KK30/ B8d2 mtl)fCttpoflmigork College of ^tPsJician^ anb burgeons! Hibrarp Pr. C.F. M^cDoYta-li A TEXT-BOOK DENTAL PATHOLOGY AND THERAPEUTICS FOR STUDENTS AND PRACTITIONERS BASED UPON THE ORIGINAL OF HENRY H. BURCHARD, M.D., D.D.S. LATE SPECIAL LECTURER ON DENTAL PATHOLOGY AND THERAPEUTICS IN THE PHILADELPHIA DENTAL COLLEGE REWRITTEN BY OTTO E. INGLIS, D.D.S. PROFESSOR or DENTAL PATHOLOGY AND THERAPEUTICS IN THE PHILADELPHIA DENTAL COLLEGE FOURTH EDITION, THOROUGHLY REVISED ILLUSTRATED WITH 671 ENGRAVINGS AND A COLORED PLATE LEA & FEBIGER PHILADELPHIA AND NEW YORK 1912 d^cwOciu. ^u.^^-^ hn^i:^. i?\^ ■ Entered according to the Act of Congress, in the year 1912, by LEA & FEBIGER in the Office of the Librarian of Congress. All rights reserved. THIS VOLUME IS RESPFXTFULLY DEDICATED TO RUSSELL H. CONWELL, D.D., LL.D. IX RECOGXITION OF HIS UNSELFISH EFFORTS IN THE OPENING OF OPPORTUNITIES FOR EDUCATION PEEFACE TO FOURTH EDITION As Stated by the Author this vokime was designed as a text-book of the principles and practice of dental medicine for the use of students, and as a reference work on applied special pathology and therapeutics for the use of dentists. Accepting the dictum of the advanced teachers of the day, he considered that an entirely rational system of dental medicine could have but one basis— namely, the same principles which underlie general medical and surgical practice. The book represents, therefore, an attempt at formulating, from data obtained from every available source, a system of dental pathology and therapeutics of which the several parts shall be in harmony with one another and also with the several collateral sciences involved. The impulse prompting the work was no desire to multiply books, but arose from a conviction expressed by many teachers, that such a volume was needed by students, practitioners, and teachers. In revising the work for this new edition, the Editor has endeavored to maintain the original idea of a text-book furnishing a description of each dental disease and its treatment in such manner that teachers may find it a useful adjunct in the presentation of dental pathology and therapeutics to their students. The development in this branch of dental science during the last few years has necessitated many changes in the text to reflect the present advanced position of the entire subject. ]\Iany new illustrations have been added to increase its value for didactic purposes. In place of the original section on Pharmacology, which was necessarily limited in scope, the various remedies and drugs men- tioned are fully indexed in order that their various uses as applied to the therapy of the pathological conditions discussed may be studied. vi PREFACE TO FOURTH EDITION The thanks of the Editor are due to those who have kmdly loaned vakiable illustrations. In no instance has a request been denied. The Editor also takes this opportunity to express his warm appreciation of the continued favor bestowed on this work by professors and teachers of the subject throughout this Continent and in Europe. O. E. I. 1524 Chestnut Street, Philadelphia. CONTENTS SECTION I GENERAL PATHOLOGY CHAPTER I General Prixciples 17 CHAPTER II Causes of Disease, General and Local 27 CHAPTER III Microorganisms as Exciting Causes of Disease 34 CHAPTER IV Disturbances of Nutrition 61 CHAPTER V Disturbances of the Vascular System 107 SECTION II E.MBRYOLOGY, ANATOMY, AND HISTOLOGY CHAPTER VI The Development, Anatomy and Histology of the Jaws and Teeth 147 CHAPTER VII Dentition: Its Progress, Variations, and Attendant Disorders . 185 CHAPTER VIII Malformations and [Malpositions of the Teeth 229 viii CONTENTS SECTION III AFFECTIONS OF THE ENAjNIEL AND DENTIN CHAPTER IX Abrasion, Erosiox, axd Stains 283 CHAPTER X Stains of the Enamel and Dentin 312 CHAPTER XI Dental Caries: History; Exciting and Predisposing Causes . 320 CHAPTER XII Dental Caries: Pathology, Morbid Anatomy^, and Clinical History 342 CHAPTER XIII Dental Caries: Diagnosis, Symptoms, and Prognosis 373 CHAPTER XIY Dental Caries: Therapeutics and Prophylaxis 395 SECTION IV DISEASES OF THE DENTAL PULP CHAPTER XV Constructive Diseases 423 CHAPTER XVI Destructive Diseases of the Dental Pulp 444 CHAPTER XVII Methods of Removal of the Dental Pulp and Root-canal Filling 490 CHAPTER XVIII Gangrene of the Pulp 537 CONTENTS ix SECTION V DISEASES OF THE PERICEMENTUM CHAPTER XIX Septic Apical Pericementitis (Acute) 561 CHAPTER XX Chronic Septic, Purulent, Apical Pericementitis (Chronic Apical Abscess) 584 CHAPTER XXI Non-septic Pericementitis 614 SECTION VI PERICEMENTAL DISEASES BEGINNING AT THE GUM MARGIN CHAPTER XXII Gingivitis 641 CHAPTER XXIII Salivary and Serumal Calculus 658 CHAPTER XXIV Pyorrhea Alveolaris 678 CHAPTER XXV Pericemental Abscess 708 CHAPTER XXVI Reflex Disorders of Dental Origin 715 CHAPTER XXVII Infections of and from the Mouth, and Sterilization .... 729 DENTAL PATHOLOGY AND THERAPEUTICS SECTION I GENERAL PATHOLOGY CHAPTER I GENERAL PRINCIPLES General pathology {pathos, disease, and logos, a discourse) is that branch of science which treats of the modifications in function and changes in structure occurring in disease. It embraces all patho- logical processes occurring in the human body, and as many of these occur in and about the teeth, modified only by the peculiar anatomy of the parts, Dental Pathology may be said to be that branch of dental science which treats of modifications in function and changes in structure occurring in the diseases of the teeth and associate parts. This being true, it follows that the study of dental pathology must be preceded by a study of the general disease processes which affect the tissues of the body, and such of these as are applicable to the study are known as the General Principles. The word Therapeutics is derived from the Greek therapeuin, to take care of, meaning the measures adopted to remedy or remove the changes induced by pathological processes. The study of the pathology of a part begins with a study of its anatomy and histology, then naturally follows a study of its physi- ology and embryology. These form the basis from which degrees of abnormal function and altered structure may be judged by com- parison with similar processes occurring in other parts of the body. The body is composed of cells held together by intercellular sub- stance. These cells are the essential functionating parts of the organism; each cell is composed of a small mass of protoplasm containing in nearly all cases a nucleus, and has a form adapted to 2 18 GENERAL PRINCIPLES its environment and function. The exact chemical composition of protoplasm is unknown and efforts at analysis destroy its peculiar property as a substance exhibiting a sequence of phenomena called life. It is a \iscid substance composed physically of a network, the spongioplasm, containing a slightly more fluid substance, the hyalo- plasm.^ Chemically it is 70 per cent, water containing a collection of proteids, and differs as to these in the different classes of cells. Proteids are but imperfectly understood, but are known to consist essentially of carbon, hydrogen, oxygen, and nitrogen, combined with sulphur and other varying elements in enormous molecules approximately represented by the formula ^'°' ^ C400H310O120N50S." This formula represents merely the quantities of these elements, which are probably combined into various chemical compounds in the cell, including one or more carbohydrate radicals, and each having its peculiar affinity for food materials, capacity for energy or function, and reduc- tion of waste or useless cell material. The study of the properties of cell protoplasm P^ZXr;'""™,:; '^^r ^e made by observing in dtu the N, nucleus. action of Hviug cells under normal con- ditions, and when subjected to artificial stimuli, and by observing the action of free single cells, such as an ameba, under like conditions. If a drop of water be taken from the sides or bottom of an aqua- rium, placed on a slide and covered with a cover-glass, and then placed under a microscope with, first, a j" objective, there will be noted at some portion of the fluid a small transparent mass having the appearance of a colorless fragment of jelly; this is an ameba. The outline of the mass may have almost any form. At some por- tion there will be a defined and easily distinguished spot, the nucleus; at another point a vesicle is seen; the body of the ameba appears to contain numbers of fine granules. The nucleus appears more mark- edly granular than the body of the ameba. If kept under obser- vation, the ameba will be seen to change its outlines; at one or more and it may be in several places, projections like blunt arms or feet are seen to be extending from the ameba (Fig. 1). On account of their appearance they are called by the physiologist pseudopodia, from psrudo, false, and pous, a foot— false feet. These changes of form are much varied (Fig. ?.). The cell has, therefore, the property > Kirke's Physiology. 2 Schoficld: Elementary Physiology. PROPERTIES OF CELLS 19 of altering its form — i. e., it has mobility and contractility. If the temperature of the slide be raised the movements of the cell become more rapid, and if raised to a temperature of 55° C. the cell contracts in a round lump; it responds to stimuli, and has therefore the property of irritability. Fig. 2 Ameboid movement of a white blood corpuscle of man; various phases of movement. (Klein.) When certain solid substances contained in the water come in contact with the ameba, the latter is seen to flow around and engulf them; as is shown in Figs. 3 and 4, where the analogue of an ameba, a leukocyte, has taken in bacteria (phagocytosis). After a time the ingested body is found to have disappeared; it has been digested. Evidently the cell must produce a substance capable of dissolving some foreign substances — i. e., it has the function of secretion. This is due to a digestive enzyme analogous to trypsin, which has been experimentally isolated from ameba. ^ More than this, the ameba Fig. 3 Fig. 4 Fig. 3. — Leukocyte of a frog from theneighbor- hood of a piece of the lung of a mouse infected with anthrax, about forty-two hours after the piece of lung had been placed under the skin of the frog's back. The leukocyte is in the act of eating up an anthrax bacillus. (Brunton, after Metchnikoff.) Fig. 4. — The same leukocyte a few minutes later, after it has completely enveloped the bacillus. (Brunton, after Metchnikoff.) does not take in substances indiscriminately; some it rejects. All cells change the chemical nature of the media in which they grow, both by exhausting the nutritive supply and ejecting their excreta. If the observations are continued, it will be noticed that changes occur in the nucleus of the cell. A series of alterations in its figure are noted, as shown in Fig. 5. Two nuclei are formed, and soon the body of the cell divides and two cells appear — the ameba has repro- duced itself. This primitive cell has, therefore, the properties of 1 Hiss and Zinsser; Text-book of Bacteriology. 20 GENERAL PRINCIPLES irritability, contractility, secretion, and excretion (as will be seen in later studies), and reproduction; moreover, it responds to stimuli, as seen on warming the stage. If the stage be cooled, the movements of the protoplasm are lessened, and when foreign substances come in contact with the cell it fails to encompass them — its irritability and contractility are lessened. It is noted that some simple cells are attracted and stimulated by light; others are repelled by it. If a mild induction (interrupted) current be passed through the water in which the ameba is, the movements of the cells are checked; Fig. 5 Forms assumed by a nucleus in dividing: a, resting nucleus; b, skein-form, open stage; c, wreath-form; d, aster, or star-form; e, equatorial stage of division; /, separation more advanced; g and /(, star and wreath forms of daughter nuclei. (Reduced from Flemming's drawings in the Arch. f. Mik. Anat.) if a strong current be passed, the cell contracts sharply. If a gal- vanic (constant) current be passed, movement at first ceases, but pseudopodia are extruded toward the cathode and the cell crawls toward that pole.^ The cell responds to mechanical stimuli, such as violent shaking, by contraction. 2 If substances such as ether or chloroform are added to the fluid, the irritability of the cell is so lessened that it does not respond to stimuli. It is either chilled by evaporation or actually anesthetized. If the supply of oxygen be cut off, or if carbon dioxid be admitted to the fluid, movement ceases and the cell remains contracted. These examples serve to illustrate that protoplasm responds to stimuli of physical and chemical nature, and that its functions may be altered by substances which are brought in contact with it. > O. Hertwig: The Cell. " Ibid. PROPERTIES OF CELLS 21 Upon these facts depends the practice of therapeutics, in which stimulation or sedation is usually aimed at. A living organism, it will be seen, has a certain degree of action and function. The general average of its action and function is spoken of as a condition of health. When from any cause the func- tions are raised or lowered from the general average, a condition of disease exists. Stimulation. — Certain agencies applied to the cell increase its activity; this is called stimulation. The movements of the cell become more rapid, food particles are taken in more rapidly and disappear more quickly; irritability, contractility, and secretion are increased. The cell subdivides, or reproduces more quickly. In- crease the stimulation, and the vital activity becomes fretful; in some cases cell division is incomplete — the nucleus divides, but not the cell body. Increase the stimulation beyond this degree, and the wearied cell ceases its movements — refuses to respond; is paralyzed by overwork. Sedation. — If the conditions be reversed; if, instead of applying a stimulus to the cell, an opposite influence be introduced, the phenomena are reversed. If the temperature be reduced, the movements of the cell become sluggish; the body changes its form more slowly and less extensively — i. e., contractility is lessened; particles taken into the cell remain apparently unchanged; irritability, secretion, and excretion are lessened; and, furthermore, reproduction does not occur nearly so rapidly — that is, the cell in contact with sedative influences has all of its activities lessened. There are two great classes of influences, then, which aft'ect the vitality of cells: stimulation, which, if continued long enough, leads to death through overwork; and sedation, which, if continued, paralyzes all the energies of the cell — it is starved to death. Every cell has a range of resistance to these influences which tend to destroy it, which is fitly termed the resistance of vitality. Disease itself is some alteration in any one or more of these several cell proper- ties, of irritability, contractility, growth, secretion, maintenance, or reproduction. If any one of these properties is not exhibited, it is said that the cell is diseased. If a brood of cells derived from one parent be examined, some will be seen to grow more rapidly than others, their movements are more rapid and they reproduce more quickly; others have sluggish functions and movements. The cell lives its cycle and reproduces, and the parent is no more, the life being continued in the offspring. 22 GENERAL PRINCIPLES The life and properties of this small mass of protoplasm represent in miniature the primitive functions and life of the highest animals. The contractility is represented in the motive apparatus of the higher animals. The reception, engulfing, and dissolving, or casting out, of bodies with which the ameba is brought in contact correspond in the higher animals to the digestive apparatus and process and the excretory function. This digestion is perhaps more analogous to body cell action in its reception of food from the blood and further digestion by enzymes in the cell and by cell excretion. The highly evolved irritability is represented in the nervous system of the higher animals. The movements occurring in and about the vacuole are the pro- genitors of the circulatory apparatus and all of its adjunct organs. If the irritability of a simple cell be increased or diminished, it corresponds to a disease of the nervous system, and so with the other functions. In the human body certain collections of cells are found in which one function is active, the others in abeyance; thus, large colonies of cells exist in which contractility is the dominant property noted; these are muscle cells. Others have but the property of irritability; these are nerve cells. Still others develop peculiar chemical functions, and become glandular or secretory cells. Such collections of cells are known as tissues. These special cell colonies or tissues are built together into defined masses for the performance of their specialized functions. In the development of these masses, means of holding and maintaining the cells in definite mass forms and provisions for their food supply and waste-removing apparatus are provided in what are called the connective tissues, binding the cells in definite forms and transmitting their vascular supply (food- and waste-carrier). When thus bound together the tissues are said to form organs. While all tissues are capable of analysis into cells and intercellular substance, a more practical view may resolve the tissues into (1) func- tional cells; (2) a supporting intercellular substance; (3) intercellular spaces in which flows the lymph derived from the blood ; (4) the chan- nels of circulation and conductors of nervous impulses — i. e., arteries, capillaries, veins, lymphatics, and nerves. The arteries bring to the tissues the blood freighted with oxygen and nutrient material. As it passes through the capillaries a portion of the blood plasma, under arterial pressure and osmotic force, passes into the intercellular spaces into contact with the cells. This exuded fluid is now called lymph. Stated in general terms, the food materials contained in arterial NUTRITION 23 blood and furnished to the tissues by way of the lymph are water, proteids, ghicose and fats or their elements, inorganic salts, and oxygen. From this store the cells take what they require, and within themselves they elaborate substances essential to their growth and maintenance as masses of functionating protoplasm, and as the pro- toplasm is of more complex composition than the majority of food elements, they are said to form from simple compounds substances of a higher degree of complexity (anabolism). From their substance the cells eject into the lymph stream such waste products as result from the breaking down of the pre\dously formed protoplasm (catabolism). The total process is termed metabolism. While the exact nature of the chemical change occurring in cells is not known, the present thought is that much of the process of cell metabolism is conducted within the cell through the action of one or more enzymes which have the power of catalytically effecting prompt and smooth chemical changes at low temperature which can at times be produced in the laboratory only by complicated experi- ments not at all comparable with the action of cells. Various organs of the body evidently prepare the food material absorbed by the intestines for the use of the cells — for example, gly- cogen is formed from the absorbed glucose by the ferment of liver cells, and when needed again is transformed into glucose. Ehrlich's side-chain theory for immunity (which see) presupposes the presence of atom groups of protoplasm surrounding a complex group of atom groups, the nucleus, each atom group having affinity for a particular form of substance presented to it. These he terms receptors, and each is supposed to possess a combining or prehending group of atoms called an haptophorous group and a ferment group capable of altering the chemistry of the food element to suit its needs or that of the cell as a whole; this latter group is termed a zymoph- orous group. This obviously is merely stating in a scientific manner that the cell receives and digests food materials. The carbohydrates and fats are in the main the producers of energy, and are, lastly, resolved into glucose and fat or their elements for the consumption of the cells, and by them appropriated into their protoplasm, whence, by catabolic changes, they are started upon their retrogressive course to the final products CO2 and water. The proteids are mainly useful for the building of the cell protoplasm and its maintenance, and when catabolized end in products which in other organs are transformed into urea and uric acid. Experimental evidence has shown that after energy has been liberated to the point of fatigue, there is an actual loss of substance by the cells, in consequence of which they become smaller and of different histological appearance. 24 GENERAL PRINCIPLES It is evident, therefore, that any condition which will produce an expenditure of energy without a compensating restoration of cell material must result in a malnutritional process. There is evidence that changes occur in the cell waste either in the blood or in various organs of the body. While, then, the bodily ejecta contain substances fairly constant in composition, they are held to represent elaborations of cell waste rather than actual cell ejecta. For example, urea is pretty certainly derived from muscular tissue, 3'et is nearly absent in muscle and is supposed to be due to the dehy- dration of ammonium carbonate in the liver.^ Lactic acid and ammo- nium carbonate have been experimentally shown to be probably com- bined into uric acid in the liver. The cell waste is carried by the lymph into the lymphatics connecting with the intercellular spaces. Thence it is delivered by way of the venous system to the circulation for further elaboration and elimination from the body. Any inter- ference with such elaboration or elimination must of necessity result in a retention of waste products within the system, probably leading to irritation and disturbance of metabolism in all cells. Cell naetabolism is a chemical change and is therefore accompanied by heat production. Energy is stored up in the cell as latent force capable of liberation under stimulus, which force is expressed in various forms of functional activity — i. e., contractility in muscular tissue, irritability and mentality in nervous tissue, secretion in the various secretory glands, eliminative selection in the various excretory organs, etc. Cells after a period of activity undergo degenerative processes, and are removed or reproduced by the process of mitosis (Fig. 5). The life conditions of cells are necessarily those under which they best perform these functions without exhaustion, and are the following : (1) A proper food supply, including water and oxygen; (2) a proper removal of waste products; (3) proper physical conditions, includ- ing a proper temperature; (4) possibly a proper innervation. Any interference with these conditions, which may be termed the normal physiological conditions, results in a morbid process of physiology or pathology in its limited sense. With such interference disease may be said to begin. The definition of disease as an alteration of nutrition is therefore appropriate. For this reason the proximate exciting causes of disease are classed as (1) abnormal food supply; (2) abnor- mal waste removal; (3) abnormal physical conditions; (4) abnormal nerve supply. The morbid physiology results in morbid products or in retained ' Kirke's Physiology. DISEASE 25 normal products and an altered cell function. When pronounced this is spoken of as Functional Disease, although it may he said to be in existence even if discomfort be not produced. Sooner or later an abnormal change in the histological characteristics of the cells or intercellular substance may occur which has been referred to as ]\Iorbid Histology or Pathological Histology. As definite micro- scopic and often macroscopic appearances are associated with certain diseased conditions, these are referred to as the Morbid Anatomy of a Disease or Pathological Anatomy. The phenomena associated with a disease are called its Semeiology {semeion, a mark or sign) or Symp- tomatology, and are either described by the patient as sensations or pains of varied character or situation (Subjective Symptoms), or may be noted by normal or aided vision, by physical examination, or chemical analysis (Objective Symptoms). That which excites a disease or promotes the action of the excitation is called a Disease Cause. The study of disease causes is Etiology {actios, a cause, and logos). It is noted that diseases having a fairly defined pathology and morbid anatomy have from their beginning to ending tolerably constant phenomena; they have each a natural history; this is called the Clinical History of a Disease. The study of the origin and development of a disease together is known as its Pathogenesis {pathos, disease; gennao, I produce). Through the study of the characteristic symptoms of diseases, as well as those common to several diseases, a particular disease may be distinguished. This is called Diagnosis {dia, through; gignosko, I know)— Direct Diagnosis when there is no question as to the symp- toms, Differential Diagnosis when several diseases are possible and the characteristics of one are considered as more pronounced. Under certain circumstances a disease may be inferred to be present by excluding all other possible conditions (Diagnosis by Exclusion). In the course of a disease experience has shown that certain signs and symptoms are apt to be followed by good or ill results, as the case may be. By these signs and symptoms it may be foretold with some degree of assurance what will be the probable outcome of the disease. The inference based upon these symptoms is known as the Prognosis {pro, before, and gignosko, I know). The care of or treatment of a disease is its Therapeutics. This involves a knowledge of remedies applicable, known as the ^Materia ]Medica. When applied upon the basis of a scientific study of the pathogenesis, clinical history, and prognosis of disease and a parallel knowledge of the physiological action of drugs and of other remedies, the treatment is known as Rational Therapeutics. AMien the treatment is based upon the 26 GENERAL PRINCIPLES known good effects of a remedy in a certain disease, and not upon its physiological action, it is known as Empirical Therapeutics. The pathogenesis of a disease being known, intelligent efforts may be exerted for its prevention. The causes may be removed or neutral- ized before they have an opportunity to act; this is Prophylaxis. The science of prevention of disease upon the broad basis of a knowledge of disease causes and observance of laws of health is Hygiene. It will be seen that a knowledge of special pathology can only be obtained from (1) a knowledge of pathology in general or at least of those principles of general pathology which underlie all disease pro- cesses; (2) a knowledge of the local anatomy and histology; (3) a knowledge of local embryology and physiology; (4) a study of local pathology and morbid anatomy. To this must be added a study of materia medica and special therapeutics. CHAPTER II CAUSES OF DISEASE, GENERAL AND LOCAL A DISEASE cause may be defined as any influence of whatsoever nature which is capable of disturbing the nutritive balance of any portion of the body. The branch of study which deals with the causes of disease is called Etiology. The causes of disease are classed as Exciting (or Determining) and Predisposing. These are each divisible into Extrinsic, originating from without, and Intrinsic, originating within the body. EXCITING CAUSES OF DISEASE These are influences, either extrinsic or intrinsic, which are com- petent to suddenly or gradually interfere with the nutrition of the cells of a part or with the general nutrition of cells. These influ- ences are very numerous, but may be grouped according to their action under a few convenient headings: (1) Abnormal Food Supply. (2) Abnormal Waste Removal. (3) Abnormal Physical Conditions. (4) Abnormal Nerve Supply. These are termed the Proximate Exciting Causes, as their effects are immediately exerted upon the cells. Other causes may be back of these and are spoken of as Primary (or Contributory) Causes — e. g., tuberculosis of the lungs (primary) may cause insufficient ox}'genation of the blood which constitutes an abnormal food supply (proximate) . Abnormal Food Supply. — By abnormal food supply is meant an altered quantity or quality of nutritive elements delivered to the cells either of a part or of the entire body. The primary causes of this may exist as disturbances or faults in any of the food-elaborating organs, the lungs, the eliminating organs, or the oxygen carriers of the blood may exist in lessened numbers. In the first case the quality or quantity of nutritive material is impaired, in the second and fourth cases oxygenation is insufficient, and in the third case materials in- jurious to cells are retained in the body and are again presented as food to the cells, acting as poisons. Poisonous or even non-poisonous drugs, and the products of bacterial action, whether absorbed from 28 CAUSES OF DISEASE, GENERAL AND LOCAL the intestines or from foci of infection, have all more or less delete- rious action upon cell protoplasm, violent if entering the blood in quantity, chronic if entering continuously. Faults in the circulatory apparatus interfering with the circulation generally cause an interference with general nutrition, while local disturbances of the circulation from any cause disturb the relations of the blood supply to the nutrition of a part. Thus the fresh blood supply (food supply) to a particular location may be excessive, as in the milder form of arterial hyperemia, or deficient, as in venous hyperemia and inflammation. Abnormal Waste Removal. — Abnormal waste removal is ordinarily included under the heading of abnormal food supply, and it is evident that retention of waste in the blood causes the presentation to cells of an abnormal food or poison. In local conditions, such as venous hyperemia and inflammation, the stasis causing waste reten- tion prevents the access of a fresh food supply as well. In kidney disease the substances ordinarily physiologically eliminated by the kidneys are retained in the blood and act as poisons to cell proto- plasm generally. Abnormal Physical Conditions. — This class of disease causes includes all injuries due to any of the physical or chemical forces: Traumatic injuries, such as cuts, bruises, surgical openings, etc. Mechanical causes, such as compressions, obstructions to ducts or the natural outlets of the body, faults in the circulatory mechanism, stoppages in the arteries or veins. Chemical causes, such as the action of abnormal temperatures, burns, freezing, or irritations of various sorts, such as those due to mustard, arsenic, acids, or caustics, and the local effects of microorganisms may all be classified under this heading. The disturbance is due to either a direct destruction of the life of the cells or an interference with the circulation in a part. Abnormal Nerve Supply. — It is known that division of, injury to, or disease of certain nerves causes trophic or nutritional changes in the part to which they are supplied. Whether the nutrition of the parts is controlled by special trophic nerve fibers has not been demonstrated. Halliburton,^ in support of the trophic infiuence of nerves, instances that when the fifth nerve (sensory) is divided beyond the Gasserian ganglion, ulceration of the cornea results; while if the seventh nerve (motor) be divided or paralyzed, the eye- ball is equally exposed to irritants, yet does not ulcerate. He also instances that division of the vagi produces fatty degeneration of the heart. 1 Kirke's Physiology. PREDISPOSING CAUSES OF DISEASE 29 While admitting the lack of anatomical proof, he regards the trophic influence of nerves upon parts to be unexplainable upon the ground taken by others, that all apparently trophic changes are due to disturbances of the vasomotor nerves controlling the caliber of vessels. According to these other observers degrees of dilatation are produced which modify the amount of blood delivered to a part and thus modify its nutrition. Effects are produced upon nutrition by causes which can act only through the nervous system — e. g., the effect of anxiety upon appetite and digestion. The interdependence of these classes of causes is almost self-evident; for example, constant suppuration at a focus of infection (abnormal physical condition) may induce a toxemia (abnormal food supply) which may be responsible for kidney or other disease (abnormal physical condition), resulting in the retention of waste products in the blood (abnormal waste removal or food supply), which has a vicious result upon all metabolism, including that of the nervous system, inducing in turn an abnormal nerve supply and lessening resistance even in the tissues about the original focus of infection. Such a train of events is known as the establishment of a vicious circle. ' PREDISPOSING CAUSES OF DISEASE A predisposing cause of disease is one which influences the cells or juices of the body or part in such a manner as to lessen the resistance to the action of the exciting causes of disease. It must be considered that a predisposition or lessened resistance is in itself a condition of disease, not recognizable, perhaps, yet a departure from the standard of the best health of an individual or part. For the most part predisposition is regarded in its relation to the extrinsic causes of disease, such as bacterial influences. In such a condition the individual is said to be susceptible. Pre- disposition is either general or local. General Predisposition. — This is either (1) a natural or inherent lack of resistance to infectious or non-infectious diseases, or (2) an acquired lack of resistance to infectious or non-infectious diseases. The human race in general is naturally predisposed to many infec- tious diseases, such as tuberculosis, cholera, malaria, measles, small- pox, typhoid fever, scarlet fever, and syphilis.^ When a person is exposed to the disease and contracts it, he is said to be predisposed I Ziegler; General Pathology. 30 CAUSES OF DISEASE, GENERAL AND LOCAL to it. If he does not contract it, his system is immune either tem- porarily or permanently. (See Immunity.) There being several forms of immunity, the lack of any natural form may be considered as a predisposition. This immunity is ordinarily operative when the individual is in the best state of health, and when a departure from this standard is brought about by any cause, exciting infective causes may then act. This is acquired predisposition. Some individuals have a natural or congenital lessened resistance to external influences of a non-infectious character, such as heat or cold, mental effort, or nervous irritations of a degree ordinarily borne by the great majority of individuals. This may also be acquired, as, for example, by extreme subjection to the above or other enervating causes. An inherited predisposition to such diseases as insanity, cancer, or gout may exist. Some persons cannot bear certain kinds of food without illness, or react strongly to small doses of drugs, or are not affected by large doses. This is called an idiosyncrasy, and may be either congenital or acquired. The predisposing causes capable of producing a lessened resist- ance may be grouped under a few headings. Sex as an Intrinsic Predisposing Cause. — In this connection the influence of sex upon predisposition to disease must be considered. ^^^lile the general resistive power of the bodies of both sexes may be regarded as practically equal under similar conditions, yet the anatomical structures and physiology of each sex have an influence upon predisposition to certain diseases. Aside from the diseases peculiar to sex, on account of their peculiar organs, each sex exhibits predispositions to diseases which the other sex escapes; for many of these the habits of life furnish an explanation, for others an ex- planation is not available. For example, males are much more subject to hemophilia than female. Age. — During the first two years after birth the nervous system and the appendages of the alimentary canal are developing, and improper feeding, difficult teething, or other influences readily act as exciting causes of alimentary or nervous disturbances. Later, children are subject to acute infectious diseases, especially tuberculosis, diphtheria, and the eruptive fevers. At adolescence other predispositions occur, notably chlorosis in young girls. Later come the diseases of early maturity, such as typhoid fever, pulmon- ary tuberculosis, and to a degree dental caries. In old age or middle life occur arterial and other degenerations and diseases consequent upon them or upon overstimulation of organs or tissues. PREDISPOSING CAUSES OF DISEASE 31 Temperament.- — Temperament is the peculiar congenital consti- tution of an individual imparting certain physical characteristics and certain natural tendencies. There are four basal temperaments: The sanguine is that in which individuals are decidedly inclined to the blonde type with evidence of an abundance of the nutritive fluid, the blood — i. e., the vascular system is said to dominate the other functions of the body. Such are predisposed to acute pul- monary and cardiac diseases and inflammatory disturbances of serious import. The mental characteristics of this temperament are hopefulness, cheerfulness, and solidity but floridity of mental endowments. The recuperative power is good. The bilious temperament is characterized by a decided inclination to the brunette type, with evidence of a domination of other func- tions by the liver. There is a tendency to hepatic and digestive derangements and despondency; at the same time there is possessed great physical and mental strength, together with a reliable recu- perative power. The nervous temperament is indicated by the smallness and delicacy of frame and the quickness of motion and perception, evidencing a domination by the nervous system to diseases of which such temperament predisposes. In such individuals disease is usually of rapid course, and recuperation is rather more rapid than reliable. The lymphatic temperament is indicated by bulk, pallor, and flac- cidity of tissue, a colorlessness of temperament, indicating an inherent feebleness. There is a tendency to serious chronic conditions. This temperament is accompanied by poor recuperative force. There are no individuals of pure basal temperament, so that the nearest approach is a dual or binary temperament, such as the biliosanguine, in which the characteristics of the sanguine predomi- nate strongly modified by those of the bilious temperament. In like manner the sanguonervous, nervolymphatic, and other classes, twelve in number, are recognized as having typical representatives in each community. A third or ternary classification is possible — e. g., sanguonervobilious. It will be seen that temperament has a distinct relation to the vital resistance normally implanted in an individual, and therefore may to a certain extent be counted upon in a prognosis. Temperament is a predisposing cause probably only in so far as it introduces a natural general lack of resistance to disease, or irresistibly drives an individual into certain habits of life which may become the cause of a lessened resistance. Heredity. — Certain diseases exhibit a predisposition to descend from parent to child direct or from grandparent through the un- 32 CAUSES OF DISEASE, GENERAL AND LOCAL affected son or daughter to a grandchild (in the latter case it is called atavistic hereditary transmission, also remote heredity). The mode of transmission is in all probability the inheritance of a type of tissue, a tissue anatomy and physiology which permit the more ready action of the exciting causes of the disease. This ten- dency is called a diathesis — e. g., hemorrhagic diathesis (hemophilia), gouty diathesis, or tuberculous diathesis. Diathesis may also be acquired. The influence of race may also be considered as coming under this heading. (See Immunity.) Existing Disease. — The presence of one disease may weaken the resistance of a part or the organism so that another disease may the more readily become implanted — e. g., measles followed by pneumonia. Previous Disease. — At a period subsequent to disease the same disease may recur or another disease may be implanted — e, g., pneumonia predisposes a lung to a recurrence of pneumonia, or tuberculosis may readily follow. Previous disease may confer immunity, as, for example, in smallpox or measles. Extrinsic Predisposing Causes of Disease. — Under this head are included all those conditions of external origin which lessen the resistance of an individual to the action of exciting causes. Excessive heat is weakening; cold and dampness, by chilling the surface of the body, cause hyperemia of internal parts and thus predispose to such diseases as pneumonia, rheumatism, etc. Fatigue, unhealthy, cramp- ing, or sedentary occupations, continued loss of sleep from any cause, evil habits, continued hunger, etc., are other examples of debilitating influences which may be partly intrinsic. Local Predisposition. — Alterations in the normal physiology of a part are apt to occur through certain actions upon it, thus bringing it into a condition of lessened resistance, permitting the action of entirely different exciting causes. Apart from this fact, a part may be predisposed, by nature apparently, to permit the growth of bacteria which do not grow well in other tissues. Local depression of tissue vitality predisposes to the growth of organisms in the tissues. Thus slight injury producing either arterial or venous hyperemia or ischemia may permit bacteria to produce even grave consequences. More severe injury also may predispose, but the contrary effect has also been observed — i. e., that severe injury excites a phagocytic reaction and copious exudation of lymph (a later stage of inflamma- tion) which antagonizes the bacteria. (See Inflammation.) The structure of a part has also been shown to have an effect upon the life of microorganisms gaining access to its tissues. The tissues about the mouth are normally notoriously resistant to infections, IMMUNITY 33 but at times are exceedingly susceptible, as in pyorrhea alveolaris. Ordinarily surgical operations about the mouth were successful in pre-aseptic times, while abdominal or gynecological operations were attended by an enormous percentage of death from infection. General depression of vitality also necessarily affects the resistive force of all local tissues. Thus extensive suppuration is more liable to occur in those rendered feeble and anemic by any cause. IMMUNITY Immunity is the opposite of predisposition, and, like it, can be either natural or acquired. It signifies an insusceptibility to a disease. Natural immunity to a particular infectious disease can only be determined by repeated exposures, and may then fail at last owing to some systemic change.^ Immunity may be exhibited toward only one disease. In some persons disease appears to be influenced by sex, as, for example, males have a general immunit}^ from goitre, females from Addison's disease. Immunity is influenced by age in certain diseases; for example, the diseases of childhood are rare in the elderly; they do occur, however. The degenerative diseases of old age are almost unknown in childhood. Race has its influence; the negro is almost immune to malaria and yellow fever, but particu- larly susceptible to smallpox and tuberculosis. The natural immunity may be more apparent than real, owing to failure of the bacteria to find a local condition favorable to development and to enter the blood. If special care in experiment be taken to introduce the bacteria, and failure of inoculation result, the natural immunity is absolute. Example: Rats to diphtheria, or negroes to yellow fever. A striking example of lost immunity occurred in the case of a friend, who, in early and middle life, could handle poison ivy with impunity. On approaching seventy years of age, and while in a condition of general debility, he was affected from head to foot with the peculiar dermatitis as the result of pulling up a plant. The further discussion of immunity as related to bacterial infection should properly be discussed after the consideration of bacterial causes, and will be found at the end of Chapter III. 1 Green: Pathology and Morbid Anatomy. CHAPTER III MICROORGANISMS AS EXCITING CAUSES OF DISEASE The infectious and contagious diseases have for the most part been shown to be caused by low forms of vegetable organisms known collectively as fungi, while in a few diseases minute animal organisms (protozoa) are the causes. The following table shows the position of the vegetable organisms in the scale of vegetable life and gives the lowest forms of animal life: Phanerogams: plants reproducing by flowers and seeds. Vegetable kingdom Cryptogams, reproducing by spore formation or division. Leafy cryptogams. Thallophytes, having no dis- tinction be- tween the leaf and stem, Lichens. Algse. Fungi . (Cocci. I Bacilli, y Bacteria. Spirilla. J Hjrphomycetes (mould fungi). Blastomycetes (bud fungi). Animal kingdom Lowest forms " Sarcodinea. Flagellata. Sporozoa. Infusoria. Mycetozoa, fungi not certainly defined as animal or vegetable "~ forms. 1 Higher forms. Certain insect and worm forms are pathogenic. Protozoa: single cells without circulatory or nervous systems. Fig. 6 Trichophyton tonsurans ("barber's itch"). Diagram- matic. (Lehmann.) Of the protozoa four classes are known, though but few species are pathogenic; these classes are (1) the sarcodinea (ameboid), which includes the ameba coli of dysentery (Fig. 10); (2) the flagellata, non-ameboid but motile by means of flagella; (3) the sporozoa living within the bodies of other animals, a class which includes the hemo- sporidia, ameboid motile parasites living in the blood, and of which the malarial germs, plasmodium malarise (quartan fever, seventy-two-hour cycle), the plasmodium 1 The terms mycetozoa and protozoa seem to be practically synonymous to pathologists, who use the term protozoa in the sense of mycetozoa as above defined. MICROORGANISMS AS EXCITING CAUSES OF DISEASE 35 praecox (estivo-autiimnal fever, twenty-four or forty-eight-hour cycle, Fig. 11), the cytorrhyctes variolse seu vaccinae (the probable cause for smallpox and chickenpox) are examples; (4) the infusoria. Fig. 7 Fig. 8 Penicillium with spores. (Lehmann.) a, saccharomyces; b, cell with four spores. (Lehmann.) Fig. 9 Fig. 10 Saccharomyces albicans. (After Grawitz, in Lehmann.) 1, ameba from dysenteric stool, with vacuoles and enclosed red cells; 2, ameba from straw infu- sion; 3, the same encysted. X 600. (Kiinster.) 36 MICROORGANISMS AS EXCITING CAUSES OF DISEASE The vegetable fungi are divided into (1) schizomycetes, or fission fungi; (2) hyphomycetes, or mould fungi (Figs. 6 and 7); (3) blasto- mycetes, or bud fungi (or yeasts) (Figs. 8 and 9). Being without Fig. 11 Plasmodium precox (forty-eight hours). Cycles of estivo-autumnal parasite: 1, very young form; 2, infection of one cell with seven young parasites (drawn from a marrow smear); 3, triple infection, two parasites joined by single chromatin mass; 4, double infection, peculiar rings with two chromatin grains at opposite poles; 5, double infection, small ring adherent to cell; 6, 7, signet- ring forms, subdivision of chromatin; 8, 9, later ring forms, with subdivided chromatin and few pigment grains; 10 to 12, full-grown forms, with finely subdivided chromatin and gradual concen- tration of pigment; 13, 14, stages of presegmenting forms, with concentrated eccentric pigment; 15, double infection, with separate presegmenting bodies; 16, estivo-autumnal rosette; 17, 18, young crescent and ovoid; 19, ''pulsating" crescent; 20 to 22, various forms of crescents; 23, two bows about single crescent; 24, fully developed crescent, two masses of chromatin, achromatic substance, double wreaths of pigment; 25, diagrammatic flagellating body; 26, extracellular sterile body. (Schmaus and Ewing.) chlorophyl (the green coloring matter of plants which synthesizes CO2 and water into starch), the fungi are unable to utilize the simple compounds, such as carbon dioxid and ammonia, as foods, and are MICROORGANISMS AS EXCITING CAUSES OF DISEASE 37 therefore compelled to break down the complex organic compounds, for which purpose they are competent by reason of their enzymes. All three classes of fungi have representatives which produce disease in the human body, but the schizomycetes furnish by far the greater number of infectious disease causes. Fig. 12 a, spiral forms with a flagellum at only one end; b, bacillus of typhoid fever with flagella given off from all sides; c, large spirals from stagnant water with wisps of flagella at their ends (Spirillum undula). (Abbott.) Chemically, bacteria are about 85 per cent, water, together with albumin called mycoprotein, ferments, soluble extractives, salts, sometimes niiclein bases, coloring matters, organic acids, sulphur, starch, and cellulose. Fig. 13 Typhoid bacilli stained by Van Ermengem's method to show flagella. The schizomycetes (Greek sckizo, to split, and muhes, a fungus) are minute single-celled plants without nuclei, but possessed of a cell wall and cell protoplasm (mycoprotein). They have a size of about 1 micron (1 /<= 250 on inch) or less in their smallest diameter. Some of them possess flagella, hair-like processes, often very numer- 38 MICROORGANISMS AS EXCITING CAUSES OF DISEASE ous, arising from the protoplasm rather than the wall, with which they lash the fluid surrounding them, and by which means they effect locomotion (Fig. 12). Other bacteria again are non-motile. Entering the organic compounds, carbohydrates, hydrocarbons, and nitrogenous (albuminous) substances, they ferment or decompose them, forming new products, and extract from them substances oo od6o iSo3<^ Fig. 14 00 ' %00 00 o°. 00 fc o°0 »o^ Q?o a, staphylococci; &, streptococci; c, diplococci; d, tetrads; e, sarcinse. (Abbott.) Fig. 15 necessary to their growth and subsequent reproduction. The sub- stance in which they thus grow is called the medium or soil. The conditions under which this is accomplished are: (1) The fungi must have a proper vitality. (2) Their food supply or soil must be suited to their growth and must be moist— in general terms they require water, CNO, and salts. (3) The temperature must be suitable; they grow more actively at about 102° F.; at 160° F. maintained they usually die, but in some cases, as with the typhoid bacilli, they may live in the spore form at even 212° F. or over unless main- tained for some time. Some that develop best at high temperature are called ther- mophilic. Low temperature, as 32° F. or far below that, inhibits their growth, but does not necessarily kill them. (4) Their waste products must be removed or they die in them. This is said to be due to the reaction, whether acid or alkalin, and not to any of the other by-products — e. g., in lactic fermentation 2 per cent, of lactic acid is about the greatest amount endured by them. They are also sensitive to and inhibited by agitation, daylight, electric light, and electric currents. Morpho- logically the schizomycetes are grouped into several classes accord- ing to form. Zooglea of bacilli. (Abbott.) MICROORGANISMS AS EXCITING CAUSES OF DISEASE 39 1. Micrococci {niikros, and kukkos, a berry), including all of the spherical forms or those having equal or nearly equal diameters (Fig. 14). 2. The bacilli {hacillum, a rod) or rod-Uke forms; one diameter being greater than the other (Fig. 16). 3. The spirilla (Greek spira, a coil), or the curved forms (Fig. 17). All of these groups may again be subdivided. The micrococci are subdivided according to their modes of grouping. Double cocci are Fig. 16 ah c d a, Bacillus subtilia with spores; 6, Bacillus anthracis with spores; c, Clostridium with spores; d, bacillus of tetanus with spores. called diplococci {diploos, double). If in division the cocci agglom- erate like a bunch of grapes, they are called staphylococci (staphyle, a grape). If they arrange themselves in a chain, they are called streptococci {sireptos, a chain). If they divide in two directions and form a bunch of four cocci, they are called tetrads. If in three direc- tions, they form sarcinse. The bacilli are of many and varied forms, and differ as to their mode of grouping. During reproduction bacteria may excrete a material which unites them into a gelatinous mass called zooglea. Fig. 17 a b a, spirillum of Asiatic cholera (comma bacillus) ; 6, involution forms of this organism as seen in old cultures. (Abbott.) The bacilli in the course of reproduction may form long threads, showing, as a rule, the traces of segmentation. Under certain unfa- vorable conditions of development many bacilli form glistening oval bodies within themselves (endospores) which resist stains. The body of the bacillus may disappear, leaving the spore only. These spores are very resistant to devitalizing agents. The bacilli forming spores are said to be in the resting stage. These spores under favor- able conditions again form bacilli like their progenitors, but do not 40 MICROORGANISMS AS EXCITING CAUSES OF DISEASE form other spores without this return to the bacillus form. A single cell forms, as a rule, but one spore. Some bacilli do not form spores (Abbott). If the entire bacterium is changed into the spore form they are called arthrospores; when cocci take on the appearance of spores they are also called arthrospores. Under unfavorable conditions bacteria may undergo degeneration and take on abnormal or involu- tion forms, and when the conditions are again favorable to develop- ment they may resume their typical forms. ^ While these form changes occur, bacteria are never permanently changed from one form to another.^ Those bacteria which have several forms in their life cycle are termed pleomorphic. Those having but one form are monomorphic. Those bacteria which exist on living tissue are known as parasitic. They enter the body by way of open wounds or sur- faces deprived of epithelium, or may lodge at certain points of the mucous surface of the lungs, skin openings, or the alimentary canal. If not killed out they multiply in the natural juices of the part on which they locate and produce an infective inflammation. Poisonous substances may be generated, which are absorbed into the system and may act as poisons, producing toxemia. When the toxin is excreted by the bacteria and floats in the blood it is called extra- cellular toxin; when confined to the bacteria, it is called endotoxin. The character of both the inflammation and the poisoning depends upon the particular bacterium or bacteria present. The bacteria may in certain cases be taken into the blood, and, coming to rest at certain spots, the above-described process is repeated. The Bacillus anthracis divides in the blood stream,^ and other organisms, such as the Bacterium pneumoniae and Bacillus influenzae may exist in it. Many forms of organisms exhibit a preference for certain spots at which they flnd the conditions best suited to develop- ment — e. g., the typhoid bacillus in the glands of the ileum, Beyer's patches; the anthrax bacillus in the lungs of animals; the diphtheria bacillus in the mucous surfaces of the pharynx and contiguous parts. Those parasitic bacteria which produce disease are called pathogenic, others are non-pathogenic. The mouth offers a suitable habitat for many bacteria. The bacteria which live on dead organic matter are called sapro- phytic (sapros, rotten, and phuton, a plant). They break up the dead animal and vegetable matter into simple compounds like carbon dioxid, ammonia, etc., which are utihzed by the higher chlor- ophyllous plants. The nitrogen of the air is also utilized by some > Abbott: Principles of Bacteriology. ' Ibid. • Green: Pathology and Morbid Anatomy. FERMENTATION 41 plant bacteria, and can be introduced to aid crops. As animals are dependent upon plants for existence, their vast importance in the economy of nature is evident. Bacteria may often pass from a para- sitic existence to a saprophytic one — a fact which is utilized in their study by bacteriologists, who prepare artificial media in which to cultivate them. These are called cultures, which by transference from one culture plate to another of like kind are said to be passed through generations. When by careful segregation one form of bacterium is separated from others present in a mixed culture and thereafter cultivated alone, it is called a pure culture; when the bacteria are thinly spread on a gelatin or agar culture and then isolated, the grouped bacteria developing at each point are called a colony. Bacteria may pass from a saprophytic to the parasitic form of exist- ence. Bacteria which have this power of adaptation to a new form of medium are called facultative. When without this power, they are obligate bacteria. According to Pasteur, those which require oxygen in order to live are called aerobic. Those which cannot live in its presence are anaerobic. Those which live either way are facultative. When bacteria produce pigment either within themselves or their medium, they are termed chromogenic; when they produce light or phosphorescence, they are termed photogenic. If they have the ability to produce fermentation, they are termed zymogenic; when they produce gas they are called aerogenic. FERMENTATION Fermentation in the broadest acceptation of the term has been defined as the decomposition of substances possessing complex molecules under the influence of organized or unorganized ferments (enzymes). The decompositions occur when organic substances are exposed to the action of bacteria or their enzymes, or are subjected to the action of certain ferments such as are found in the digestive fluids secreted into the alimentary canal, which are really enzymes also derived from living cells. According to W^oodhead,^ the molecules of the fermented compound are separated from one another for a brief period and then allowed to combine and form simpler and more stable compounds. The process is accompanied by heat due to chemical changes. Ferments, then, are of two kinds: (1) Organized or formed fer- ' Bacteria and their Products. 42 MICROORGANISMS AS EXCITING CAUSES OF DISEASE ments or living bacteria which multiply at the expense of the sub- stance which they are fermenting; (2) unorganized or unformed ferments or enzymes, nitrogenous bodies produced by living cells which have the power of producing chemical changes in organic substances. They thus affect many times their own weight of the particular organic substance being fermented without being them- selves much affected, though eventually exhausted (catalysis). Typical examples are the pepsin of the gastric juice, which changes albumin to peptone, and the ferment of the yeast plant, proved capable of changing sugar into alcohol and carbon dioxid, even when the cells themselves are crushed and filtered out. The unorganized ferments usually act by oxidizing, deoxidizing, or hydrating the substance modified. They act best when their products are removed from the neighborhood. Many bacteria have been shown to possess such unorganized fer- ments. It is probable that they produce their effects on organic substances by the aid of these ferments, which serve them as pepsin serves man (extracellular ferments). It is thought that in other cases the germs take up organic food, digest it, and excrete waste products in somewhat the same manner that the body cells nourish themselves by intracellular ferments (p. 23). As a rule, more than one species of bacterium infects a fermentable substance. The more active varieties predominate in the fermentation, but mixed fermentations may proceed. In some cases the bacterial multipli- cation is favored by the activity of other bacteria, in some cases the development is retarded. Some may die out, finding an unfavorable soil. After a time the predominating bacteria may die in the waste products accumulated about them, leaving the field clear for a second or third variety. In this way progressive decompositions may occur — -e. g., the alcoholic fermentation may be succeeded by the acetic, in which the alcohol is changed to acetic acid, as in cider- vinegar formation. The nature of the chemical changes produced in a fermentable substance depends upon the chemical nature of the latter and upon the nature of the fungus causing the fermentation. Thus, in an infusion of vegetable juices containing sugar a yeast fungus (one of the blastomycetes) will produce carbon dioxid gas and alcohol if the oxygen of the air be freely admitted (aerobiosis), while if to a fresh portion of the same solution scrapings from carious dentin be added, lactic acid will be formed, and, as a rule, no gas. Moreover, the reaction will occur if oxygen be excluded (anaero- biosis). In albuminous compounds an alkaline reaction and entirely different substances will be formed upon the addition of carious dentin. FERMENTATION 43 The ferments produced by bacteria are quite numerous. The proteolytic ferment dissolves albuminous substances; proceeds under an alkaline reaction and sometimes under an acid reaction. The diastatic ferments change starch into sugar. Inverting enzymes convert saccharose into dextrose or non-ferment- able forms of sugar to fermentable ones. Coagulating ferments coagulate milk. Coagulation is also pro- duced in the tissues and exudate in inflammation by the ferments of pyogenic cocci. Sugar-splitting ferments change sugar into other products, as alcohol, carbon dioxide, and lactic acid. Fat-splitting ferments split fats into glycerin and fatty acids. Hydrolytic ferments cause a combination with the elements of water in substances they decompose. Emulsifying, oxidizing, and nitrifying ferments also occur. Toxins are also classed with the ferments, and are capable of producing new substances when distributed in the blood, (See Immunity). The progressive decomposition of albuminous matter into simple compounds is effected by many bacteria through processes of oxida- tion, deoxidation, and hydration. Peptones^ are first formed, next alkaloid-like bodies called pto- mains; succeeding this such nitrogenous bases as leucin, tyrosin, and the amins (methyl, ethyl, and propylamin) are formed; next fatty acids and such acids as butyric, lactic, and succinic acid appear; next aromatic products such as indol, phenol, and cresol are formed, and the final decomposition is represented in the end products — carbon dioxid, CO2; hydrogen sulphid, H2S; ammonia, NH3; and water, H2O. When bacteria produce decomposition of living animal tissue they effect this putrefaction, as distinctly noted in certain cases of abscess. Such products of bacterial action, either produced in a living or a saprophytic medium, as are capable of acting as poisons in the animal organism are called toxins. Some animal parasites also pro- duce them. It is understood that they differ according to the fungus and the medium. If the toxin be proteid in nature, it is termed a toxalbumin. Some of the ptomains are toxic; the greater number are not. When the toxins alone are absorbed from a focus of infection the subject is poisoned — a condition called toxemia, whether due to a toxic ptomain, as in the case of Asiatic cholera, or to a toxalbumin, 1 Ziegler: General Pathology. 44 MICROORGANISMS AS EXCITING CAUSES OF DISEASE as in the case of diphtheria. Such toxemia is commonly accompanied by more or less fever, according to the amount taken up. When the organisms enter the circulation and multiply in the blood, or at least move about and live in it, to be carried to capillaries in which they can rest and multiply, the condition is termed a septicemia.^ In toxemia and septicemia the symptoms depend upon the nature of the organism and their products. Bacteria are found everywhere and exist upon the surface of the body, in its external cavities, and in the alimentary canal. Here under conditions of health there seem to be conditions favoring certain forms, which, when implanted, occupy the field and exclude, except temporarily, other forms to which the soil is not so well suited. These are known as the "normal flora." It has been shown, however, that the growth of some bacteria is favored by the presence of certain others (symbiosis). Fig. 18 Fig. 19 Staphylococcus pyogenes aureus. From a culture. X 1000. (Green.) Streptococcus pyogenes. From pus found in a pyemic abscess. X 1000. (Green.) With certain changes occurring, other forms may become im-. planted. Pathogenic bacteria may exist in the healthy cavities and produce no ill results. Again, the soil may favor and disease begins. Certain bacteria have been found constantly present in relation with certain diseases — e. g., the spirillum of Asiatic cholera with that disease. These are specific bacteria. Taken from individuals with the disease, they produce it in susceptible animals inoculated with them if circumstances favor their growth. Bacteria spread in the tissue along the lines of least resistance. They may follow the cellular tissue or enter the lymphatics, or pass 1 Abbott: Principles of Bacteriology. FERMENTATION 45 at once into the veins and be carried into the circulation. They may be strictly localized at the point of infection. Thus there may be a localized inflammation — e. g., in simple abscess due to the Staphylococcus pyogenes aureus; a diffuse inflam- mation, as in case of infection by the Streptococcus pyogenes; a gland infection or septicemia, as in anthrax or general infection by Streptococcus pyogenes or Bacterium pneumoniae; or a metastatic mflammation, as in pyemia, in which the germs (usually Strepto- coccus pyogenes) gain access to the blood from a local focus of infection and are carried to distant parts, in which they cause abscesses while the products produce toxemia. To produce effect, Fig. 20 Mouse's lung; vessels plugged with bacilli anthracis: a, alveolus; v, vein full of bacilli, c, capillaries also full; br, bronchus. X 400. (Horsley.) germs in the blood must come to rest at some point, which may occur in the capillaries owing to their injury, in thrombi or emboli, or, in case of entrance of bacteria into a leukocyte, they may migrate into the connective tissue (Fig. 20). It has been shown that pyogenic germs may exist in the blood without local effects, while again a local injury may cause the arrest of the germs and a secondary local inflammation or abscess be set up. This is due to simple arrest or to extravasation of blood, which permits the germs to pass from the vessels into the connective tissue. General or local depression of tissue vitality acts as a predisponent to local infection. The infections themselves are classified as primary, secondary, and mixed. The primary is the original infection, say, e. g., Bacillus tubercu- 46 MICROORGANISMS AS EXCITING CAUSES OF DISEASE losis. The secondary is that implanted when the original disease is well under way — e. g., Streptococcus pyogenes aureus upon tuber- culosis; a third or tertiary infection is possible.^ The original infection may be by mixed germs, more than one of which may multiply. Thus, the Streptococcus pyogenes aureus and Bacterium pneumoniae may both be found in an abscess. This is a mixed infection. BACTERIA OF THE MOUTH In even the best cared for mouths bacteria are numerous and find the conditions suited to their growth. In unclean mouths containing food debris, dead epithelium, etc., their life conditions are much more favorable. According to Miller^ there are a number of bacteria which almost invariably occur in every mouth. These are: 1. Leptothrix innominata. 2. Bacillus buccalis maximus. 3. Leptothrix buccalis maxima. 4. Jodococcus vaginatus. 5. Spirillum sputigenum. 6. Spirochete dentium (denticola). To this list Goadby^ has added: Leptothrix racemosa of Vicentini, further described by Williams.^ Streptococcus brevis of Lingelsheim and Cladothrix buccalis (pro- visionally added.) With the exception of Streptococcus brevis and perhaps Clado- thrix and Bacillus buccalis maximus, these are uncultivable on labor- atory media, and strictly obligate parasites. Of the last-named organism, Goadby obtained biological characteristics of the pure culture, but he did not establish its disease-producing power, if it possesses any. Certain pathogenic organisms have been shown to be present in the mouths of healthy persons, such as bacteriological investigators; those nursing infectious diseases, such as diphtheria, scarlet fever, etc., and even in the mouths of healthy individuals apparently not exposed to any infection. In about 10 per cent, of all individuals examined at random Netter found Staphylococcus pyogenes aureus (golden pus). Staphylococcus pyogenes albus was also found. The Pneumococcus, or Bacterium pneumoniae, was found in the mouths 1 Park : Surgery by American Authors. ^ Microorganisms of the Human Mouth. 3 Mycology of the Mouth, 1903. * Dental Cosmos, 1899. See Dental Caries. BACTERIA OF THE MOUTH 47 Fig. 21 of about 15 per cent, of healthy individuals. This organism has been found by Kirk to be apparently causative of pericemental abscess, and has been reported by Schreier"^ as found in 75 per cent, of cases of apical abscess examined. It has also been related with cases of osteomyelitis and Ludwig's angina. The Bacillus diphtherise of Loeffler has been found in about 10 per cent, of mouths examined at random, and 33 per cent, of 600 children in a school examined during an epidemic of diphtheria were found to have the bacillus present in the mouth, while but about 2 per cent, developed the disease.- This latter fact show^s the absolute necessity for at least a local predisposition as well as an exciting cause. The Bacillus tuberculosis exists in the mouths of many suffering from pulmonary tuberculosis, and exists also at times in the mouths of the healthy. Primary tuberculous osteitis has been observed. The Sac- charomyces albicans may be present and at times produce thrush (Fig. 9) . The Bacillus typhosus (typhoid) has been found in the healthy mouth, and at times has oral patho- genicity. Many other organisms have been isolated from the human mouth. Some of these have a specific character, of others little is known. The mouths of professional nurses have been shown to con- tain bacteria, which increased the danger of infection of their patients, and that the sanitation of their mouths reduced the danger.^ Some of the bacteria of the mouth possess the power, under certain con- ditions, of felting themselves in gelatinoid masses or films upon the surfaces of the teeth. Here, if properly supplied with carbohydrate food, some of them produce lactic acid and decalcify the teeth. Some of the masses may develop an alkaline reaction due to putrefaction. Some have a later putrefactive action upon the organic matrix of the dentin. Goadby* gives an interesting classification of bacteria found in dental caries (which see). Some bacteria not yet isolated are the probable causes of pyorrhea alveolaris. (See chapter on Pyorrhea Alveolaris.) Diplococci pneumoniae entangled in the meshes of the fibrinous exudation. From a section of lung in the "red hepatization" stage of acute pneumonia. In the upper part of the field is a cell containing several cocci — possibly a phagocyte. X 1000. (Green.) > Dental Cosmos, 1S93. 3 Guttman. See Dental Cosmos, 1910, p. 1165. 2 Goadby. * Mycology of the Mouth. 48 MICROORGANISMS AS EXCITING CAUSES OF DISEASE The bacteria in the mouth probably are taken into the food and swallowed in great numbers. Many are doubtless killed by the gas- tric juice, which is a weak germicide; notwithstanding, some pyo- genic cocci and some of the blastomycetes may develop in the stomach Fig. 22 Bacillus diphtheriae: A, its morphology on glycerin-agar-agar; B, its morpiiology on Loeffler's blood serum; C, its morphology on acid blood-serum mixture. (Abbott.) Fig. 23 and produce disease. Many also may enter the intestines and either excite disease of specific character or produce abnormal intestinal fermentations, the toxins of which may be absorbed, and produce malnutritional conditions. They may remain localized in the mouth and produce oral disease, dental caries, or pericemental diseases, etc. Collections upon the teeth, plates, etc., abscesses, pyorrheas, etc., are unquestionably the causes in many instances of fever, septic infection, intestinal disturbances, heart complications, pulmon- ary tuberculosis, glandular enlargements, etc. The relation of an unclean mouth to effects upon the mouth and alimentary canal and air passages is, therefore, a direct one of an importance that renders exact studies in this direction of extreme value. The saliva, while not germicidal (Miller), may or may not contain substances acting as pabulum for the growth of bacteria, but probably does in \ / / > Bacillus tuberculosis. 1000. (Green.) THE RESISTANCE OF THE TISSUES TO INFECTION 49 many cases apart from extraneous food materials introduced. It has been considered by Hugenschmidt that the saUva is positively chemotactic, attracting many leukocytes to the oral mucous mem- brane; also the great vascularity of the part probably aids in reducing effective inoculation. THE RESISTANCE OF THE TISSUES TO INFECTION The resistance of the tissues to bacteria is to be considered from two main standpoints: (1) The prevention of the entrance of bac- teria into the tissues. (2) The destruction of the bacteria after entrance into the tissues. 1. The prevention of entrance. It has been shown that pathogenic bacteria may enter the mouth, alimentary canal, lungs, etc., but few develop. The skin acts as a mechanical barrier, though its openings may at times harbor bacteria. The mucous membrane secretes mucus, which envelops bacteria and with it they are carried away. The healthy mucus also has apparently a devitalizing power for some bacteria, not for others. Fig. 24 1, a spore which has penetrated the intestinal wall and entered the abdominal ca\-ity, where four leukocytes have surrounded its end: m, the muscular layer of the intestine; e, epithelial layer; 3, the serous layer. 2, a spore surrounded by leukocj'tes from the abdominal ca\'ity of a Daphne. (Metchnikoff.) The acid gastric juice kills many, but some may pass through, two or three hours after a meal, at times when the gastric juice is not active. Probably the intestinal juices also inhibit, in large degree, the action of such as have entered the alimentary canal. In all cases the agitation of the fluids of a part seems to act mechanically to prevent localization of bacteria. 2. The prevention of development in the tissues. Within the healthy tissues bacteria find several elements opposing their develop- ment. It seems the consensus of opinion among pathologists that the blood serum normally contains germicidal substances probably of the nature of a nuclein and called by Buchner "alexins." 4 50 MICROORGANISMS AS EXCITING CAUSES OF DISEASE Fig. 25 This belief is mainly based upon the demonstration of Nutall that filtered blood serum possesses the power of producing the degenera- tion of bacteria. Buchner found that heating to 55° C. destroyed this property, a fact pointing to the albuminous nature of the alexins. After reviewing all the evidence, Vaughan and Novy^ conclude : " (1) the exact nature of the germicidal constituents of the blood or alexins is not known; (2) the alexins have their origin in the white blood corpuscles; (3) disintegration of the white blood corpuscles liberates alexins ; (4) it is probably true that alexins are also secreted by living leukocytes." Authorities disagree, some claiming multi- plicity of alexins, others that only one alexin exists in a given serum (Metchnikoff). Metchnikoff, in 1884, demon- strated that the leukocytes take up bacteria within themselves and claimed that they thus de- stroy them. This process he termed phagocytosis (phago, I eat; cytos, a bud). The poly- morphonuclear leukocytes, called microphages by Metchnikoff, and the large mononuclear leukocytes, which he called macrophages, have this power. The macro- phages take up dead leukocytes. It is now considered that this property, which is also pos- sessed by the endothelial cells of the bloodvessels and serous cavities, is but evidence of the nutritive function of simple cells occurring after the bacteria have been partially degenerated by the serum (Fig. 25). This is borne out by experiments: Mixed pyogenic cocci and leukocytes free from blood serum exhibiting no phagocytic activity, whereas when the bacteria are first exposed to blood serum and then to phagocytes, there is marked phagocytosis (see Opsonins). In some cases bacterial disintegration may liberate the intracellular toxins and thus permit the toxic effects upon the host. 1 Cellular Toxins. Active phagocytosis. Endothelial cells en- closing the bacilli of swine septicemia, from an hepatic vein of a pigeon: a, a, endothelial cells; b, 6, leukocytes. (Metchnikoff.) IMMUNITY 51 Researches of Leber, Buchner, and others have shown that leuko- cytes may be attracted by certain bacterial products even in high dilution, and by other chemical substances such as mercury and copper salts. This is called positive chemotaxis. The opposite is negative chemotaxis. It has been shown that the negative may be followed by marked positive chemotaxis. Toxins are negatively chemotactic, and when bacteria produce much toxin phagocytosis and suppuration is lessened,^ e. g., in streptococcus infection. Many other bacterial products and bac- terial proteins are positively chemotactic, and when they are pro- duced in place of much toxin phagocytosis is increased, and the bacteria, if few, are coincidently destroyed by the alexins and taken up by the phagocytes with resolution, or, if the bacteria be numerous, suppuration is increased and the bacteria expelled as a protection to the body. It has been shown, however, that the taking up of living bacteria may occur and may spread an infection. Also it has been shown that the microphages take up some bacteria and the macrophages take up others. If the combined local forces be incompetent to kill out the infecting organisms, the local infection spreads until limited or the patient dies; or a metastasis may occur, in which case the process is prac- tically repeated in another locality. IMMUNITY Immunity is the opposite of predisposition, and may be defined as that condition of the local fluids, the blood, or the body cells, in w^hich inoculation with bacteria or bacterial products has no injurious effects. There is also some relative immunity to non-infectious diseases, e. g., females to hemorrhagic diathesis. Immunity to infective agencies may be natural or acquired. Natural Immunity.— This is usually an inheritance from immune ancestors of a type of tissue anatomy and physiology, or a peculiar substance in the blood, etc. Typical examples of this kind of immunity are those of the rat to diphtheria; man to rinderpest; lower animals to syphilis; the negro to yellow" fever (though he is susceptible to smallpox); the hog to snake venom, etc. Natural immunity may change to susceptibility through some 1 Stengel: A Text-book of Pathology. 52 MICROORGANISMS AS EXCITING CAUSES OF DISEASE change in the systemic condition. Thus, two students attending a scarlet-fever ward for months became susceptible through the effects of a long walk and hunger; both took the fever, one dying. ^ Rats, run in a wheel until exhausted, were successfully inoculated with anthrax bacilli, to which they are normally insusceptible. Natural immunity may therefore fail upon severe test, and survival of the test is the onlj^ certain assurance. This natural immunity may be of two kinds: 1. Natural toxin immunity, e. g., hog to snake venom. 2. Natural bacterial immunity, e. g., negro to yellow fever. Acquired Immunity. — This is of two kinds: 1. Acquired toxin immunity. 2. Acquired bacterial immunity. Acquired Toxin Immunity. — Toxin immunity may be acquired in two ways : 1. By the injection of small doses of toxins at intervals until no reaction results. The horse is so immunized in diphtheria antitoxin production. The antitoxin is produced by the cells of the horse. 2. By the injection into man or animals of serum containing anti- ' toxin produced by method No. 1. The former is an active immunity; the latter passive. Acquired Bacterial Immunity. — Immunity to bacterial inoculation may be acquired in several ways: 1. Naturally, through having had an attack of the particular specific disease, thus, as a rule, measles, smallpox, syphilis, yellow fever, and many other infectious diseases produce bodies which remain in the blood and render the individual immune to a second attack, though in some cases this immunity is lost. The child of a syphilitic mother is often rendered immune to syphilis and cannot be subsequently infected by her (Profeta's law); also, the mother of a syphilitic child may show no symptoms of the disease and be immune to it (Colics' law). The toxin is, in both cases, absorbed through the placenta, immunizing the child or mother, as the case may be. 2. Artificially, through the injection into the body of attenuated bacteria, cultivated through several generations under unfavorable conditions; for example, at increased temperatures or in the presence of weak antiseptics or by passing them through other animals, whereby their virulence is lost: a mild immunizing attack ensues. Thus in rabies, or, rather, for prevention of rabies, after the bite of an animal suffering from it, accurately graduated doses of emul- 1 Green: Pathology and Morbid Anatomy. IMMUNITY 53 sions of the spinal cord of infected rabbits, dried for varying periods to produce accurately degenerated rabies germs, are injected into man, preventing the development of the germs introduced by the bite. The emulsion of older cords are injected first, then those of younger cords (dried for a shorter time). 3. Artificially, by the injection of dead bacteria from a pure culture of the specific bacterium from which immunity is sought. What is known as the opsonic index is raised, and the person becomes more resistant to that particular infection; that is to say, phagocytosis is increased. (See Opsonins.) Fig. 26 A, complement; B, amboceptor; C, receptor; D, part of cell. Showing how complement destroys bacteria through the agency of amboceptors. Cell with different kinds of receptors: C, receptors. The dark objects represent food molecules, toxins, etc. 4. Artificially, by the injection of graduated doses of toxins, pro- duced in a saprophytic medium by the specific bacterium, all bacteria being filtered out. This is most readily done when the toxins pro- duced lie in the medium external to the bacteria (extracellular toxins). The horse is so treated in the production of diphtheria antitoxin for use in the diphtheria of man. 5. Artificially, by the injection of the serum of animals immunized by method Xo. 4, which serum contains a substance antagonistic to the specific toxin and known as an antitoxin, also, possibly, a sub- stance antagonistic to the bacteria producing the toxin. Thus the injection of horse serum containing antitoxin of diphtheria produced by method No. 4 into a diphtheric patient aborts the disease by 54 MICROORGANISMS AS EXCITING CAUSES OF DISEASE antagonizing both the bacteria and its toxin. Injection into the attending nurse produces immunity to the disease. The methods 1, 2, and 4 produce a much more lasting immunity, as the antagonizing substance is the result of cell reaction on the part of the individual, and is called active immunity; that produced by method No. 5 is passive immunity, because not produced by cell reaction, but directly introduced into the blood, and is much less lasting. It is not effective for all bacteria. The various forms of immunity are explainable by the now gener- ally accepted theory of Ehrlich known as the side-chain theory. Ehrlich's Side-chain Theory. — This theory is based upon certain demonstrated facts and upon the supposition that each cell is com- posed of a complex nucleus made up of groups of molecules in turn composed of aggregations or groups of atoms and surrounded by side groups of atoms (molecules), which compose the cell protoplasm. Each atom group is supposed to have its own chemical affinity for food elements, poisons, etc., as shown by the selective affinity of drugs. These chemical atom groups, therefore, have a receptive function and are called receptors (on the cell). Other groups have a ferment- ative action and chemically change the substances presented: these are called zymophorous atom groups. Each toxin molecule has an affinity for some cell receptors, other- wise no effect is produced by it. (Snake venom has no effect upon the hog.) The receptor is considered to possess a group of atoms suited to a prehending action, whereby it combines with the toxin molecule (or food molecule in nutrition), which possesses a similar combining group of atoms. In each these are termed the haptophorous group. The toxin molecule is capable of inflicting injury upon or stimulating cell action, as shown in the case of tetanus, in which tonic muscular contractions are excited. The group of atoms in the toxin molecule, which accomplishes this is termed the toxophorous group (Fig. 27). That the body cells neutralize the toxin if not in overwhelming quantity, is shown by the experiment of Wassermann and Takaki, in which a mixture of brain emulsion and tetanus toxin was inert when injected into a susceptible animal. Therefore, a zymophorous group of atoms is said to exist in the cell or its receptor. The Theory of Toxin Immunity. — The toxin produced during an infective disease, such as diphtheria, and floating in the blood, presents itself to cells, for some receptors of w^hich it has an affinity. The haptophorous atom group of its molecule joins with the hapto- phorous atom group of the receptor. The toxophorous group exerts IMMUNITY 55 its action upon the receptor and is neutralized by the zymophorous group of the latter unless the toxin is in too great quantity. The cell, in case of injury, repairs itself by forming an excess of the par- ticular kind of receptors having affinity for the particular toxin. These receptors become detached and float in the blood, and there have the same affinity for the toxin. These are called receptors in the blood, and constitute what is known as antitoxin. They are known to be formed by the body cells and not by the blood, as they have been found in the tissue juices of blood-making organs immediately after the introduction of toxin, while at the same time not found in the blood, though they afterward appear, as might be expected (Fig. 28). Fig. 28 Fig. 29 Showing separation of antitoxins, and combina- tions of toxins (dark) with free antitoxins in the blood. -D Showing the action of anticomplement: A, complement; B, intermediary body; C, receptor; D, cell; E, anticomplement. The antitoxin receptor (with affinity for the toxin molecule) has an haptophorous atom group which combines with the haptophorous group of the toxin molecule, which, having found its affinity in the blood, is satisfied, does not further affect the cells proper, and thus cell injury is prevented. This occurs naturally in each case of diphtheria, and probably recovery or death is dependent upon the ability of the body cells to furnish antitoxin sufficient to antagonize the toxin and another body to be described which antagonizes the bacteria. In the case of diphtheria serum therapeutics, the horse is com- pelled by method No. 4 to form these antagonizing substances, and the serum is then injected into the individual suffering an attack 56 MICROORGANISMS AS EXCITING CAUSES OF DISEASE or threatened, thus furnishing him ready made the antagonizing substances (antitoxin, etc.). A special antitoxin is supposed to be formed for each kind of toxin. Ehrhch beheves an antitoxin mole- cule to be capable of satisfying 200 toxin molecules, and that they combine chemically. In old sera the toxin undergoes a chemical change into toxoid, and the injection of this causes an increase of receptors on the cell, and thus renders the animal more susceptible to the action of the toxin. An antitoxin unit is the amount of antitoxin necessary to neutralize an arbitrary amount of a particular toxin. Toxon is a third body produced by the bacteria which has some affinity for antitoxin, but the combination is still somewhat toxic (has a different toxophorous group of atoms), and in diphtheria is credited with the production of postdiphtheric paralysis. The attempt to make antitoxins has not been successful in most cases. The Theory of Acquired Bacterial Immunity. — ^When bacteria enter the tissue of an animal by inoculation and are not destroyed by the alexins and phagocytes, they develop and produce toxins and may themselves enter the blood. A reaction of the body cells occurs, as shown by fever, and not only antitoxin, but another body is pro- duced by the cells, which, with the aid of still another substance called complement, is capable of destroying the particular bacterium causing the infection. This body is another form of receptor having two haptophorous groups, by which it links the complement with the receptor of the bacterium, and thus enables the complement to destroy the bacterium through its zymophorous atom group. The doubly haptophorous receptor is called from this fact the amboceptor (also intermediary or immune body) (Fig. 26). A different ambo- ceptor is produced for each bacterium and the host is immunized against this bacterium only. The complement, of which there are several in association in the blood (Ehrlich), is probably produced by the leukocytes, and is classed among the alexins. As stated, it has a zymophorous atom group, and also has an haptophorous atom group with which it joins the amboceptor. The complement is destroyed at 55° C. (is thermolabile) . The amboceptor requires a higher heat (is thermosta- bile); a different amboceptor is probably formed for each variety of bacterium. In natural bacterial immunity it is thought that some of the amboceptors are inherited from immune ancestors, and that they exist together with complement in the blood ready to act. Metchni- koff claims that amboceptor and complement are products of the leukocvtes. The elements in blood serum which destrov bacteria IMMUNITY 57 are termed haderiolysins , and the new bodies formed by cells as a protection are called antibodies. Toxins and not ptomains stimu- late their formation. Agglutination. — When body cells react to infection, and attempt to or effect immunity, the blood plasma acquires the property of clump- ing the bacteria together, and they settle to the bottom of a test serum, leaving the fluid clear. It is supposed to be exhibited only toward the bacterium causing the infection, but experimentally out of the body {in vitro) others are sometimes affected. The substance producing agglutination, called agglutinin, evi- dently exists in blood as the result of cell reaction. It is of the nature of liberated amboceptors, but has a zymophorous group. It therefore acts by combining by an haptophorous group and acting through a zymophorous group. The reaction is useful in making an early diagnosis of the kind of existing infection. Thus if typhoid bacillus be suspected as a cause of disease present and be the cause, the blood serum drawn from the patient will agglutinate living t^^phoid bacilli placed in it. This is known as Widal's reaction. Precipitins. — A substance of nature and origin similar to agglutinin causes precipitation instead of agglutination. It is used in diagnosis and in differentiating the blood of animals, a matter of importance in murder cases. Opsonins. — In the absence of serum, phagocytosis does not occur. Wright determined that leukocytes washed in sodmm-citrate-chlorid solution to free them from serum, and then introduced into serum containing bacteria but no leukocytes, would then produce the phenomenon of phagocytosis. Obviously, then, the serum contains a substance or substances capable of favoring phagocytosis. It is regarded that this substance prepares the bacteria for the phagocytic process, and from this fact Wright named these sub- stances opsonins, which are therefore classed among the alexins. Opsonins have an haptophorous of group atoms prehending the bac- teria and a zymophorous group acting upon them. Other observers have determined that opsonins are multiple in normal blood. The degree of activity of the opsonin related to a particular infection when compared with that of a healthy person is called the opsonic index. The Opsonic Index. — To test the opsonic index, an even emulsion of the bacteria, the serum of the infected patient, the serum from each of several healthy persons, and healthy leukocytes from the healthy persons are necessary. 58 MICROORGANISMS AS EXCITING CAUSES OF DISEASE 1. The Emulsion. — The pure culture is isolated. A 2 per cent, nutrient agar medium has sterile milk, milk serum, or blood serum added in the proportion of 1 part to 3 of the nutrient agar. In tubes of the selected medium slant cultures are made, and incubated at 37.5° C. for eighteen to twenty-four hours. (Gilder sleeve.) These are then washed from the surface of the medium with 0.85 per cent, sodium chloride solution and the solution placed in a sterile bottle with sterile glass beads or sand and shaken to remove clumps. The number of bacteria in each cubic centimeter is then estimated (standardized) and a dilution made on the basis of this estimated count with 0.85 per cent, sodium chloride solution, so that when opsonized with normal serum each leukocyte will take up from 5 to 8 of ordinary bacteria. (Gildersleeve.) 2. The Sera.— These are obtained from the patient and healthy persons by congesting the finger with a rubber band and bleeding into a capsule or pipette, which is then sealed and the blood allowed to clot in the incubator for 15 to 20 minutes. 3. The leukocytes are obtained by filling with blood a centrifuge tube, three-fourths full of a 1 per cent, solution of sodium-citrate in 0.85 per cent, solution of sodium chlorid. After shaking, the tubes are centrifugalized, the fluid drawn from the buffy coat, and the latter then carefully pipetted and drawn in and out to mix thoroughly. The preparations being ready, equal volumes of bacterial emulsion, the serum to be tested, and leukocytes are drawn into a marked pipette, each volume being separated by a bubble of air. These are then mixed by drawing in and out, and the end of the pipette is sealed and the pipette placed in an opsonizer for fifteen or twenty minutes. The pipette end is then broken, and the contents spread evenly on several glass slides by means of another slide (Gilder- sleeve) . These are then air dried and stained. The bacteria in a given number of leukocytes are counted and the total divided by the number of leukocytes counted, thus obtaining the average of bac- terial ingestion per leukocyte. This gives the 'phagocyting index for the infected individual. The same procedure exactly is carried out with the normal sera, and the average phagocyting index determined. The index is cal- culated by dividing the patient's phagocyting index by the normal phagocyting index, or the same thing may be done by the following proportion : Normal index : patient's index '.: 1 : x. If X is above 1, the patient's index is high. If X is below 1, the patient's index is low or subnormal. IMMUNITY 59 Vaccine Therapy. — Wright found that when a large number of the bacteria causing the infection were killed and then injected into the patient, their bodies contained substances which produced a cell reaction resulting in an increase of opsonin and phagocyting power in the leukocyte of the individual — this determined by the opsonic index. For a time — twenty-four or forty-eight hours — the index became lower. This Wright called the negative phase; afterward it gradually rose to a maximum. This stage he termed the positive phase. The object sought, then, is to increase the resistive power of the patient to the infection through an increase in the phagocytosis. The Vaccine. — This is prepared by producing an emulsion of the pure culture as for the opsonic index. The emulsion is then stand- ardized by an estimation of the bacteria in each cubic centimeter. The bacteria are then killed by heating the sealed container in a water bath and are then diluted with 0.85 sodium chlorid solution (with 0.2 per cent, of tricresol or phenol added) to the desired strength. The proper number of bacteria for one maximum dose should be contained in 1 c.c. of the diluted emulsion. To determine the dilu- tion the estimation in 1 c.c. of standardized emulsion is divided by the number desired as a dose, and the quotient less 1 equals the number of c.c. of the diluting solution to be added to 1 c.c. of the emulsion. The Injection. — The hypodermic syringe is sterilized and filled with the diluted emulsion and an injection made into a convenient site, which should be previously sterilized with 2 per cent, phenol solution, followed by sterile water and absolute alcohol (Gildersleeve) . The needle should be inserted into the subcutaneous tissue of the outer side of the arm, or, if preferred, of the leg or thigh, or below the angle of the scapula, which ever would prove most convenient for the purpose. Gildersleeve^ recommends smaller doses when the index is low, in general infection, in acute conditions, in children, and in individuals markedly depressed, than in the opposite conditions. He gives the following dosage of the various vaccines employed in treating infections of the oral cavitv: Micrococcus aureus and albus 50,000,000 to 600,000,000 Streptococcus pyogenes 10,000,000 to 100,000,000 Pneumococcus 10,000,000 to 100,000,000 Micrococcus catarrhalis 25,000,000 to 100,000,000 Influenza bacillus 25,000,000 to 100,000,000 ' American Text Book of Operative Dentistry. 60 MICROORGANISMS AS EXCITING CAUSES OF DISEASE The Reaction of the Blood. — According to Michaels^ (following Gautrelet), individuals in whom the oxidations are below normal, and who have a tendency to arthritic diseases because of an excess of the acid constituents or waste products in the body fluids, are denominated hyperacid individuals. The hypoacid have oxidations above the normal, together with a superabundance of saline chlo- rides; and these he regards as more subject to infection. There are three ways in which the predisposition of the hypoacid might be accounted for: 1. The increased amount of alkaline elements may permit an alkaline reaction of the blood, rendering it favorable to bacteria as a culture medium. 2. The systemic change may introduce a substance into the blood whfch is a suitable pabulum for the bacteria (according to Kirk^ this occurs in the saliva in those susceptible to caries). 3. Certain immunizing substances, opsonins, alexins, etc., may fail to be formed. Per contra, the hyperacid may be immune for opposite reasons. Whether this be a rational explanation or not, it is certainly shown by Wright that therapy will increase the opsonic index, and it may be that in the hyperacid the continuous cell irritation by the acid elements, as CO2, uric acid, etc., may cause a tissue reaction increasing alexin or opsonic power. The foregoing is merely a synopsis of the main facts governing immunity. There are many details which are omitted and for which the reader is referred to works on bacteriology. EXTERNAL ANTIBACTERIAL INFLUENCES Many chemical substances and physical forces prevent the growth and reproduction of bacteria without necessarily killing them; these are called antiseptics; a weak solution of boric acid is an example, agitation is another, dryness another. Low temperatures also pre- vent fermentation. Other substances or forces kill the bacteria after an exposure to their influence for a sufficient length of time; these are germicides — e. g., a 1 to 1000 solution of mercuric chlorid in water, boiling water, or streaming steam; sunlight for some bacteria. Other substances destroy both the bacteria and their products; these are disinfectants — e. g., sodium dioxid or other substances liberating nascent oxygen. Formaldehyde and iodin are also disinfectant. 1 Sialosemiology. ^ Dental Brief, 1907. CHAPTER IV DISTURBANCES OF NUTRITION Disorders of nutrition are of three classes: (1) Due to an excess of nutritive material of all classes, or of one class; (2) due to a deficiency of nutritive material, active or relative; (3) due to the presence in the blood of material which, instead of serving the purpose of metabolism, disturbs it; (4) an inability of the cells to appropriate a proper quantity and quality of food. EXCESS OF NUTRITION; HYPERNUTRITION An excess of nutrition may be either general or local. If local, it is associated with an overfulness of the bloodvessels (hyperemia). If the individual possess a general richness of blood, he is said to be plethoric. Sthenic plethora is such a richness associated with activity of the circulation and a consequent increase of the vital processes due to plentiful cell nutrition, and with an active repair of even excessive waste of cell protoplasm. In asthenic plethora, on the contrary, the individual is full-blooded, but the circulation is sluggish; waste products are probably accumu- lated in the blood and the vital processes are sluggish in consequence. Instead of the rich color and active movements associated with sthenic plethora, the asthenic have a purplish appearance and the movements are more labored. Local Hypernutrition. — An increased stimulation of the nerves of a part invites more blood to it, which within certain limits increases the nutrition to the cells of the part. This results in increased irri- tability, contractility, and general functional activity of the func- tionating cells. If this be maintained, the cells grow or multiply, or both, and the part is enlarged and capable of an increased amount of work. Stimulation beyond this point causes irritation or overstimulation of cells, and the vital processes become fretful; incomplete chemical changes occur in the cells, and the functional activity is disordered. The cells are wearied, and if the overstimulation be continued paralysis from overwork results. 62 DISTURBANCES OF NUTRITION Hypertrophy. — Though strictly meaning an excess of nutrition, this term signifies an increase in the size of a part as the result of stimulation and destruction, with a compensatory rebuilding of cell material in excess (a cell hyperplasia) (Weigert^). The new- growth must be practically normal in structure. As a rule, both the size (simple hypertrophy) and the number of the cells (numerical hypertrophy or hyperplasia) are increased. The caliber of the bloodvessels is increased to comply with the stimulus to their con- trolling nerves — the vasomotors. Hypertrophy is frequently ex- hibited in tissues subjected to an unusual amount of work short of marked fatigue. An increase in its function occurs; its capacity for work becomes greater, and if the strong stimulus (mild irritation) implied be continued the cells increase in size and it may be in number, all three phases of the expenditures of an increase of vital energy being represented — functional, nutritive, and reproductive. If the heart be subjected to an increase in the strain ordinarily brought upon it, an increase in the volume of the muscular fibers follows, causing hypertrophy of the walls. The same is true of the muscles of the gravid uterus, in which the cells increase to many times their normal length. When one organ, as a kidney, takes up alone the work usuall}^ performed by two it increases in size (hypertrophies). This is called compensatory hypertrophy. It may occur in an organ which endeavors to supply the deficient function in another organ of different sort. Hypertrophy also occurs in many inflammatory conditions, and is due to the area of hyperemia surrounding every focus of inflammation. Thus the epithelium about the edges of an ulcer may thicken or new bone may be formed about an area of inflamed bone tissue or periosteum. The bone tissue may become more compact, a condition termed sclerosis of bone, as it results in the formation of formed (intercellular) tissue at the expense of the cellular elements. The removal of an accustomed resistance often produces an irri- tation resulting in mild hyperemia, and thickening or hypertrophy results — e. g., non-occlusion of teeth frequently produces hyper- cementosis. A form of cellular hypertrophy appears to occur in certain leuko- cytes, resulting in the formation of a multinucleated cell or ''giant cell." Under irritation the nucleus subdivides, but the cell body fails of division, and instead of complete reproduction a large cell with many nuclei is formed (Fig. 30). These giant cells appear where tissue is ' See Abbott's Principles of Bacteriology, p. 601, for an amplification of this idea. EXCESS OF NUTRITION— HYPERNUTRITION 63 to be removed, as in the case of aseptic foreign bodies or the roots of deciduous or even of permanent teeth. (See Resorption of Temporary Teeth.) An hypertrophy or excessive development may occur during intra-uterine hfe and is spoken of as congenital hyper- trophy. A low grade of inflammation may lead to a numerical hypertrophy, as in the case of hypertrophy of the dental pulp (which see). Hyperplasia. — Hyperplasia, sometimes called false hypertrophy, is an increase in size partly due to an increase in the number of the cells, though the individual cells may be smaller than normal. It occurs mostly in the connective tissues, though it ordinarily plays a part in most hypertrophies. The part is usually asymmetrical. Examples: elephantiasis and hyperplasia of the dental pulp. Fig. 30 "-r=- Dog's hair encapsulated in subcutaneous tissue: a, hair; 6, fibrous tissue; c, proliferating granu- lation tissue; d, giant cells. Preparation hardened in alcohol, stained with Bismarck brown, and mounted in Canada balsam. X 06. (Ziegler.) Cyst and Tumor Formation. — A cyst is an enlargement contain- ing a cavity which in turn contains liquid, gelatinous, or pultaceous material, about which is a capsule condensed from the surrounding structures. The accumulation of the fluid or semifluid contents produces the enlargement of the part even if bony (Fig. 31). They differ from tumors in being strictly localized, though they may be large, and in their generally benign character, though tumors may at times have a cystic character. Cysts may be formed by the retention, secretion, or extravasation of fluid in several ways: (1) By the retention of normal secretion of a gland owing to the obstruction of its duct — e. g., ranula. These are called retention cysts. (2) By abnormal secretion into ductless cavities — e. g., bursse (exudation cysts). (3) By the extravasation of blood into a ductless cavity (extravasation cyst). (4) Indepen- dently in tissue as a result of mucoid or fatty changes or liquefaction necrosis, the surrounding tissue becoming condensed into a capsule (liquefaction cysts). (5) Independently as a collection of fluid in 64 DISTURBANCES OF NUTRITION connective-tissue spaces, which enlarge and fill. The surrounding tissue condenses into a cj'st wall. (6) Independently as a result of chronic irritation by foreign bodies, extravasated blood, or parasites, as in dentigerous cysts^ (Fig. 31). Cysts may have but one cavit}^ (simple cysts) or have numerous intercommunicating cavities known as loculi (compound or multilocular cysts). Forming within bony walls, these may be largely distended, and the walls are usually thin. Dentigerous and other cysts are usually lined by epithelium peculiar to the part. The explanation of Malassez, that epithelial remnants Cyst of the lower jaw, having its origin about an undeveloped tooth. (Garretson ; (as the enamel organs) develop forcing the connective-tissue elements outward as a covering to them, is probably the correct one. Mean- while, fatty degeneration of developed epithelium and the collection of fluid account for the fluid or pultaceous character of the cyst contents. This proliferation of epithelial remnants is well proved by the development of epithelial products in the interior of dermoid cysts. Dermoid cysts are cystic tumors of widely varjdng sizes found in various parts, such as the ovary, neck, base of brain, orbit, etc. They contain fatty and epithelial debris, and are lined with epithe- lium, outside of which is a corium with its papillae, and outside of this subcutaneous adipose tissue. The whole is enclosed in a fibrous capsule of connective tissue. The epithelial lining may contain and ■ Green. DERMOID CYSTS 65 develop the characteristically dermoid structures, hair, teeth, sebaceous and sweat glands (Fig. 34). BroomelP states that the hair is often several feet long, usually of a light brown color, regardless of the color on the outside of the body, and becomes white as age whitens the outside hair, and is usually absent in dermoids in bald persons. Hair follicles are present. He states: "Dermoids of the mouth are usually found in the hard and soft palates, infrequently in the former, but when found are complicated, while the more frequently found in the soft palate Fig. 32 Longitudinal section of a tooth from an ovarian cyst: a, b, d, tissue filling absorption cavities; c, narrow band of connective tissue through which the organ o received its nourishment; d, absorp- tion of enamel. (Miller.) are simpler. In these situations they range from the size of a pea to that of a hen's egg, the larger being pendulous. They are also found on the floor of the mouth and dorsum of the tongue. Brown instances a case in which one la}' under the jaw and extended down the side of the neck.^ "The teeth range in shape from the simple cone to multicusped complex forms, the crowns of the same being well formed. The 1 Dental Cosmo.?, 1905. 2 Ibid., 190S. 66 DISTURBANCES OF NUTRITION roots are usually not fully calcified or developed, or, perhaps, partly developed. A follicular wall is present. The enamel may be smooth or pitted. "The cementum is usually absent or but slightly developed. "Radicular odontomes evidenced by tumor-like growths on roots are due to aberration of the dentinal germ. The pulp canal was always present in cases examined. Fusion of teeth has occurred in these cysts. In histology the teeth are similar to ordinary teeth, with some slight aberration due to the peculiar condition." Fig. 33 Absorption tissue, from cavity a in Fig. 32. Miller^ states that the c^^stic contents include fatty acid, oxalic acid, large quantities of ty rosin and leucin, which substances furnish the acid for the decalcification of teeth occasionally found, but that no bacterial action, such as occurs in the second stage of dental caries, could be found. He stated that in those teeth having living pulps transparency might be found. Tumors. — A tumor is a newgrowth conforming to a degree to the normal histology of a part, but having no physiological function and no typical limit of growth. They are classed as benign or malig- > Dental Cosmos, 1905. TUMORS 67 nant, accordingly as they are strictly localized and comparatively harmless, or tend to sap vitality and to spread dangerously, or to be transferred to other localities (metastasis). The growth of a tumor is attended by a sapping of the vitality of a sufferer — the degree of the debility produced being apparently in direct ratio to the size and the rapidity of the growth. Besides the size and the rapidity of development of individual tumors, another element determines their malignancy, their position, and, further- FiG, 34 Portion of a wall of an ovarian dermoid cyst: a, wall of the cyst; b, projecting portion made up of fatty and cutaneous tissue; c, hairs; d, teeth. (Ziegler.) more, their occurrence in other parts resulting in multiple tumor formation. A tumor victim acquires a peculiar appearance — a cachexia whose intensity and rapidity of advance are directly dependent upon the degree of malignancy, and the effects produced upon general nutrition by the toxic substances entering the circulation. Tumors introduce no new form of tissue element; they are repro- ductions of the cells of the tissues of the body. They may have the same cell formation as the tissue from which they spring, and are 68 DISTURBANCES OF NUTRITION then called homologous tumors; or they may have a different histo- logical structure from the tissue in which they are found, being then called heterologous tumors. For example, a bony tumor growing from bone would be homologous; a cartilaginous tumor growing from gland tissue would be heterologous. Causes. — The causes of tumor formation are unknown; it has been believed that their growth is due to parasites, especially the protozoa; this, however, has not been proved. A certain proportion of tumor formations, 7 to 14 per cent.,^ appear to be caused by traumatic injury; as, for example, in cases of mammary tumor, a history of a blow or fall may be at times obtained. Long-continued, sluggish inflammation appears to be causative of tumor formation in an unknown percentage of cases. A chronic irritation of certain portions of the body, such as the junction between the mucous and skin surfaces of the lip, the sides of the tongue, etc., is a frequent antecedent to their formation. Ziegler gives a reason- able explanation of the origin of certain epithelial tumors in organs which are undergoing atrophy; for example, in advanced age the connective tissue of the body is undergoing atrophy and there is relaxation of its strata; the epithelium of the surface (or of glands), still possessed of its power of reproduction, proliferates and invades the connective tissue, producing cancer. Cohnheim advanced the theory that embryonic remnants or "rests" are included in the tissues and in time reassert their pro- liferative powers. Tumor formation consists in the reproduction of the cells of one or more tissues, and in the growth thus formed bloodvessels are developed. Tumors do not contain nerves, though they may develop in nervous tissue. "The bloodvessels of tumors have comparatively fragile and poorly developed walls. In the malignant growths or rapidly developing tumors of any sort the vessels are mere spaces between the tumor cells, with little attempt at the development of firm walls."^ About the more slowly developing tumors a condensation of con- nective tissue occurs in many cases, forming a distinct limiting wall or capsule from which the tumor may be enucleated. The two great classes of tumors, those of mesoblastic and those of epiblastic and hypoblastic origin, may be subdivided into orders according to their histological peculiarities. > Ziegler. 2 Stengel: A Text-book of Pathology. TUMORS 69 Classification of Tumors TUMORS OF THE MESOBLASTIC TISSUES Those usually benign: Bony tumor, or osteoma. Cartilaginous tumor, or chondroma. Fibrous tumor, or fibroma. Fatty tumor, or lipoma. Mucous tumor, or myxoma. Tumor of lymphatic vessels, or lymphangioma. Tumor of bloodvessels, or hemangioma. Tumor of nerve fibers, or neuroma. Tumor composed of neuroglia, or glioma. Tumor composed of muscle fibers, or myoma. Those usually malignant: Tumors of connective tissues with rapid cell proliferation and little intercellular substance: Spindle-celled sarcoma. Round-celled sarcoma. Giant-celled sarcoma. Sarcomata i Angiosarcoma. Sarcomatous cylindroma. Melanosarcoma. Mixed sarcomata, as fibrosarcoma, etc. TUMORS OF THE EPITHELIAL AND ENDOTHELIAL TISSUES Those usually benign: Papilla of skin or mucous membrane — papillomata. Tumors of epithelial glands— adenomata. Those malignant: "Epithelial growths atypically reproducing certain glandular or other structures and showing a manifest tendency to irregular extension."^ Epithelioma Consists of surface epithelium Carcinomata J Glandular carcinoma (histologically resembles racemose gland). Colloid cancer. Syncytioma malignum (carcinoma of placental site). Squamous. Cylindrical (columnar) . ' Stengel : A Text-book of Pathology. 70 DISTURBANCES OF NUTRITION Tumors are rarely composed of but one type of tissue; several types may be present, the tumor receiving its name from the tissue predominating. When the distinguishing feature of a tumor is two predominating tissues, the tumor is given a compound name; as, for example, when, in a sarcomatous growth, numerous large multi- nucleated cells characteristic of bone marrow are found it is called a myeloid sarcomatous tumor. When fibrous and sarcomatous tissues are distinguishing features the tumor is called a fibrosarcoma. Tumors are dangerous in several ways : The size of the tumor may cause pressure upon important structures. The rapidity of growth may sap the vitality of the individual. If the tumor degenerate or suppurate, it may produce hemorrhages, or the absorption of the poisonous products may produce toxemia with anemia, emaciation and weakness, and a train of malnutritional conditions due to intoxications (p. 94). The metastasis of portions of tumors as emboli reproduces the tumor in a new locality. In the connective tissues the sarcomata are the malignant types and the sarcomatous element in a mixed tumor determines the malignancy, e. g., in fibro- sarcoma. In the epithelial tissues the carcinomata are the malignant tumors, and in mixed tumors determine the malignancy. Malignant tumors are often associated with disturbance of the general health from their inception. They tend to recur after abla- tion and either invade the adjoining tissues which may cause grave local disturbance or the morbific material they form enter the cir- culation or lymphatics and thus are transplanted to other localities (metastasis) . Since the malignancy of a tumor is due primarily to the size and the rapidity of its growth, it is clear why sarcomata are more malignant than fibromata, and why some forms of sarcomata are more malignant than others. To illustrate: Begin observation at the different stages of connective-tissue development, when connective-tissue cells have first divided, repro- duced; the tissue produced is at the indifferent stage, as seen in section of the embryonic jaw (Fig. 35). Mesoblastic cells at this early period are in an indifferent stage; some of the cells shown in the figure will form bloodvessels, others will become bone corpuscles, others will form fibrous and others muscular tissue. This structure has its analogue among tumors in a soft, fleshy, rapidly growing growth, called the round-celled sarcoma. As cells expend their vital energy in three ways (nutritive, functional, and reproductive activity) the embryonic cells of such a growth may expend their energy in nutrition (growth), and will then grow out of the indifferent stage into a more mature form of TUMORS 71 connective tissue, the ultimate form of one type being a fiber; an embryonic round cell undergoing a series of form changes from a small round cell to a long fiber (Fig. 36). The growth may cease at any stage of this form change, the tumor composed of such cell forms receiving a corresponding name. The embryonic connective-tissue tumors, as stated, are called sarcomas, the form of the fig- 35 cells composing them giving them a qualifying title. In Fig. 36 are represented the stages of development of a connective-tissue fiber from a round cell. If growth cease at stage 1, and the cell energy thereafter expend itself in reproduc- tion, a rapidly growing tumor composed of small round cells is formed — a small round-celled sarcoma, markedly malignant. If the cells expend a portion of energy in growth of cell size, a large-celled sarcoma is formed, less malignant than the former. If the cells expend a portion of their energy in forming intercellular substance, reproduction and malignancy are less active. So the spindle forms, 3 and 4, represent less rapid reproduction and lesser malignancy than 1 and 2, although Porcine embryo: ct, embryonic connective tissue of mesoblast. 2.5 cm. X 250. Fig. 36 ® ® the form 4, which should be of less rapid reproduction than 3, because of more mature organization, is frequently more malignant, because less intercellular substance is formed, as shown in Figs. 37 and 38, the energy represented in that process being used up in reproduction. The nearer the approach to the mature form (6, Fig. 36) the slower the growth of the tumor, which, w4ien composed of tissue of this type, loses its fleshy (sarcomatous) appearance and becomes fibrous, and is hence called a fibroma. ■ When a sarcoma begins its growth from bone, its histological character is frequently modified (Fig. 39). It contains large marrow cells which have undergone incomplete reproduction, forming giant 72 DISTURBANCES OF NUTRITION multinucleated cells; this is a common form of tumor emerging from the sockets of teeth. Some of the cells of a sarcomatous growth may go on to maturity, while others remain at some stage of their Fig. 37 Fig. 38 Small spindle-celled sarcoma (from a tumor of the leg). X 200. Large spindle-celled sarcoma. To the left the cells have been separated by teasing, so that their individ- ual forms are apparent; to the right they are in their natural state of apposition, such as would be seen in a thin section of the tumor. (Virchow.) developmental career. Mahgnancy will be modified according to the amount of mature tissue formed. Epithelial Tumors. — Growths arising from epiblastic or hypoblastic tissues may be benign or malignant. What are called the adenomata Fig. 39 Fig. 40 Myeloid epulis from lower jaw: a, multi- Adenoma of the breast: a, group of gland- nucleated giant cells; b, oval cells. X 265. ular acini; b, fibrous stroma; c, cells broken (Pepper.) away from their attachment. X 265. (Pepper.) may be taken as the type of the benign epithelioma; that is, compara- tively benign. They present all of the characters of typical glandular tissue; numerous acini lined with epithelial cells and surrounded by connective tissue (Fig. 40). Tumors of this type may lose their TUMORS 73 Fig. 41 comparative benignancy and become of the succeeding epithelial type. Carcinomata. — These are growths arising from preexisting epithe- lial tissue, which possess the characteristics of epithelium developing NAithout limitations of a basement membrane. Beginning upon a skin, or mucous surface, or in a gland, the reproduced epithelial cells are not sharply marked off from the connective tissue by a limiting membrane, but, gaining entrance to the alveoli of connective tissue, they proliferate there, find their way into lymphatic vessels and lymphatic glands, and reproduce epithelial growths in such places of lodgement, so that a tumor having its origin in one part may give rise to tumors in other parts of the body — metastasis (Fig. 41). Like the connective-tissue tumors, types of carcinoma differ as to rapidity of growth in their original situation and in the degree of transference; these factors determine their malignancy. Tumors of the sarcoma group may also give rise to growths in other parts, the tumor cells being carried thence by lymph vessels or bloodvessels. After a period, tumors frequently suffer such interference with their nu- trition that degeneration occurs in them. After removal, some varieties of tumors, both those which infiltrate sur- rounding tissues and those which are metastatic, show a tendency to recur- rence; that is, removal does not effect a cure, and the tumor may upon reap- pearance assume another and a more malignant character. Epithelial tumors never become tumors of the connective-tissue type; and, vice versa, connective-tissue tumors cannot become epithelial tumors. The distinction formed between epiblast and .mesoblast in the embryo is maintained throughout life. Tumors show a great variety of histological characteristics, for which works on general pathology should be consulted. While the treatment of tumors is not a part of this book, it may be said that, unless the cause of a tumor can be located and its benign character determined, it is wise to view it as dangerous. Section through an aggregation of very young cancer cells, lodged like an embolus within a capillary of the liver. The parent growth was an adenocar- cinoma of the stomach. Preparation stained with hematoxylin. X 300. (Ziegler.) 74 DISTURBANCES OF NUTRITION They should be usually removed surgically unless inoperable! The a;-rays are useful in some cases after operation or in inoperable cases. Cooley, of New York, has suggested a toxin for injection which inhibits sarcoma and at times cures. Its use after operation is held advisable.^ The writer has been urged to introduce material upon tumors of the jaws. This seems inadvisable, as space does not permit. A tumor is readily seen and should be viewed with suspicion. If not dental as described hereafter, it should be referred to a surgeon, for further diagnosis. DEFICIENCY OF NUTRITION; HYPONUTRITION If the quantity or quality of the blood delivered to a part be deficient, the nutrition of the cells of the part is impaired. First, atony, a lessened activity of the vital processes of the part, occurs. Cell chemistry is disordered, and waste products are either retained in or about the cells. The function of the cells is diminished : If secretory, its secretion is lessened; if muscular, the cell has a lessened contractility; the relations between nutrition and waste are disturbed; the part be- comes physiologically wearied sooner than usual. Hypoplasia. — ^If the process cause interference with the develop- ment of an organ, so that it is much below normal in size, or the development of a part is arrested, whether from lack of nutrition or disturbance of developmental cells, the resulting condition is termed hypoplasia. If the parts fail entirely of development, the condition is called agenesia. Atrophy. — If the process of hyponutrition be marked, the waste in a previously normal part may exceed repair, and the part affected becomes diminished in size or atrophied (Fig. 42,5). Atrophy may be general or local. In general atrophy there is a general loss of tissue, due to an excessive waste or faulty assimilation of food by the tissues. There is a loss of body weight, due first to a loss of the fat, later to shrinkage in the tissue cells. The shrinkage in size of the tissue cells causes shrinkage of the entire organ. The cells and fat may recover their size when the faulty waste or assimilation is corrected. During atrophy many cells are lost through the process of fatty degeneration and removed by the phagocytes (leukocytes), 1 Clinton: Dental Cosmos, 1910, p. 316. HYPONUTRITION— DIGESTION 75 SO that atrophy may, Hke hypertrophy, be both simple and numeri- cal. An atrophied part is pale and shrunken, contains less fluid, and is tough and fibrous. At times the fibrous portion or connec- tive tissue may increase as the cells diminish (sclerosis). Causes.^General atrophy is caused:^ (1) By a deficient supply of food material delivered to the tissue cells. This may be due to a primary food deficiency or any interference with its preparation for absorption or with its proper absorption or circulation. (2) By excessive waste of the tissues generally, as in fevers, prolonged suppuration, etc. (3) By impaired vital activity of the cells them- selves, as in senile conditions. Fig. 42 Adipose tissue: A, normal: B, atrophic, from a case of phthisis; o, single fat cell, with cell wall, nucleus, and drop of fat. X 300. (Virchow.) Local atrophy may be caused: (1) By a lessened circulation in a part due to obstruction of the arteries, veins, or capillaries, as, for example, by pressure. (2) By diminished functional activity or disuse of a part, as in the case of unused muscles or even bones. Certain organs are atrophied or resorbed as a part of the cycle of life, e. g., the umbilical cord, the roots of deciduous teeth, the thymus gland, the mammary glands after the menopause. (3) The loss of nervous connection of a part with the nerve centres controlling it (trophoneurosis), or through interference with nervous centres having trophic influence upon a part. (4) Excessive functional activity may cause atrophy by producing a degenerative condition due to overstimulation. Degeneration. — If cells have reached the limit of their life cycle or have been subjected to influences markedly disturbing their nutrition, the proteids of which they are composed are replaced by new substances of somewhat obscure origin, which appear in the parenchymatous cells, and connective tissue markedly altering the histology and producing a pathological anatomy ' Green. 76 DISTURBANCES OF NUTRITION a \l peculiar to each form of degeneration. If the change is due to chemical changes within the tissues, it is a true degeneration. If the new substance enters the cell, it is an infiltration. Fatty Infiltration.— In this condition the fat is found in globules in the cells, which globules tend to coalesce. The nucleus may be » pushed aside. It is regarded as I'iG. 43 simply the storing of fat in healthy cells, though possibly an infiltration may occur in a debilitated or degenerated cell (Fig. 44.) Fatty Degeneration. — Fatty degeneration is a condition in which the pathological accumu- lation of fat is found in the substance of cells. The cell appears granular and fat-drop- lets appear within the substance of the protoplasm and give a black reaction with 1 per cent, osmic acid. These do not tend to coalesce, as in the case of fat infiltration. " The larger the amount of cell albumin replaced by fat the nearer is the whole cell to death"^ (Figs. 45 and 46). Three theories are held as to •• the origin of the fat: 1. That the proteid of the cell is changed to fat. 2. That fat is a normal part of cell proteid and simply becomes more visible because set free through the action of poison (such as bacterial ferments or phosphorus) acting upon the combination of fat proteids in the cell. The administration of phosphorus to animals produces it. 3. That the fat is infiltrated from the blood, as in fatty infiltra- tion, but into diseased cells. Thus animals were poisoned with phosphorus and then fed with fat foreign to the animals; the foreign fat was found in the degenerated cells. Causes. — Depression of vitality is always the proximate cause, and as primary causes producing this depression may be mentioned : Muscle fibers in simple atrophy. (Schmaus.) ' Green: Pathology and Morbid Anatomy. H YPONUTRI TION—DEGENERA TION 77 Tissue starvation from any cause, as from an altered food supply. The lack of oxygen in acute hemorrhage (suboxidation). The intro- duction into the blood of toxic substances, such as mineral poisons, e. g., arsenic, mercury, or phosphorus; chemical compounds, as carbon monoxid; leukomains, as in diabetes and chronic anemia; toxins, as in fever of bacterial origin or from a focus of infection. Fig 44 Fig. 45 Liver cells in various stages of fatty accumulation. X 300. (Rindfleisch.) Fatty degeneration of cells: a, from a cancer; fc, from the brain in chronic softening. X 200. (Green.) Fig. 46 l;li«52J*:A-^^^^^^~'^ Fatty degeneration of the heart, from a case of pernicious anemia. The protoplasm is replaced by globules of various sizes stained black by osmic acid. The outlines of the fibers are irregular, owing to inequality in their distention. X 400. (Green.) Locally, interference with the circulation, if not sufficiently over- whelming to produce death, may cause fatty degeneration of cells by interfering with the food supply, as in venous hyperemia, aseptic infarcts, and simple inflammation. The products of infection can produce fatty degeneration in the cells of the inflamed area. (See Pathology of Inflammation.) 78 DISTURBANCES OF NUTRITION In areas which have undergone fatty degeneration a cheesy sub- stance may be formed out of the degenerated elements existing in the part. The fluid is gradually absorbed and a mass composed of atrophied cells, fatty debris, and cholesterin crystals is left. This process is known as caseation. Encapsulation of the caseous mass by fibrous tissue may take place, or its liquefaction or its calcifica- tion may occur. Fatty degeneration may occur in many tissues, and the danger is proportionate to the importance of the tissue involved. Cloudy swelling of kidney epithelium: a, normal epithelium; &, epithelium beginning to be cloudy; c, advanced degeneration; d, cast-off degenerated epithelial cells. From a preparation which had been treated with ammonium chromate. X 600. (Ziegler.) Cloudy Swelling (Parenchymatous or Granular Degeneration). — Cloudy swelling is a change occurring in the parenchyma (essential cells) of a part as the result of the presence of toxic substances in the blood, or even as the result of aseptic disturbance of nutrition, such as a severe burn. The same causes which produce fatty degeneration may produce it. Pathology. — The cell absorbs fluid, swells, its contents become granular, and the histological structure is lost. In the early stages the change is albuminous; no fat is demonstrable; later, however, it appears, so that the change is regarded as a first stage in the production of fatty degeneration, by which process many of the INFILTRATION— DEGENERATION . 79 cells are lost, though the organ may recover if the patient withstands the original disease (Fig, 47). Glycogenic Infiltration — Normally, glycogen is found in some other tissues than those of the liver, notably in muscle. If it appear in tissue not normally containing it, or in excess in those in which it is normal, a glycogenic degeneration or infiltration exists. It may be produced by any influence which alters the behavior of cells, especially those having secreting activity toward the carbohydrate food element (glucose), as in diabetes, and, while mostly within the cells, may exist in the intracellular tissue. (Stengel.) It is stained brown by iodin and converted by ptyalin or amylopsin into sugar, the color reaction then not occurring. It does not seem to be clearly shown as a direct infiltration of glycogen, but rather as an appearance of glycogen in the cells, which may readily be glucose changed to glycogen within the cells. It has not been satisfactorily shown to be a degeneration from proteid constituents. (Stengel.) Cook^ calls attention to the fact that the tissues become capable of diverted action, and that the glycogen may, even experimentally, be so acted upon by oxidizing agents as to be converted into acid derivatives, probably lactic acid, paralactic acid, and sarcolactic acid, and that these may be broken up by the zymotic action of tissue cells or by certain bacteria. The degenerative change in the tissues renders them susceptible to bacterial action, as in case of the gum tissue. The mucous membrane of the gums has been shown by the same author to be capable of this degeneration if overstimulated by chem- ical agents followed by the use of a stiff brush, and he argues that acid derivatives may be liberated either by the tissue or by bacteria in contact with them, and thus possibly account for certain phases of tooth destruction, as erosion. He emphasizes the fact that infil- tration of tissue, with abnormal quantities of a normal constituent of the body, is more likely to take place in the lymphoid and mucous cells of the body than in any other tissue structure. Hyalin Degeneration. — In various forms of arthritis, in arterio- sclerosis, during infection, in septic processes, and in other condi- tions a retrogressive process, characterized by the appearance of a homogeneous proteid substance, occurs. It is closely allied to amyl- oid, mucoid, and colloid degeneration, and to coagulation necrosis. The new tissue is of a glistening, waxy, homogeneous appearance, and stains with great affinity with acid anilin stains, as acid fuchsin, 1 Dental Cosmos, 1907. 80 DISTURBANCES OF NUTRITION taking a brilliant red color. The cells of the part may show fatty degeneration. Location. — Seats of interest are the endothelium of bloodvessels, which is proliferated, making the wall thickened, and the lumen nar- rowed or obliterated. (See Endarteritis Obliterans.) Upon mucous membranes it causes opaque plates or pseudomembranes. It occurs in interstitial tissues and also within the cells. Its proximate etiology and pathology are obscure. The hyalin material can be reconverted, absorbed, and removed. It does not injure the cells to an extreme degree. It may be con- verted into other albuminoid degenerations, may undergo caseation and calcareous infiltration. Fig. 48 (Stengel.) It has been found in the epithelium of the mouth by Cook, but without established signifi- cance. Mucoid Degeneration. — In this form of degeneration the proteid protoplasm of cells is transformed into mucin, a glycoproteid char- acterized by affinity for basic anilin stains, as methylene blue. It occurs in catarrhal mucous membranes, connective tissue, tumors, etc. Mucin absorbs water, but is not soluble in it or dialyzable. In the catarrhal mucous membranes the goblet cells show excess in number, and are swollen and distended with mucin. (Stengel.) The cell becomes vacuolated and the nucleus granulates and stains with a basic stain. About the necks of teeth the mucus becomes stringy and tenacious, its chemical and physical character being changed and chondroitin present. (Cook.)i According to this author this substance combining with water might give rise to sulphuric acid in contact with the teeth. C18H27NSO17 +H20 = H2S04+Ci8H27NOi4. Mucic acid might be produced from glycuronic acid found in mucin. Cook observed mucoid degenera- tion of epithelial cells and submucous structure in cases in which strong astringents were used on the mucous membrane; the con- traction of the cells caused a retention of mucin leading to a chemical change in the mucin itself. (See Erosion.) Hyalin degeneration of small vessels in the cord. X 350. 1 Dental Cosmos, 1907. INFILTRATION— DEGENERATION 81 Colloid Degeneration. — This consists of the abnormal appearance of a non-dialyzable substance Hke mucin, but differing from it in preference for acid stains, by not being precipitated by acetic acid and alcohol, by lack of absorption of water, also by causing a more profound disturbance of cells in which this is found and in which it remains much longer. Salts, as calcium oxalate, are apt to be precipitated in it, and may be again dissociated. The etiology is obscure, but probably analogous to that of mucoid degeneration. Fig. 49 Colloid cancer, showing the large alveoli, within which is contained the gelatinous colloid material. X 300. (Rindfleisch.) Dropsical Infiltration. — This is an infiltration of an excess of plasma into cells. It is a part of cloudy swelling, or may occur as large droplets of plasma enlarging the cell compressing the nucleus and protoplasm, and may even cause the cell to burst. Fatty degen- eration of the protoplasm may occur as a sequence to dropsical infiltration. The process occurs in general dropsy, in burns, in skin lesions connected with vesiculation, and in inflammation of organs. Lardaceous Degeneration. — This type of degeneration is known as amyloid, albuminous, or waxy. The formation of the material from which this condition derives its name is preceded by an unknown type of degeneration of the cells of the part affected. The degenera- tive processes appear to be the result of long-continued suppuration due usually to tuberculous disease. In the connective tissue about the degenerated cells (not in the cells) a substance akin to albumin is deposited, which causes swelling and a pseudohypertrophy of the organ affected. The substance gives a reaction with iodin resem- bling that of starch; hence the name amyloid {amylum, starch). It may affect any organ of the body. It usually appears first in the 6 82 DISTURBANCES OF NUTRITION connective tissue lying between the inner and middle coats of small arteries. The swelling caused by the infiltration markedly lessens the caliber of the vessels and diminishes the nutritive supply of the parts supplied by the artery, which may lead to fatty degeneration and atrophy of the insufficiently nourished parts. Calcareous Infiltration. — In tissues which have undergone pre- vious degeneration, calcium, sodium, or magnesium salts may be deposited as an infiltration from the blood plasma. The parts are thus petrified. The cells take no active part in the process.^ Fig. 50 .^X^^^'^^Y, Calcareous infiltration of renal epithelia. From the edge of an old infarct: a few tubules still to be recognized. X 250. (Schmaus and Ewing.) It is believed, however, that the deposit of salts in the dying tissue is more than a mere precipitation, and that calcification results from a combination of the salts with an albuminous base and with fatty acids, such an affinity being favored by the degenerative changes. Ordinarily, the carbonate and phosphate of calcium are the infiltra- ting salts, but in gout, uric acid salts are deposited, owing to an excess of uric acid in the form of biurates and quadurates in the body fluids. A sluggish circulation in the part favors the deposition of the salts. The calcification may occur in both the cells and in the intercellular substance.2 (See Calcific Degeneration of the Pulp.) In the early stages the salts are found as fine granules in the intercellular sub- stance. 1 Green: Pathology and Morbid Anatomy. 2 Ziegler: General Pathology. INFILTRATION— DEGENERATION 83 "The white, fibrous tissue is the form of connective tissue usually affected, but concretions may occur in the connective tissue sur- rounding the bloodvessels."^ As a secondary process after degeneration, calcification of the middle coats of the arteries may occur, rendering them inelastic. This renders them incapable of regulating the blood supply to parts, and these suffer more or less nutritive disturbance, and, in some cases, actual death of the part (gangrene). Calculi are found in tumors at times. Many forms of free calculi are formed in the body. These occur most frequently in ducts or cavities lined with epithelium, e. g., the salivary ducts and the bladder. "All free concretions have an organic basis or nucleus," with which are combined the calcium salts, oxalates, cholesterin, etc., making up the inorganic or crystallizable part of the combination. The organic part may consist of inspissated feces, as in enteroliths, mucus, or mucin, as in the calculi upon the teeth; epithelial scales, mucus, etc., in the urinary passages.^ The fine crystals or granules are probably soluble in some cases. The larger calculi are probably permanent and cause degeneration of adjacent tissue. Calcareous infiltration is clearly to be distinguished from the normal calcification of the hard tissues, bone, enamel, dentin, and cementum. These are composed of calcoglobulin, in which calcium and magnesium salts are combined under the superintendence of certain living cells with albuminous bases derived probably from their own substance. Pigmentary Infiltration. (See Tooth Development.) — Pigmentary infiltration is the infiltration of coloring matter into the tissues. There are four varieties: 1. Extrinsic, derived from outside the body, e. g., coal dust in lung tissue or general staining from silver salts taken up in the intestines. 2. Hematogenous, derived from hemoglobin or its derivatives. They are: (a) Hemoglobin, dark red. (6) Hemin, reddish brown or bluish black. (c) Methemoglobin, brownish red. (d) Hematin, dark brown or bluish black. (e) Hematoidin, orange or reddish brown. (J) Hemosiderin, yellowish or brownish. These are decomposition products of hemoglobin. Hemoglobin and hemosiderin contain iron. 3. Hepatogenous, or biliary. 1 Ziegler: General Pathology. ^ Ibid. 84 DISTURBANCES OF NUTRITION 4. Metabolic, resulting from cellular activity within the body, and termed melanin. The hematogenous pigments are of chief interest, inasmuch as they occur in the staining of teeth by devitalized pulps and sometimes by living pulps in a state of venous hyperemia. In these discolora- tions there is an analogy to the colors manifested in an old bruise, which undergo various color changes as the chemical character of the pigment is altered. (See Moist Gangrene of the Pulp.) NECROSIS Necrosis (from nekros, dead) signifies, in its broadest sense, death of tissue. It is due to profound disturbance of its nutritional func- tion or to direct injury to its elements. Necrosis proper (per se) signifies death of tissue in mass from any cause. Necrobiosis means the death of cells through the process of atrophy or degeneration, which are successive changes leading to death. Necrosis of bone signifies the circumvallation and death of bone through the process of inflammation, which causes thrombosis of its vessels and cessation of its nutrition. The dead part, when separated, is called a sequestrum. The solution of continuity is effected by leukocytes massed about the portion in which nutrition has ceased. Caries of bone is that form of bone death in which the bone is honeycombed and molecularly broken down rather than seques- trated. (See Osteoporosis.) Gangrene is a term used to signify death, en masse, of a part, the soft parts being included. The dead part undergoes drying (dry gangrene) or putrefactive softening (moist gangrene). (See Gangrene.) Etiology. — The causes of necrosis are as follows: 1. Circulatory obstructions, as (a) stoppage of an artery supplying a part, the nutritive supply being cut off by any cause; (6) venous hyperemia of a part, the vein being unable to carry off the blood charged with cellular waste, which accumulates about the cells, intoxicates them, and prevents access of fresh blood (food supply); (c) occlusion of the capillaries by any cause has a similar efi^ect. Inflammation may be placed in this general class of causes. 2. Troxjhic Disturbances. — The nerves controlling the metabolism of a part being diseased, the part undergoes degeneration and NECROSIS 85 slight causes produce necrosis, e. g., necrosis of eyeball when ex- cision of the Gasserian ganglion has been practised. 3. Direct destruction of the vital activities of cells by any physical or mechanical agents, or chemical substances, including among the latter the poisonous substances produced through the action of bacteria (see Fig. 77). Injuries, blows, the tension of exudate, pressure, excessive heat or cold, the passage of powerful electric currents, and the x-rays are all influences which directly injure or permanently destroy vital activities of cells. The application of chemical agents which so act upon cell substance as to change its character produces necrosis. While this is particularly true of such substances as powerful acids and alkalies, or alkaloids, which immediately destroy cell integrity, it is also true of milder agents acting for longer periods. Certain poisons, particularly those of bacterial origin, paralyze the vital activities of cells, and necrosis results. The occurrence or non-occurrence of or the liability to necrosis will largely depend upon the degree of vital energy of cells prior to the action of the active causes of necrosis. Parts debilitated from any cause are more liable to necrosis than those which have suffered no debility. A part chronically ill-nourished, subjected to the causes producing degenerations, is liable to sufter necrotic changes, for the several degenerations and atrophy are but successive stages leading to necrosis. A necrosed part acts as an irritant to the tissues about it, inaugu- rating an inflammatory reaction which marks off the dead from the living parts. The dead part is sequestered, and hence is called a sequestrum, or, in case of soft parts, a "slough," or sphacelus. Necrosis may be of several types, of which the following are the chief forms: Coagulation Necrosis. — When a dying tissue contains coagulable material and the necessary ferments, the parts undergo coagulation. (See Coagulation.) The cells and parts about become solidified, the cells lose their nuclei and do not stain as usual, and the part appears glazed, pale, and waxy. It occurs in suppuration, and is due to the coagulating ferments of pyogenic cocci. (See Bacterial Ferments.) (See Fig. 63.) The thrombosis of the vessels about an urea of infective inflam- mation is probably due to the same ferments. Fat Necrosis. — This is a peculiar form of fat death in wdiich the fat is split into glycerin and fatty acid by lipase (a ferment). The fatty acid remains and combines with inorganic salts. 86 • DISTURBANCES OF NUTRITION Liquefaction Necrosis. — ^This is the death of tissue with Hquef action of the proteid material in the area, which is usually rich in exudates. The process is probably due to enzymes capable of liquefying the tissue. GANGRENE When death, en masse, of a part occurs as the result of an inter- ference with its nutritive supply, the process is termed gangrene. Causes. — It may occur as the result of an inflammation produced by a particular bacterium, as in noma or malignant edema; from arterial obstruction, as arterial thrombosis; or capillary obstruction, as in freezing or venous obstruction, may produce it. (See Venous Hyperemia of the Pulp.) Ergot may produce it through contraction of the bloodvessels. Dry Gangrene. — In parts which ordinarily contain but little fluid the obstruction of the artery may be associated with but little obstruction of the veins and lymphatics. Under such circumstances the dead part is drained of the little fluid it contains, and a fresh access of fluid is prevented. Exposure to the air aids a further loss of moisture by evaporation. The conditions are not favorable to the development of microorganisms, and the part changes from a pale appearance to a dark, shrunken one. The process of gradual drying is also called mummification. (See Dry Gangrene of the Pulp.) It is usually circumscribed. Moist Gangrene. — Under opposite conditions — i. e., a venous obstruction with a fair arterial supply — there is much venous engorgement and extravasation of blood into the tissues, which are stained red by the hemoglobin from disintegrated red corpuscles. Abundant effusions also cause the part to be swollen. Death of tissue occurs from interference with nutrition; when bacteria are the direct cause, the part is inflamed and edematous. The moisture present favors the development of bacteria, and they enter the tissue through the skin. Putrefaction with the evolution of malodorous gases, such as hydrogen sulphid (H2S), hydrogen phosphid (HP3), and ammonium sulphid (NH4)2S, causes the part to have an offensive odor. If the gangrene be due to infective inflammation, or the surrounding tissue be debilitated from any cause, the area of gangrene may spread — i. e., invade the living tissue (spreading gangrene). This is prob- ably due to the presence of bacteria, which irritate and progressively destroy the surrounding tissue. The poisons produced, if absorbed, may cause death. If the adjacent tissue be healthy and resistant, GENERAL MALNUTRITION 87 a line of demarcation is established, consisting of leukocytes, which dissolve all fibers or firm connections between the dead and li\ing parts. Suppuration occurs at the line, and the dead portion is separated as a sphacelus or slough. Occurring in bone, this is called a sequestrum. Occasionally the part being internal is encysted and the contents may be absorbed and the sac calcified.^ An ulcerated surface is left. The latter form is circumscribed gangrene. If gan- grene be deep-seated and septic, suppuration occurs, which estab- lishes one or more fistulse upon the surface of the body or in one of Fig 51 Senile gangrene of the great toe, from a case of arterial thrombosis. The toe is shrunken and its epidermis is being exfoliated. At the line of demarcation the skin has retracted (a) and the deeper parts are separating (6). (Green.) its cavities. (See ^Nloist Gangrene of the Pulp.) A sequestrum may be cast out through one of these. In the aged' atheromatous or cal- careous changes in the arteries produce a slow circulation in the extremities. A slight injury to a vessel wall may induce extensive thrombosis (which see). The result is gangrene of a part or all of an extremity, known as senile gangrene (Fig. 51). GENERAL MALNUTRITION By the term malnutrition is meant a more or less general dis- turbance of the metabolic processes of the cells of the body, which may simply lower the body resistance or health standard, or may be of such profound character as to incapacitate an individual for ordinary functions. 1 Stengel : A Text-book of Pathology. 88 DISTURBANCES OF NUTRITION If imperfect digestion, assimilation, or elaboration of food materials or its circulation, or an imperfect relation between the amount of oxygen and food material at the cell exist, or if a great excess of food material be assimilated which cells cannot appropriate, and the excess acts as material to be gotten rid of, or if the food taken be of an irritating nature, or if such material as retained body waste products, toxins derived from foci of infection, or from alimentary canal, or drugs absorbed are presented to the cells in excess, or if the drain upon the body cells reduce the amount of cell protoplasm, and the replacement of the cell constituents is not rapid enough to restore the protoplasm wasted in energy, it is plain that a general disturbance of body cells may result, and the altered metabolism in turn furnishes its share of irritating, unfinished catabolic products to further increase the general disturbance through the production of a pathological condition of the blood (a humoral condition, Michaels). The gradual action of one or other of these classes of causes, acting either by starving the cells or by irritating them (auto-intoxication), produces a condition with tendency to diseases of certain type, and the tendency is called diathesis (acquired). According to Michaels,^ following Gautrelet, the abnormal vital processes tend in mankind to pathological conditions, which we may classify under two humoral conditions (or diatheses), viz., hypoacidity and hyperacidity. The first state (" lymphatism") is the expression of a vital overactivity, and has, as consequences, the contagious diatheses (scrofula, tuberculosis, syphilis) . The oxidations are overactive, and the hydrations are superior to the normal, hence there is a decrease in organic acidity and an increase of saline chlorides excreted by the economy. Hypo-acidity favors chemical changes in the tissues. (Ducleaux.) In the hypo-acid diathesis all the oxidations are exaggerated, and are above the normal. "In the hyperacid diathesis (arthritism), gout, rheumatism, sclerosis, oxidation is insufficient; there is incomplete oxidation with a consequent increase of organic acidity or hyperacidity, and a peculiar state of the organism characterized in a general way by a slowness in the biochemical changes. The reaction of the blood with the ordinary reagents (litmus, for example) is normally alka- line, but if we study the distribution of the acids and bases of the blood plasma we see that the reaction is really acid (Gautrelet, Drouin, and Hugeounenq), and thus acidity is increased and the blood may become relatively acid by the accumulation of acid-waste products which are not eliminated, the secretions and excretions ■ Sialosemeiology, Proceedings Third International Dental Congress, 1900. GENERAL MALNUTRITION 89 becoming then of acid reaction. It is on this account that a certain number of chronic diseases have constant characteristics in regard to semeiology; increase of the normal acidity of the urine, as well as the increase in the normal acidity of the saliva." Following Gautrelet, he gives four effects of the exaggerated and retrograde processes that diathesis produces: (1) A chemical modification of the plasma; (2) modifications affecting the chemistry of secretions and excretions (as detailed above); (3) histological modifications in the tissues; (4) modifications due to the creation of a special field for microorganisms. It will be seen that the above effect begins with a change in the blood or its contents, which successively acts upon glandular and other cell physiology and later alters their histology, and in total may bring about a predisposition to bacterial invasion through the loss of vital potential or resistance. The hyperacid diathesis may be inherited or acquired by individuals who take a liberal supply of food requiring oxidation and take insufficient exercise in the open air, while in the hypo-acid the oxidation is superior to normal. These diatheses are the forerunners of many of the diseases of malnutrition, and evidence of approaching disease may be obtained from both saliva and urine by analysis of their contents through physical, chemical, and micropolariscopic examination of either or both fluids. The contents of each fluid being taken out of the blood through glandular activity represent fairly the faulty elements. The presence of altered physical characteristics when fresh or upon standing, of unusual chemical substances determinable either by the aid of reagents or microscopic or micropolariscopic examination, leads to the inference that unusual chemical changes have occurred in the cells, or that the waste products found represent an undue waste of tissue, or that cell waste has been altered after leaving cells or not sufficiently changed into the normal waste products. In the accentuated disease condition one or more organs, as the liver and kidney, may be diseased, and it may be a nice point to determine whether the disease begins with the liver and proceeds to the diathesis, or with the diathetic condition or its cause and proceeds to disturb the liver. At the same time the same course might act upon both; for example, overfeeding with food requiring oxidation, and this not supplied by exercise, could induce a dis- turbance of the function of liver cells quite as readily as of any other body cells. According to Kirk,^ the disproportion between pabulum and oxygen resulting in hyperacidosis produces a greater ratio of carbon dioxid ' Dental Review, 1903. 90 . DISTURBANCES OF NUTRITION to oxygen in the blood than is normal. Temporarily this would be corrected by the action of the renal epithelium in which a reaction occurs between the carbonic acid of the blood and the basic phos- phates, as follows: HNaaPo^-f- HjCog = H2NaPo4+ HNaCog. The sodium bicarbonate formed is returned to the blood, maintaining its alkalinity, and the acid sodium phosphate is eliminated as the normal acid salt of the urine. In the same way acid calcium phosphate is formed. When the disproportion between pabulum and oxygen are con- tinued, the suboxidation becomes chronic, the kidney is no longer sufficient to maintain alkalescence of the blood by eliminating the excess of acidity as acid phosphate, the carbonic acid seeks other channels of elimination, and the epithelium of the buccal glands and sweat glands may take up the action normal to the kidney and excrete acid sodium phosphate and acid calcium phos- phate, producing in the case of the buccal glands a certain class of erosion of the teeth, and in the case of the sweat glands frequently giving rise to eczematous eruptions. Dental caries is not ordinarily induced in this stage, but if begun the carious matter is changed to a dark brown color, crumbly, semihard texture, and the further process is one of decalcification rather than a true carious process. "The continued suboxidation and hyperacidosis by carbonic acid thus leads to the great loss of basic phosphates as. acid phos- phates, which are more readily soluble and osmosed through kidney epithelium than basic phosphates, and for that reason are rapidly eliminated, thus establishing a phosphaturia, with consequent phosphatic starvation and ill health, as shown by neurasthenia, with its irritability, despondency, migraine, cerebral hyperemia, or hysterical phenomena. A point of depletion is reached and they are found only in minute quantity in the urine and saliva. At about this time lactates of sodium, calcium, and magnesium, in the order named, appear in the saliva, then double lactates of sodium and calcium, then lactophosphates of calcium and magnesium, then oxalate of sodium or double oxalate of sodium and calcium, while oxalate of magnesium may appear in the urine. With the appearance of the lactophosphate a general rather than a localized erosion appears. (See Erosion.) The nervous irritability is markedly increased, and a rapid loss of weight occurs. Later, acetone and diacetic acid appear in the secretion along with creatin, and in some cases cystin, at which period profound mental torpor, at times almost amounting to coma, is not infrequently manifested, or there may be extreme nervous irritability amounting almost to hysterical mania. GENERAL MALNUTRITION 91 " Coincident with the loss of the phosphates, nitrogen with carbon as a cyanogen radial (ammonium cyanate), which probably should have gone to form urea, is lost. Evidences of imperfect oxidation of proteids are manifested in the saliva and urine by the presence of lactate of ammonia (a forerunner of urea), lactate of calcium, creatin, acetone, and oxalates, with increase of urate of ammonia and amor- phous urates. The urine often contains indican, especially in cases complicated with disordered liver and habitual constipation. The saliva is usually constantly acid, due to the presence of acid phos- phates, and the dental lesions are ordinarily erosion, or, where the acidity is absent, pyorrheal invasion of the peridental membranes. Many of these cases develop epithelioma or leukoplakia buccalis, or both together, and in view of the fact that there is constant irri- tation of epithelium by the exudates, they may have an etiological relation." (Free quotation, Editor.) The diet indicated by Kirk for these cases would apply to those diseases and cases of pyorrhea in which the predisposition is due to this diathetic fault, and consists in reducing the necessity for oxygen by largely eliminating the carbohydrate portion of the diet. Suc- culent vegetables, gluten bread, milk, albumin, and a moderate ration of proteids in the shape of fish, oysters, game, light meat of fowls, are allowed. Small doses of phosphorus, or of arsenic iodide, and glycerophosphates of lime and soda are continuously adminis- tered. The exercise and rest are adjusted, and attention is given to general hygiene. "Michaels has found the saliva of but few individuals to be in a perfectly normal condition and the teeth perfect, while most of them are out of equilibrium and the teeth are affected either by caries or erosion or pyorrhea alveolaris. He states that lesions of the liver and kidneys cause the appearance of acid waste, also that the organism constantly produces acids, such as uric, oxalic, lactic, volatile fatty acid, etc., which, under normal conditions, are also destroyed, but that abnormal conditions arise which retard the oxidations of these organic acids, which must then accumulate in the organism among the waste products arising from incomplete dissimilation; many have acid properties. "The serum of venous blood, while weakly alkaline, has a real acidity (acid elements) stronger than that of arterial blood. Fever is accompanied by an acidity of the blood, as in diabetes (/?-oxy- butyric acid), rheumatism, arthritism (gout). The alkalinity is reduced (real acidity increased) in anemia, leukemia, and all cachexias. "He regards the liver as determining the majority of nutritive 92 DISTURBANCES OF NUTRITION changes, and that it suffers from the influence of all sorts of toxins, whether the result of microbic activity or due to an excess of alkaloids (leukomains) . The cells of diathetic individuals constantly elabo- rate products, some of which are positively poisonous to the hepatic gland. The acid salts and biliary pigments are toxic. Their absorp- tion is deleterious and the inactivity of the hepatic cells creates a danger to the organism. The danger arises from the fact that the liver has to eliminate from the circulation all kinds of debris. If the neutralization of the products of fermentation is incomplete; if the harmful ammoniacal compounds have not been changed into urea; if the liver does not have a reserve of glycogen, or if its generators, which are supposed to play a role in the metamorphosis of alkaloids, if through its inactivity there is a retention of waste products, the secretions are necessarily contaminated with the morbid principles; the toxic products present in the blood poisons the organism and constitutes the different diatheses (auto-intoxication)." This conception includes the views of physiologists that the liver is both a secreting, excreting, and food elaborating organ. He argues that if the bacterial fermentations, by their presence or by the pres- ence of their toxins, are capable of modifying the enzymic secretions, they necessarily influence the action of the physiological fermenta- tions. It follows from this that these toxic principles saturate, in a given period of time, the organic secretions and produce a cacochymic state (morbid state of the body fluids) . Michaels has found in the saliva of hypo-acid individuals glycogen, albumin, perhaps inosite, mucin, basic chlorides with ammonia in greater quantities than normally, sulphocyanides and biliary acid in less proportion than normally, and concludes that it is an ideal medium for the development of microbic contagion. He has found glycogen in the saliva of adolescents generally, and susceptible of reduction and fermentation under the influence of ptyalin in the presence of earthy salts, a fact emphasized by Kirk with a view to its establishment as a prominent factor in susceptibility to caries (which see). In the saliva of hyperacids he found sulphocyanides and mineral and organic acids, acid phosphates of sodium and potas- sium, ammoniacal oxalates, biliarj^ elements, and urobilin in greater proportions than normally. The increased importance of the consideration of metabolic diseases in their relation to dental diseases by the dentist warrants the introduction of a brief summary. Inanition. — This is ultimately tissue starvation, whether due to any of the following causes: 1. Want of proper amount of food. GENERAL MALNUTRITION 93 2. Gastric diseases interfering with digestion by altering the quaUty or quantity of hydrochloric acid or pepsin. 3. Disease of the liver, etc. 4. Abnormal intestinal digestion. 5. Occlusion of the sorbefacients by retained excrementitious matter or other local disease. Effects. — The tissues are not properly supplied with food to maintain themselves, and waste exceeds repair; the unimportant parts are first consumed and make good the deficiency. The surplus food materials, first the fats, are first consumed, then the carbo- hydrates, next the nitrogenous tissues, first muscles and glandular organs, and lastly, the osseous and nervous tissues. This is general atrophy necessarily accompanied by degeneration. There is loss of energy and temperature, and the vital organs are weak; death occurs from exhaustion. Overfeeding. — The excessive use of proteids in food leads to a necessity for elimination from the blood of the excess absorbed, and to intestinal fermentation of the unabsorbed excess. The proteid food maintains the proteid equilibrium, and any more than is required for this is in excess. Energy is largely supplied by the carbohydrates (eventually glucose) and the fats. An excess of these leads to the storing of fat to a degree normal and useful as a reserve, but in combination with a sedentary mode of life, pathological fat or obesity, in which oxidation is reduced. A tendency to fat production exists in in- dividuals. Excessive Tissue Destruction. — The tissues may be excessively wasted by many causes, and in many cases the food supply is defi- cient as well. These causes are, briefly: 1. Fevers. 2. Continuous hemorrhage. 3. Long-continued suppuration. 4. Tumors, especially carcinoma. 5. Chronic infectious diseases, as tuberculosis. The increased waste is due either to increased oxidation of the proteid elements, due to stimulation of nervous centres controlling catabolism, or to the ferment contained in the toxic substances produced and entering the blood, which may cause cellular waste in the effort to produce antitoxins (see Ehrlich's Side-chain Theory), while at the same time normal food appropriation is interfered with if the amount of food supplied is not indeed lessened, as in continuous hemorrhages. 94 DISTURBANCES OF NUTRITION Intoxications. — These may be divided into extrinsic and intrinsic intoxications. The principal classes are: 1. Intestinal Intoxications. — In intestinal putrefaction, particularly in constipation, the aromatic products, acetone, tyrosin, indol, skatol, phenol, cresol, and paracresol, may be absorbed and produce a form of intoxication of tissue cells which lowers the vital potential of all cells and the resistive force of tissues to bacterial infection. In intestinal putrefaction in children a marked readiness of the muscular system to fatigue has been noted, also in cases of persons who have suffered from indicanuria for a long time, showing a mark- edly poisonous effect upon muscle and probably upon other tissue. The absorption of indol and its modijfication in the liver leads to its appearance in the urine as indican, or indoxylsulphate of potassium/ which, therefore, indicates an abnormal intestinal putre- faction with absorption of deleterious products.^ That indican in the urine is caused by abnormal tissue metab- olism is not well supported by evidence.^ It is found in carcinoma and chronic peritonitis. It is generally present when suppurations are in progress; probably indol is ab- sorbed from the focus of putrefaction. The ingestion of pus from pyorrheal pockets in the mouth may easily lead and has led to chronic gastritis and intestinal putrefaction, in which latter Bacillus coli communis plays an important, assistant part. The liver may be disordered primarily, thus favoring the condition owing to lessened formation of bile, or, secondarily, owing to its increased function as a poison destroyer. The intestinal putrefaction causes the forma- tion of indol, etc., thus leading to the presence of indican in the urine. The excessive use of proteid food not only overloads the intestine, but invites putrefaction therein; also, the amount absorbed being excessive, the eliminative functions are overtaxed, leading to disease. 2. Drug Intoxication.^ — The use of arsenic, phosphorus, or other inorganic poisons, or the vegetable alkaloids, as morphin, cocain, atropin, etc., or the continued contact with lead salts, all un- doubtedly affect metabolism ^ — some beneficially — when employed in suitable doses in diseased conditions, or injuriously in continued excessive use. Thus atropin in small doses checks secretion — e. g., of the salivary and mammary glands. Phosphorus continued produces fatty degeneration. 1 Thompson's Practical Medicine. 2 Test for indican: Add nitric acid to urine — shake with chloroform — -a bluish color is imparted to the chloroform on standing. ' Leathes: Problems in Animal Metabolism. GENERAL MALNUTRITION 95 3. Bacterial Intoxication.^ — The toxic products of bacterial action (apart from the aromatic products), as the ptomaines and albumoses (toxins), act as ferments upon proteid tissue, causing cellular waste either by ferment action (destruction) or by stimulation of the cells, either directly or through the nervous system, leads to the produc- tion of antitoxic substances in excess, which by Ehrlich are claimed to be discharged into the blood. No doubt the cell is also rendered less capable of anabolism. (See Side-chain Theory.) This is seen in fevers in which emaciation (excessive waste) is proved by the increased output of urea. Intrinsic Intoxication. — In this class may be placed all intoxications produced by substances originating in excess within the body proper as a result of metabolic disturbance, resulting from disease of the nervous centres controlling metabolism or of organs which fail to perform their duty of elaboration for metabolism or elimination or elimination proper, in part or entirely. In some cases compensatory elimination by other organs occurs, which may be effectual or may lead to disease of said organ or organs. A good example of com- pensatory elimination is seen in health during sudden changes of atmospheric temperature. Thus on the w^arm days perspiration is free and elimination by the urine lessened ; the avenue of elimination is largely reversed on the cold days. These intoxications may also be classed: Uremia. — In this there is a retention of urea (as ammonium carbonate or its congeners) in the system which should be eliminated in the urine. The body cells are chronically or acutely poisoned, according to the degree of the retention, death resulting in the complete form. Nephritis is a common cause. Diabetes Mellitus. — In this disease probably the essential lesion is a hyalin degeneration of the islands of Langerhans, of the pan- creas, or injury to the floor of the fourth ventricle of the brain (diabetic centre), which may be caused by even strong mental emotion, as grief. Carbohydrate assimilation is interfered with, an increased amount of sugar appears in the blood and urine (in the urine termed glyco- suria) , and the cells are unable to appropriate it. Proteid destruction with increased production of urea occurs (excessive waste). ^ An excess of phosphoric and sulphuric acids, ^^-oxybutyric and diacetic acids are formed or retained, and hyperacidosis results. The sugar in diabetes is probably first formed from carbohydrates, later from proteids, the carbohydrate radicals being probably dis- sociated in the proteid disruption. 1 Stengel: A Text-book of Pathology. 96 DISTURBANCES OF NUTRITION Therefore, patients who form sugar after the elimination of sugar from the diet furnish a grave prognosis. The chief aim in the treat- ment is the almost entire elimination of carbohydrate food or proteid food containing glycogen.^ All cells have a lessened resistance to bacteria, as shown by an increased tendency to pneumonia and tuberculosis,^ and a similar predisposition to pyorrhea alveolaris is probable. Symptoms. — Great thirst; frequent micturition (polyuria); in- creased amount of urine and the excess of sugar in it; indicated by high specific gravity and analysis; excessive appetite; emaciation; dyspeptic symptoms; hypochondriasis; insomnia; skin diseases, as furunculosis, are common. The glycosuria in diabetes mellitus may account for the cervical caries seen in diabetics by introducing a factor in lactic acid fermentation, viz., glycogen (starch). (See p. 79.) Peculiar Intrinsic Intoxications. — Without question, intense emotion results in the production of intrinsic intoxicants having some influ- ence upon metabolism. A most notable example is the classic one of a mother, who, shortly after intense rage at an insult, nursed her child, with fatal result to it. In another case a child was poisoned by the milk of a wet-nurse who spent a night in debauchery. (J. Lewis Smith.) The causes were of slightly different classes, the modus operandi much the same. Intense anxiety also has a disturbing influence. The nervous influence no doubt alters metabolism, and the products act as poisons in a degree corresponding to their amount. Acid Intoxication. — Many acids may be accumulated in the blood, producing the condition known as hyperacidosis or general hyper- acidity. The accumulation is probably the result of an increased production by metabolism or the incomplete reduction to urea, etc., of normal, acid cell excreta. The condition probably arises as the result of gastro-intestinal disturbances or altered nerve influence, or the failure of function in an organ, as in diabetes in which acidosis exists. The acids are carbonic, lactic, sarcolactic, sulphuric, phos- phoric, uric, diacetic, and /5-oxybutyric. The symptoms probably result from the acidosis rather than from any one acid. Suboxidation always accompanies the condition. Some of the acids combine with the alkaline elements, and, therefore, reduce the normal alkalinity, while the acids left disturb metabolism, thus leading to further disturbances. (See p. 90.) Gout. — Gout or podagra is a recurrent non-suppurative arthritis associated with the deposits of sodium biurate in the joints, and 1 See Works on Practical Medicine. 2 Stengel : A Tesst-bopk of Pathology, GENERAL MALNUTRITION 97 often with constitutional symptoms. It may be acute or chronic, by some thought always chronic, with occasional acute manifestation. It is largely hereditary or the result of inherited tendency to luxurious and indolent life. The excessive rise of uric acid from proteid waste is held to be the cause of the presence of biurates of sodium, as mechanical irritants to the joints, in which, owing to increased age (thirty or over) and its tendency to lessened use of joints, a sluggish circulation with increased acidity of the fluids of the part favoring precipitation is established. The salts crystallize in the synovial tissue and excite inflammation. A slight excess of uric acid in the blood is sufficient if the local conditions are as stated. Ebstein claimed that degenera- tion or necrotic changes in the tissues cause the precipitation. The sluggish circulation leads in this direction. (See Venous Hyperemia.) The conditions leading to a rise of uric acid are many: 1. Richly cooked foods, especially proteid and sugar, with wines. 2. Sedentary life combined with the above, or overwork and under- feeding, w^ith the use of malt liquors. 3. Chronic lead poisoning. 4. Defective elimination; the output in the urine is lessened just before the arthritis and increased after it. (Haig.) Chronic Gout, — After an acute attack in one joint others may be attacked, and tophi (concretions of sodium biurate) form in the ear or nasal cartilages, joints, sheaths of tendons, etc. In some cases crepitation of the joints may be felt and heard. The joints are dis- torted and enlargements by the tophi occur; the skin over them may be smooth and shiny, but not inflamed. The neighboring veins are prominent. Constitutional Symptoms. — Com- plications. — Weakness, anemia, cachexia, digestive disturbances, dyspepsia, gastric and intestinal, with constipation, failing nutri- tion, deformity, inability to exer- cise, mental irritations and dulness, granular atrophic kidney, cardiac hypertrophy and dilatation with arteriosclerosis, chronic gastritis, asthma, bronchitis, cerebral or other Topbi of gout (ziegier.; Fig. 52 98 DISTURBANCES OF NUTRITION thrombosis, sciatica, eye-skin lesions, obesity, diabetes, cholelithiasis, gravel, and vesical calculi. (Thompson.) Goutiness. — {Gouty Diathesis). — This is the inherited or acquired condition underlying the acute and chronic forms of gout, or a tendency to gouty symptoms in parts other than the joints, as the vital organs, skin, and nervous tissues. According to Ewart, "in its functional aspect it is due to the abnormal acidity of tissue juices, while a delicacy of tissues is produced or inherited, causing increased irritability and lowered resistance." The following diseases and symp- toms may be associated as results, and in themselves show the force of Michaels' claim for a general hyperacid classification of individuals with these symptoms. Vascular System. — Arteriosclerosis, an increase of the fibrous elements of the arterial walls and indicated by their thickening and the high tension. This induces overwork of the heart, resulting in cardiac hyper- trophy, and this occurring in the coronary arteries produces failing nutrition of the heart and myocarditis with appropriate symptoms. Respiratory System. — Asthma, emphysema, and obstinate recurrent bronchitis; bronchial catarrh in the young. Genito-urinary System. — Uric acid sediment with hyperacidity, hematuria, urethritis, oxaluria, albuminuria, glycosuria in some cases, menstrual disorders, and uterine and ovarian disturbances. Nervous and Muscular Systems. — Neuralgias, muscular soreness, lumbago, sciatica, bursitis, sore heels, hemicrania, or migraine, neurasthenia. Digestive System. — Acid dyspepsia, acid eructation. Tongue may show glossitis or leukoplakia, gingivitis, suppurative tonsillitis (infection added), bilious headaches, chronic gastritis, colic. Skin.^ — Harsh, dry, tending to eczema, pruritus, urticaria, erythema, acne, pityriasis, furunculosis, herpes, exfoliative dermatitis, per- spiration acid. Early gray hair, alopecia. Nails have longitudinal strise and are brittle. Eyes. — Iritis, glaucoma, conjunctivitis. Lesions of retinal vessels, retina and optic nerve, keratitis and panophthalmitis. These symptoms vary widely in different subjects. The chief points of interest to the dentist, apart from diagnosis of goutiness, is the peculiar tissue delicacy, and the general hyper- acidity as a cause. Without doubt this form of auto-intoxication (acidosis) in some cases leads to thickening of small arteries in the pericementum, leading to endarteritis obliterans, as shown by Talbot, and while not the only form of chronic gingival irritation, is prob- ably one cause predisposing to gingival infection leading to the more complicated, persistent, and recurrent forms of pyorrhea alveolaris. GENERAL MALNUTRITION 99 It may be regarded as established that goutiness may exist and lead to" declared" gout, or merely act as a chronic tissue irritant. Treatment. — The accepted medical therapeutics of goutiness, which lies within the special province of the dentist, may well be given here.^ Diet. — Three moderate meals a day. Eating between meals to be avoided. Any meat, except pork, once a day only; fresh fish, eggs, lean ham or bacon, oysters or shell fish at the other meals if desired; oatmeal, hominy, cornmeal, cracked wheat, stale bread and crackers, fresh green vegetables and potatoes, leguminous vegetables, apples, oranges, cream or other cheese as proteid, soups, tea and coffee in moderation, custard and gelatin preparations. Alkaline mineral waters, or plenty of plain water, before meals and at bedtime, or the tablets of lithium citrate or bitartrate may be taken dissolved in water. To be avoided are much meat, sweet dishes and confec- tionery, pastry, fried foods, pickles, spices, curry, cakes, griddle cakes, alcoholic and malt liquors. Hygiene. — Brisk exercise in the open air to increase oxidation and elimination through the induction of perspiration, and Turkish baths if no organic disease as of the heart and kidneys exists, and then only as advised according to the advance of the disease. Daily cold bathing with brisk rubbing; wearing of woollen clothing. Sea bathing or medicated baths. The bowels should be kept freely open with cascara sagrada or aloes if necessary. Special Therapeutic Indications. — For anemic and neurasthenic cases, Fowler's solution, with iron and cod-liver oil, or blood-making preparations. For feeble digestion: 3 — Tincture nux vomicse TTlx Compound tincture gentian or cinchona f5j S. — Talie before meals. For constipation, cascara sagrada, aloes, Carlsbad water, thialion, a laxative salt of lithium. For gastric catarrh with constipation and high vascular tension: I^ — Sodium sulphate 3J S. — Take in a half tumblerful of hot water one hour before meals, two or three times a day. For persistent high vascular tension: Nitroglycerin gr. y^n every three hours. Or, Sodium nitrate gr. iij three times a day. Or, Choral hydrate gr. v three or four times a day. 1 Acknowledgment in part to Thompson's Practical Medicine. 100 DISTURBANCES OF NUTRITION Lithemia. — This is a condition occurring in individuals who overfeed, drink too httle fluid, exerc se httle, and are under various nervous strains or overwork. A neurotic disposition and stimulants enhance the disturbances of nutrition. Cold weather, adding to the above a lessened perspiration and increase of work by the kidneys, increases the difiiculty. Tobacco and alcohol increase the ill effects. There may be no symptoms of gout in even marked cases. There is acidosis with lithuria (uric acid in the urine) or oxaluria; eventually renal, vascular, and hepatic scleroses develop, together with liability to localized inflammation chiefly in serous membranes, as the pleura or synovia. The hypothesis is that uric acid or some proteid toxin irritates the capillaries to contraction, thereby raising vascular tension, and by this twofold toxic and mechanical action causing arteriosclerosis, which in turn induces cardiac hypertrophy, sclerotic kidney changes, and vascular hepatic cirrhosis. It tends toward neurasthenia. Symptoms.^ — Nervous Symptoms. — ^Vertigo, tinnitus aurium, in- somnia, restlessness, burning or pricking sensation in the palms or soles, darting pains in the limbs, hebetude of mind, hypochondriasis, hemicrania, or diffuse basilar or frontal headache, general nervous irritability. Digestive Symptoms. — ^Lost or capricious appetite, coated red or dry tongue often fissured, aphthous ulcers, thirst, metallic taste in the mouth, pyrosis, hiccough, gastric oppression, nausea, gastralgia, vomiting, flatulence, constipation or irregular, dark-colored, frothy stool, palpitation of the heart (an hour or two after meals), hepatic tenderness. Urine .^ — Scanty, dark, strongly acid, of high specific gravity, with often brick-dust sediment of urates. Perhaps temporary albuminuria; perhaps inflammation of urinary passage. Skin. — Eczema, pruritus, urticaria or lichen. Treatment. — The condition of life should be reversed as to previous eating and drinking, and exercise to avoid the overstimulation by proteid food waste and to increase elimination. Stimulants are to be avoided, sodium phosphate given for its action upon the liver in promoting the excretion of bile, and also for its mildly cathartic effect. It also furnishes an element for regeneration of nervous tissue, and renders the body fluids more alkaline. Lithium prepara- tions are of little value. Potassium acetate, bicarbonate, and citrate are useful. The bowels are to be kept open. Headaches may be relieved by: GENERAL MALNUTRITION 101 I^ — Phenacetin gr. xxxvi Salol, Caffein aa. gr. xxiv M. and ft. capaulse no. xii. S. — A capsule three or four times a clay. For the neurasthenic cases treat with arsenic and glycerophos- phates. The diet is to be reguhited as in goutiness. The use of much fat, meats, or carbohydrates is to be avoided, to lessen the necessity for oxidation and for work by the liver. The use of a largely vege- table diet, to render the body fluid more alkaline. Plenty of water between meals, to flood the system. Hygiene, rest, and exercise, as in goutiness. Rheumatism. — Rheumatism is an acute fever, probably of infective origin, characterized by constitutional toxic symptoms, inflammation of the joints, muscles, serous membranes, skin, or even tonsils. It may be classified as acute, chronic, or muscular rheumatism. Etiology of Acute Rheumatism. — It may be transmitted to the newborn, or a constitutional tendency to it may be inherited. It is most common to young adults (fifteen to twenty -five years), but no age is exempt. It is most common in males. Climate, exposure to cold, injuries and overwork of parts, occupa- tion inviting exposure to hardships, chronic alcoholism, nervous shock, debility, starvation, anemia, and chorea are other predisposing causes. The exciting cause is supposed to be largely due to a bacillus isolated from the blood or joint of rheumatic patients, but it is also induced by a diet of meat or the fermentation produced by overuse of sugar and starches, causing a rise of lactic or uric acid in the blood. Clinical History. — It presents the following clinical difference from acute gout.^ Acute gout. Acute rheumatism. Exciting cause . Often errors in eating and drinking. Sometimes cold and damp. First attack Commonly in one great toe. Commonly in large joints. Later attacks . Both toes, fingers, knees, etc. Rare in toes, often shoulder or hip. Appearance of joint Color, dark red, shiny, and tense. Lighter red. Pain Worse at night or early morning, localized. Migratory from joint to joint. Subsidence .... Leaves thickening and deformity with repeated attacks. Leaves normal joints. Tophi In lobes of ear, finger-joints, etc. Never present. Age and sex Common in middle-aged men; very Common in young persons, chil- rare in children. dren, and women. Effect of treatment Salicylates have but little effect; col- Salicylates have marked effect; chicum marked effect. colchicum no effect. ' Thompson's Practical Medicine 102 DISTURBANCES OF NUTRITION Symptoms. — Pain and inflammation of joint, which may be pre- ceded b}^ headache, indigestion, constipation, lassitude, muscular aching, chilliness, mild inflammation of tonsils, pharynx, and larynx. Tongue coated, pale, and indented by the teeth; breath foul. Fever 103° or 104° F., sometimes hyperpyrexia. Sweating during the height of convalescence, with acid odor from decomposition of fatty acid, but may be neutral or alkaline in parts of same person, therefore not an effort at elimination of acid. Saliva. — Acid, excess of potassium sulphocyanid. Urine. — Hyperacid, urates increased, chlorides diminished, uric acid abundant, sometimes albuminuria. Heart. — Pericarditis and endocarditis in one-fourth of all cases. Mind. — Clear except in hyperpyrexia. Skin. — Urticaria, petechise, ecchymoses, purpura, eczema at times ; subcutaneous nodules in youth. Complications. — Conjunctivitis occasionally; chorea frequently. Prognosis. — Uncertain as to period before recovery; relapses, or recurrence common. Treatment. — Sodium salicylate and oil of gaultheria, internally, relieve the pains and inflammation. Cold baths to reduce the tem- perature. Blisters as counterirritants; protection from jarring by cotton and fenders; guaiacol with glycerin, oil of wintergreen, etc., as local lotions. The diet is much the same as in gout. Chronic Rheumatism. — This form has much the same etiology, but is more common after the fortieth year. It appears in much- used joints, and is most common in females. Morbid Anatomy. — Fibrous thickening and contraction produce moderate thickening and distortion of joints; atrophy of muscles about joints may occur. Symptoms. — Symptoms are of slow onset; general health good unless inability to exercise produces alteration. Pain absent except when joint is overworked or in damp weather. The fingers may be deflected laterally and flexed by contraction of tendons. Febrile attacks, 101° F., occur from time to time, but the urine is normal. Prognosis. — Disease progressive, no recovery, but temporary im- provement by treatment so that the joints may remain quiescent for years. Never fatal. Systemic Treatment. — Simple alkalies or alkaline waters, arsenous acid, yV gr. t. i. d., cod-liver oil for the debilitated and anemic, Carls- bad salts or sodium phosphate for constipation. Local.— Drenching with hot (105° to 110° F.) and cold (70° F.) water alternately, followed by massage and wrapping the joint in flannel. Sweating in an enclosing box with hot air, 240° or 250° F., GENERAL MALNUTRITION , 103 followed by Swedish movements. The lotions used for acute rheu- matism are also used. The diet is much the same as for goutiness. Muscular Rheumatism. — In this form of rheumatism the dis- turbance is in the muscles, with little constitutional disturbance. The essential lesion is probably an inflammation of the muscles, though the nerves may suffer. Ssrmptoms. — Local tenderness and pain increased by every con- traction of the muscle. Pain stationary, worse by night and during barometric disturbances; oxaluria in some cases. Scorbutus (Scurvy). — This is a subacute or chronic disease, characterized by inanition, anemia, and asthenia, with purpura and a tendency to swelling of the gums. WTiile of doubtful origin, defective hygiene and the use of improper foods, especially the lack of fresh vegetables and fruits, and the use of salted foods, the improper absorption of food owing to chronic intestinal maladies, as dysentery, or to cachexias, as in malaria, cancer, and syphilis, are the chief causes, though infection has been held to act upon those debilitated by the above causes. In young children it is due to the use of proprietary foods instead of fresh food, and appears mostly from the eighth to the twelfth month, rarely before the sixth or after the sixteenth month. The circulation is feeble and the blood impoverished. The gums are red and swollen, protrude over and between the teeth if present, and bleed; the breath is offensive, owing to putre- faction of the blood. The stomach shows great irritability, and there is thirst and craving for acid foods. The joints are swollen and painful, owing to the hemorrhages. The urine is high colored; the acidity and temperature lowered. Treatment. — As a prophylactic and cure, lime, lemon, or orange juice, together with the use of fresh vegetables and fruit in adults, or their juices in infants. Fresh milk modified, white of egg, and beef juice, or breast feeding, are to be substituted for proprietary foods or table feeding in infants. Rachitis (Rickets). — This is a disease found in infants develop- ing typical deformities in the bones, and due to a deficiency of lime salts in them, in turn probably due to an absorption of that present, by hyperemic tissue present, and a diminution in the deposi- tion of a fresh supply. There is usually, also, hypertrophy of the liver and spleen. The prolonged lactation of the child upon unfit milk, poor in fat, and the overuse of proprietary foods lacking the proper food elements, as farinaceous food or exclusively a condensed milk diet. The teeth develop slowly and are apt to be of faulty 104 DISTURBANCES OF NUTRITION structure. The general line of treatment is much the same as for scorbutus. Neurasthenia. — This is a condition of nervous exhaustion, no reserve nerve matter being held for even slight effort. It is often accompanied by nervous excitability, insomnia or disturbed sleep, apprehension, melancholia, failure of appetite, and feeble digestion. Nervous energy is lost and irritability remains. It may be caused by continued excitement or overwork of the nervous system, and responds to rest, regulated diet, general tonics, treatment by glycero- phosphates of lime and soda in the serious cases, while in mild cases, exercise in the open air, baths, sea or mountain air, combined with the tonic treatment and abstinence from stimulants, effect a cure.^ In view of demonstrations upon animals that nerve tissue is actually used up in nervous energy, the above treatment probably permits a gradual restoration of the elements of nerve tissue. Oxaluria. — ^The increase of sodium and calcium oxalate crystals in the urine indicates : 1. That food rich in oxalic acid (as tomatoes or rhubarb) has been used in increased quantity. 2. That intestinal fermentation is existent and forming it from glucose. (Baldwin.) 3. That intrinsic increased production of oxalic acid by oxidation of uric acid, in turn derived from the purin bases of the nucleins, and nucleo-albumin of the tissues is present. It frequently accompanies the increase of uric acid in the urine, and is regarded by Simon^ as due to impairment of normal oxidation processes in the liver. Thus it may be found in goutiness and lithe- mia. It is also associated with dyspeptic and nervous symptoms, producing a condition known as oxalic acid diathesis. It also sometimes accompanies diabetes. Continued oxaluria may result in the formation of calcium oxalate calculi. It is frequently associated with nervous irritability, hypo- chondriasis, and neurasthenia. Oxalates are found in the urine and saliva. (See pp. 91 ;and 92.) Phosphaturia. — The tribasic, phosphoric acid, H3PO4, is a normal product of metabolism, and like other acids combines with salts before elimination. Its alkaline combinations are sodium phosphate, Na3P04; calcium phosphate, Ca2(P04)2; and magnesium phosphate, Mg3(P04)2, which may also be found in alkaline urine. Its neutral combinations are di-sodium hydrogen phosphate, Na2H.P04; calcium hydrogen phosphate, CaHP04 ; and magnesium hydrogen phosphate, ' See Thompson's Practical Medicine. ^ Simon: Clinical Diagnosis. fl^/ Rg.VM. a 6 c d A. /• 9 A I J k m m n BLOOD. (p^lirlich triple stiiiii.) (Prcpurcfl h>- Dh. 1. P. Lyom.) Fly. I. TYPES OF LEUCOCYTES, a. PolymorphonueieHP Neutrophile. b. Polymorphonuclear Eosinophile. c. Myelocyte iNeutrophilici. d. Sosinophilic Myelocyte, e. Large Lymphocyte (large Mononuclear). /. Small Lymphocyte (small Mononuclear). Fig. ir. NORMAL BLOOD Field contains one neutrophile. Red.s are norm.al. Fig III. ANEMIA. POST-OPERATIVE (.secondary). The reds are fewer than, normal, and are deficient in haemoglobin and somewhat irregular in form. One normoblast is seen in the field, and two neutrophiles and one small lymphocyte, showing a inarked post-haemorrhagic anaemia, with leucocytosis. Fig. IV. LEUCOCYTOSIS, INFLAMMATORY. The reds are normal. .A marked leucocytosis is shown, w^ith five neutrophiles and one small lymphocyte. This illustration may also serve the purpose of showing tha leucocytosis of rnalignant tu.ncr Fig. V. TRICHINOSIS. .■\ marked leucocytosis is shown, consisting of an eosinophilia. Fig VI. LYMPHATIC LEUKEMIA. Slight anaemia. A large relative and absolute increase of the lymphocytes (chiefly the small lymphocytes) is shown. Fig. VII. SPLENO-MYELOGENOUS LEUKEMIA. The reds show a secondary anaemia. Two normoblasts are shown. The leucocytosis is massive. Twenty leucocytes are shown, consisting of nine neutrophiles, seven myelo- cytes, two small lymphocytes, one eosinophile (polymorphonuclear) and one eosinophilic myelocyte. Note the polymorphous condition of the leucocytes, i.e., their variations from the typical in size and form. Fig. VIII. VARIETIES OF RED CORPUSCLES. a. Normal Red Corpuscle (normocyte). 6, c. Anaemic Red Corpuscles, d-g. Poikilocytes h. Microcyte. i. Megalocyte. j-n. Nucleated Red Corpuscles, j.k. Normoblasts. I. Micro- blast, m, 71. Megaloblasts. , GENERAL MALNUTRITION 105 Mg.H.P04, all found in the blood and in neutral urine. Its acid combinations are sodium di-hydrogen phosphates, NaH2P04, and calcium dihydrogen phosphate, Ca(H2P04)2, found in acid urine, and to which the normal acidity is partly and chiefly due. Ammonium magnesium phosphate (NH4MgP04+6H20) or triple phosphate is also found. ^ Many of the phosphates are derived from the food, but some are formed by proteid catabolism; one-third of all excreted is eliminated in the intestinal secretion; some are eliminated in the saliva, as shown by the formation of salivary calculi. In diseases requiring increased phagocytosis, as febrile conditions, the elimination of phosphates falls, the phosphates probably being utilized in the formation of leukocytes. The excretion is increased in diabetes and tuberculosis. A very large increase in the total amount of phosphates eliminated (7 to 9 grams in twenty-four hours) is called phosphatic diabetes, and has been associated with four classes of symptoms: (a) Cases with marked polyuria and marked nervous symptoms. (6) Cases preceding or accompanying pulmonary diseases, espe- cially tuberculosis. (c) Cases in which phosphaturia alternates with or co-exists with glycosuria. (d) Cases in which oxaluria, polyuria, and slight albuminuria are present, and in which some relationship with gout exists. (See p. 98.) An increase in the«amount of phosphates in the blood tends to the production of calculi. As nerve tissue contains a considerable amount of lecithin or phos- phorized fat essential to it, excessive drain upon this may result in a loss of this substance by catabolism, with loss of phosphates doubtless masked by the preponderance of phosphates derived from the food. This is borne out by the beneficial use of glj'cerophosphates of lime and soda, rest, and general tonic treatment in neurasthenia. (See p. 104.) Albuminuria. — The presence of albumin in the urine may be either (1) transitory, remittent, or cyclic (recurring with regularity), as the result of functional disturbances, as anemia, adolescence, in general malnutrition, after severe exercise or cold baths; or (2) due to organic disease of the kidney, as acute and chronic nephritis, renal arteriosclerosis, and amyloid degeneration of the kidney; or (3) to fevers, as typhoid and yellow fever, and is due to the presence 1 Kirke's Physiology, 106 DISTURBANCES OF NUTRITION of bacterial toxin in the blood; or (4) to circulatory disturbances, as organic heart disease, or to local circulatory disturbances, as com- pression of renal veins by a pregnant uterus; or (5) to impeded out- flow of urine; or (6) to hemic changes, increasing the diffusion of albumin, as in scurvy, leukemia, pernicious anemia, jaundice, and diabetes; or (7) to toxins in the blood other than febrile, as turpentine, salicylic acid, phosphorus, arsenic, etc., probably producing circu- latory disturbances and irritation of glandular epithelium of the kidneys; or (8) to neurotic disturbances, as epilepsy; or (9) to in- gestion of excessive amounts of cheese, eggs, and other albuminous food; or (10) to accidental admixture after urine excretion by the kidneys.^ It is, therefore, like oxaluria and phosphaturia, more a symptom than a disease. 1 Simon: Clinical Diagnosis. CHAPTER V DISTURBANCES OF THE VASCULAR SYSTEM A SUITABLE amount and quality of blood normally flows through the circulatory apparatus, and is in close relation to processes of nutrition. The amount of blood in the vessels may be increased (plethora), though not permanently. It may be decreased rapidly in quantity, as by hemorrhage, or its red corpuscles may be gradually lessened in number (acute or chronic anemia). The proportion of white corpuscles to red ones may be increased abnormally (leukemia). The hemoglobin of red corpuscles may be deficient (chlorosis). Locally the amount of blood in a part may be increased (hyperemia or inflammation) or diminished (ischemia). Normally the blood contains floating in the plasma 5,000,000 red corpuscles, or erythrocytes, and from 5000 to 10,000 (1 to 500 red) white corpuscles, or leukocytes, to each cubic millimeter. (See Plate, Fig. II.) A marked increase in the number of erythrocytes is termed polycythemia; a marked decrease, oligocythemia. The temporary increase in number of white corpuscles is leukocytosis; a persistent increase, leukocythemia or leukemia. The blood corpuscles may be classified as follows: Erj'throcytes. Non-nucleated red corpuscles. Normal to blood. Normocytes (normal size) See Plate. Fig. 53 Fig. VIII 1,2,3.4. a iMicrocytes (small size) h Macrocj^es (large size) Megalocytes (very large size) % Poikilocytes (irregular form) d e f g Erythroblasts. f Nucleated red corpuscles derived from red marrow of bones. Pathological indicators. I Normoblasts (normal size) Microblasts (small size) Megaloblasts (large size) }k I Leukocytes. White corpuscles. Normal to blood. Pathological indicators. Lymphocytes (small) Lymphocytes (large) Polymorphonuclear neutrophiles Polymorphonuclear eosinophiles See Plate, Fig. 53 Fig. I 22% 5 / 6" 6 e 70" 7 a 2" 8 b I Basophilic leukocytes or mast cells. Neutrophilic myelocytes from bone marrow Eosinophilic myelocytes 108 DISTURBANCES OF THE VASCULAR SYSTEM Fig. 53 "2 Normal blood (triacid stain): 1, normal red cell, flatly spread and evenly stained; 2, normal rouleau; 3, normal red cells varying slightly in size, thickly spread, showing central clear areas; 4, normal red cell, of slightly altered shape; 5, lymphocyte, medium size; 6, large mononuclear leukocyte, incurved nucleus; 7, polynuclear neutrophile leukocyte; 8, eosinophile leukocyte. Separate nuclear lobes. (Schmaus and Ewing.) ANEMIA Anemia is a condition in which the blood is lessened in quantity or partly deprived of its essential constituents — i. s., red corpuscles and hemoglobin — in consequence of which the tissues receive less ox;^^gen and the general nutrition is impaired. Acute Traumatic Anemia occurs as a result of copious hemor- rhage. The individual becomes temporarily pale and weak. The arterial pressure is lessened, the circulation slowed, and the pulse is frequent and small. Recovery is, as a rule, prompt, the water being first restored and later the corpuscles being regenerated.^ Frequent hemorrhages cause the blood to become watery and debility results from impaired nutrition. (See Plate, Fig. III.) ' Ziegler: General Pathology ANEMIA 109 Symptomatic Anemia. — A diminution in the number of red cor- puscles may occur as a result of protracted o\erwork, anxiety, study, or long-continued illness, such as a fever. The number of red blood corpuscles may be reduced to one-half the normal amount, and there is a corresponding debility. The condition may disappear with appropriate removal of the cause. Chlorosis. — This is a form of anemia occurring, for the most part, in girls and young women, and characterized by a great deficiency in the hemoglobin of the red corpuscles without a corresponding reduc- tion in the number of the red corpuscles. In the watery blood very small red corpuscles (microcytes) are seen; also a few very large on6s (macFocytes), and some of irregular outline (poikilocytes).^ Myelocytes are occasionally seen. (Stengel.) The pathology is uncertain. If prolonged, the red corpuscles may sink in numbers to 3,000,000 or 2,000,000 per cubic millimeter and 20 per cent, of hemoglobin. Being, as a rule, readily cured by a course of iron, it is inferred that the body is starved of iron, an essential constituent of hemo- globin. It is often associated with gastric disturbances, constipation, defective hygiene, and irregular habits, which apparently have a causal relation. The skin and mucous membranes are pale and have a slightly greenish tinge.^ In recovery the number of corpuscles is first increased, then the hemoglobin. Leukocytosis. — This is not a form of anemia, but a temporary increase in the number of multinucleated leukocytes, apparently derived from the lymphoid structures of the body in response to some demand for leukocytes. Thus it occurs after a full meal, in the later months of pregnancy, in acute fevers, in tuberculosis, and in conditions accompanied by suppuration.^ Its presence during the course of surgical disease has been held to be diagnostic of pus forma- tion^ — e. g., in abdominal surgery from SOOO to 20,000 per cubic millimeter. (See Plate, Fig. IV.) Leukemia. — Leukemia is a disease characterized by a consider- able increase in the number of white corpuscles of the blood, by a diminution in the number of the red corpuscles, and by enlargement of some of the lymphatic organs. The proportion of one white to ten red corpuscles is common (1 to 5 often, occasionally 1 to 1). The spleen may be hypertrophied (splenic leukemia). The lymphatic glands may be hypertrophied (lymphatic leukemia). In these latter cases the blood contains an excess of uninuclear leukocytes. It is rare ' Green: Pathology and Morbid Anatomy. 2 Ibid. » Ibid. ^ Cabot: Boston Medical and Surgical Journal. 110 DISTURBANCES OF THE VASCULAR SYSTEM except when combined with other forms. A^Hien the marrow of bones is hypertrophied (myelogenic leukemia) large mononuclear leukocytes with neutrophile granules are found^ (myelocytes) and the lympho- cytes and polymorphonuclear forms are increased.^ The blood con- tains toxic substances generated by the destruction of leukocytes, xanthin bodies, and acids (lactic, acetic). The urine frequently contains an excess of xanthin bases and lactic acid. (See Plate, Figs. VI and VII.) Pernicious Anemia. — This is a comparatively rare but generally fatal disease, characterized chiefly by a great fall in the number of red corpuscles to one million or less per cubic millimeter, those remaining being altered in form and size and showing evidences of degeneration. The total hemoglobin is reduced, but the relative amount may be increased. Degeneration is shown by peculiarities of staining. Normal red corpuscles (normocytes), nucleated red corpuscles (megaloblasts), large nucleated red corpuscles (giganto- blasts), microcytes, and poikilocytes are found. The blood platelets and leukocytes are somewhat diminished.^ The oxygen-carrying power is markedly lessened and all tissues suffer from malnutrition. The power of coagulation of the blood is lessened. Marked fatty degeneration of the heart muscles is apt to occur^ as well as fatty changes in the kidneys and liver. The causes are obscure, but gastro-intestinal disorders, intestinal parasites, pregnancy and lactation, hemorrhages, malaria, syphilis, tuberculosis, and infections are the chief causes supposed to produce it. Aplastic anemia is a severe type of progressive pernicious anemia, in which the bone marrow fails to develop myelocytes and erythro- blasts owing to lack of marrow cells (hypoplasia of bone marrow). COAGULATION OF THE BLOOD The blood when drawn from the body or in contact with a wounded surface or injured vessel wall undergoes a process of solidification called coagulation. This is due to the splitting up of the fibrinogen ordinarily in solution in the blood into a globulin and fibrin. The latter takes the form of a network, in the open spaces of which the corpuscles are entangled (Fig. 54). The formation of fibrin is brought about by the activity of an unorganized ferment (fibrin ferment or 1 Ziegler: General Pathology. 2 Stengel: A Text-book of Pathology. 3 Green: Pathology and Morbid Anatomy. « Ibid. COAGULATION OF THE BLOOD 111 thrombin) liberated by injured white corpuscles. For the production of this ferment calcium salts are necessary.^ Coagulation may occur in the living vessel, as a throm- ^^°- ^* bus, or in the interstitial tissue, as - Ax -.-?^ '<^/V\-<>^ in inflammation and infarction. Fig. 55 Fibrin filaments and blood tablets . ^ , net- work of fibrin, shown after washing away the corpuscles from a preparation of blood that has been allowed to clot; many of the fila- ments radiate from small clumps of blood tablets; B (from Osier), blood corpuscles and elementary particles or blood tablets within a small vein. A thrombus in the saphenous vein, show- ing the projection ot the conical end of the thrombus into the femoral vessel: S, saphe- nous vein; T, thrombus; C, conical end pro- jecting into femoral vein. At v, v, opposite the valves, the thrombus is softened. (Vir- chow.) Diagram to show phenomena of venous thrombosis: v, v, valves of veins; a, h, primary thrombus (white) ; c, d, e, f, g, secondary white thrombi connected with primary white throm- bus by various red thrombi; h, piece of white thrombus becoming detached by blood cur- rent. (Green, modified from Thoma.) Thrombosis. — The formation of thrombi or clots within the living vessel may occur in the heart, arteries, veins, or capillaries. If the blood stream be somewhat retarded, an increased number of white corpuscles and blood platelets occupy the peripheral zone and ' Kirke's Physiology 112 DISTURBANCES OF THE VASCULAR SYSTEM adhere to the vessel wall. If the vessel wall be injured, the blood platelets become attached to it. With these platelets the white corpuscles and sometimes the red become deposited. Fibrin forms and the corpuscles are included. The thrombus is red when red corpuscles are included in it; white when only white corpuscles are present. The causes of thrombosis are these: (1) A retardation of the blood current at some point from some cause; (2) local changes in the walls of the vessels and (3) probably pathological changes in the blood. ^ Older thrombi are firmer than those recently formed. Thrombi are also formed in the capillaries, a circumstance which favors the spontaneous cessation of hemorrhage. They may form in the vessels in inflammation. Remaining in the situations in which they were Fig. 57 Fig. 58 Embolus impacted at the bifurcation of a branch of the pulmonary artery, showing the formation of thrombi behind and in front of it, and the extension of these as far as the entrance of the next collateral vessels: E, embolus; i,i', secondary thrombi. (Virchow.) a V Diagram of a hemorrhagic infarct: a, artery obliterated by an embolus (e) ; v, vein filled with a secondary thrombus ( Joly: See Dental Cosmos, 1909, p. 488. 2 Reverdin: Dental Cosmos, February, 1904, p. 162. » Rosod: New York Med. Jour. * Hare: Practical Therapeutics. ^ Jour. Amer. Med. Assoc. ^ Porter: Loc. cit. ' Hare: Loc. cit. 8 See Deutal Cosmos, 1908, p. 185. » See Dental Cosmos, 1908, p. 436, 116 DISTURBANCES OF THE VASCULAR SYSTEM LOCAL DISTURBANCES OF THE CIRCULATION The amount of blood in a part may be increased or diminished. The types of local disturbance of the circulation differ as to causes, phenomena, and effect, and as to the indicated treatment for each. In health the bloodvessels are maintained at a proper caliber through the action of two sets of vasomotor nerve fibers: 1. The vasoconstrictors, which control the- involuntary muscles of the vessel wall, and which, when stimulated, cause contraction of the vessel. 2. The vasodilators, which, when stimulated, inhibit the muscular action and permit dilatation. Ischemia. — This is local anemia. The quantity of blood in a part is less than normal. It is direct when some cause obstructs the flow from an artery into a part, as when pressure of any sort is applied directly to a part or to the artery leading to it, or when an injection of fluid has been made into a part, as in cocain injections. Disease of an artery may deprive a part of blood, as in thrombosis or arteriosclerosis. Anastomotic circulation may eventually relieve a part; if not it remains pale and cold, atrophies, and may undergo degeneration or necrosis. An infarct may remain ischemic. Arterial Hyperemia. — Arterial or active hyperemia is a more or less prolonged increase in the amount of blood in the dilated arteries of a part. It expresses the reaction which occurs as the consequence of the presence of an irritant, the action of which lessens the arterial tension and permits dilatation with a consequent excess of blood. Causes .^ — The lessened arterial resistance is produced either by a stimulation of the vasodilator nerves or a sedation or paralysis of the vasoconstrictor nerves. Certain causes act to produce constriction of the vessels, but later the muscle cells of the walls are fatigued and dilatation results — e. g., the reaction after the prolonged application of cold. The removal or diminution of pressure, to which vessels have become accustomed, is also a cause of their dilatation; often sudden enough to cause bursting. Irritants and mild injuries act upon the sensory nerves of a part, and by reflex action through the vasomotors (sympathetic system) produce hyperemia of the part itself — e. g., heat as a cause. Irritation of sensory nerves may induce a reflex hyperemia in other parts to which branches of the same nerve are distributed — e. g., the peripheral hyperemia of neuralgia, induced by irritation of a tooth pulp. LOCAL DISTURBANCES OF THE CIRCULATION 117 A similar effect may be produced in deep-seated organs to which other nerves are distributed — e. g., hyperemia of deep organs through the appHcation of irritants to the skin over them or hyperemia of the intestinal wall (tenth nerve) as the result of the stimulation of a pulp vmderlying an erupting tooth (fifth nerve). Collateral hyperemia is induced by the diminished flow of blood to other parts — e. g., by the bandaging of parts or through the chilling of the surface of the body. A part having a lessened resistance may become hyperemic. Compensatory hyperemia may occur through the removal of one of a pair of organs; the other receives the excess of blood, sometimes becomes hypertrophied, and takes upon itself an increased amount of work. (See Hypertrophy.) A physiological hyperemia occurs in organs during periods of activity, the work required acting as a stimulus to the vasomotor nerves. Arterial hyperemia is produced as the first step in the process of inflammation, but can be independent of it. (See Inflammation.) Pathology. — The arteries are dilated; there is an increased flow of blood through them and also to them through their own nutritive arteries; the pressure in the veins rises as the veins are enlarged to accommodate the blood. As exudation sometimes does not increase markedly, the lymph pressure is not increased except in marked cases, in which some edema may occur. The function of the part may be disturbed in the more marked cases. (For illustrations, see Hyperemia of the Pulp.) Results. — Continued arterial hyperemia, as a rule, results in an increase of nutrition, even to the arteries themselves via the vasa vasorum. The arteries may be permanently enlarged, their walls thickened, and the tissues about them hypertrophied in consequence of the increased capacity for work in the part. Hyperesthesia of nerves and nervous tissue is often a result. In marked hyperemia with function altered there is a tendency to the degenerations. (See Arterial Hyperemia of the Pulp.) Ssrmptoms. — These naturally would be and are increased redness, temperature, and sensibility; more or less throbbing in marked and pathological cases, in some cases swefling and throbbing pain. The increased temperature is due to the increased oxidation. Degrees of Hyperemia. — It is to be borne in mind that the hyper- emia may be of several grades, varying from a very mild exaltation of function and sensation to a distinctly pathological condition with altered function. The effects may be constructive in character or destructive, the former due to the increased nutrition, the latter to interference with it. (See Constructive and Destructive Diseases of the Pulp.) 118 DISTURBANCES OF THE VASCULAR SYSTEM Hyperemia as a Resistance to Infection. — According to Biers and others the induction of hyperemia in an infected part increases the opsonic power of the excess blood, and therefore is antagonistic of infection. No doubt this is the natural process in inflammation. It has been occasionally noticed that stimulation, as in the use of a capsicum plaster in acute apical abscess, has produced resolution. Usually confined abscesses are enlarged and not cured by such stimulation. Treatment. — The principle underlying the treatment is to remove the cause and procure surgical rest. The symptoms, as a rule, then subside promptly. It may be that the conditions require treatment irrespective of the cause, which may not be determined or be absent, the vessels being dilated as the effect of a previously acting cause. The effect aimed at is the reduction of the dilated vessels. This is attempted at times through the use of drugs; for example, ergot stimulates the vasoconstrictor system and lessens the caliber of all the vessels, including those affected. Aconite, the antagonist of ergot, reduces the heart action by sedating the motor apparatus of the heart, thus reducing the arterial pressure.^ Less blood is delivered to a part in a given time. Many cases of superficially seated hyperemia are amenable to local treatment. Local sedation of sensory nerves and contraction of vessels are pro- duced by application of dry or wet cold (ice bags, ice wrapped in muslin, cloths taken in succession from a block of ice, the Leiter coil, etc.); also by the application of sedative astringents, as the liquor plumbi subacetatis in the well-known formula of lead-water and laudanum: I^ — Tincturse opii fSJ Liq. plumbi subacetatis f3j Aquse Oj — M. in which to the astringent effect of the lead is added the sedative effect of the opium, if cold sedation and contraction are added. , The principle of derivation is also employed. What is known as counterirritation is a common means of treatment. An irritant such as a mustard plaster or a blister or dry cup applied at a distance to the affected part induces a flow of blood to the point of application and lessens the amount of blood in the area of hyperemia. The volume of the blood being in definite amount, if an excess exists in any part a deficiency will be found in other parts. The hot pediluvium acts upon this principle by drawing a con- > Biddle: Materia Medica and Therapeutics. LOCAL DISTURBANCES OF THE CIRCULATION 119 siderable excess of blood into the vessels of the lower extremities. This action is increased by adding a small quantity (two or three tablespoonfuls) of mustard to the hot water. It is suggested by Endelmann that the water be at first only warm and the hot water added as the vessels relax. ^ The volume of the blood may be actually reduced and a derivative hj'peremia of the sweat glands be produced by the use of diaphoretics. Cathartics lessen the blood volume and cause mild hyperemia of the alimentary canal. Diuretics act in a similar way upon the kidneys. In deep-seated hyperemia counterirritation is valuable alone or conjoined with other forms of derivation. Venous Hyperemia. — Venous (mechanical or passive) hyperemia is an excess of blood in a part beginning in the veins, which are dilated in the hyperemic area, though they may be occluded between it and the heart. Causes. — 1. Any mechanical interference with the passage of the blood through the veins on its way to the heart — e. g., the action of bandages, tumors pressing on veins, thrombi in veins, etc. 2. Insufficiency of any of the mechanical forces aiding the pro- pulsion of the blood through the veins — e. g., diminished cardiac power or valvular insufficiency; obstructions, dilatations, or rigid- ity of arteries; insufficient muscu- lar contraction upon or valvular incompetency in veins, or lessened or excessive thoracic aspiration, etc. The second class of causes produces a collection of blood in the veins and a consequent reduction of volume in the arterial s}'stem. Pathology.— The veins are di- lated, the current is slowed, and the intravenous pressure is in- creased, in consequence of which watery (serous) exudations occur in the parts about them (edema). For the same reason in marked cases diapedesis of red corpuscles may occur (hemorrhage by diapedesis), and their hemoglobin may be dissolved out. The blood in the parts not being sufficiently changed, and in some cases in a state of stasis, there is a lessened food supply and waste removal, and cell nutrition suffers accordingly. Vital FiQ. 59 Venous hyperemia of the liver. Two capillaries near central hepatic vein, show- ing the thickening of the walls and the accumulation of red blood corpuscles within them. X 500 (Green.) 1 Dental Cosmos, 1904 120 DISTURBANCES OF THE VASCULAR SYSTEM processes are lessened, secretion is diminished, there is less oxidation, and hence less heat is produced and less work is done. Fatty degener- ation, atrophy, and in markedly continued cases necrosis may occur. Long-continued venous hyperemia with great intravenous pressure may produce dropsies. If the walls of the veins are weak and are permanently distended or thicken under pressure and become tortuous, the condition is called varicosity of the veins (varicose veins). The exudate of venous hyperemia differs markedly from that of inflammation.^ Htperemic Exudate Inflammatory Exudate Poor in albumin. Rich in albumin. Rarely coagulates in the tissue. Usually coagulates in the tissue. Contains few cells. Contains numerous cells. Low specific gravity. High specific gravity. Contains no peptone. Contains peptone (product of cell disintegration) . This is probably due to an increased permeability in the vessel wall in inflammation permitting the albumin of the blood to pass through. Treatment. — The treatment consists of the removal of the mechan- ical obstruction to the return of the blood and mechanical support of the engorged vessels, with a view to recovery of the tone of their muscular walls. This latter is accomplished by means of elastic bandages or compresses, and in situations in which these cannot be used astringents may be employed. The part is elevated, when possible, to aid in the return of the blood to the heart. In certain circumstances, as in an engorged tooth pulp, actual depletion of the engorged part must be resorted to by bloodletting. (See Destructive Diseases of the Pulp.) In cases due to failure of blood-propelling forces these are to have appropriate treatment. INFLAMMATION Inflammation may be defined as a series of hyperemic changes expressive of the reaction of living tissue to irritation, and character- ized chiefly by an excessive diapedesis of leukocytes and exudation of coagulable lymph from the bloodvessels. Causes. — Any irritant or injury capable of producing a lesion of the bloodvessel wall not involving its immediate death can produce inflammation. In case direct death is produced, the inflammation, if any, occurs in the tissue contiguous to the dead part. The causes of inflammation may be divided first into non-septic and septic or infective. The non-septic causes may be extrinsic or 1 Park's Surgery. INFLAMMATION 121 intrinsic. The extrinsic non-septic causes are: (1) Physical irritants, such as violence, mechanical irritation, pressure or traumatism, excessive heat or cold, and electrolytic action. (2) Chemical irritants — e. g., the action of acids, caustics, etc. (3) Nervous or vital irritants — e. g., rubefacients, epispastics, arsenic, etc. These act only on living tissue through the medium of the nerves. An intrinsic non-septic cause may produce inflammation — e. g., urates in tissue, mechanical strains upon tissue, temporary lack of blood in a vessel or central nervous disturbance, as in herpes from locomotor ataxia. Non-septic causes, as a rule, produce only such mild inflammatory phenomena as are concerned in circumvallation' of an irritant, absorption of it, and in repair or production of new tissue. No pus is produced unless pyogenic bacteria gain ingress. This class of inflammation is termed simple inflammation. Septic or Infective Causes. — These are fungi or their products, and the classes of inflammations produced are much more severe, continuous, and destructive in their nature, and are termed infective inflammations. Pathology of Simple Inflammation. — If to the web of a frog's foot tincture of capsicum be applied, or if its mesentery be exposed to the air, and either be examined under the microscope while the animal is living, it is noted that after a possible short period of contraction of the arterioles dilatation of arteries at once begins and is gradually followed by dilatation of the veins and capillaries. This continues to steadily increase for about twelve hours. During the first hour of this period the blood current is accelerated and the first stage of an inflammation is thus an arterial hyperemia. Following this acceleration the blood flow is increasingly retarded. The retardation is due to the action of the leukocytes, large numbers of the mono- nuclear and polymorphonuclear forms of which fall out of the central blood stream into the periaxial stream and collect along the walls of the small veins (Fig. 60, h). Several layers of leukocytes may thus form. Probably some peculiar attraction exists between the leuko- cytes and the wall of the vessel, or a positive chemotaxis exists as in infective inflammation. This massing of leukocytes compels the red corpuscles to the centre of the stream (Fig. 60, a), and their passage is mechanically interfered with; thus the further dilatation of the vessel becomes a process of venous hyperemia. The vessels are increased in size and length and become more tortuous. Pulsation is noted. Coincident with retardation of the blood flow, the leukocytes are seen to work their way by an ameboid movement through the walls 122 DISTURBANCES OF THE VASCULAR SYSTEM of the veins and to some extent of the capillaries into the perivascular spaces — i. e., into the adjoining tissue — in which they may move far from their point of escape and mass about the irritant if one be present. This process is called emigration (Fig. 60, e). At the same time a fluid rich in albumin, and thus capable of coagulation, escapes by the same route into the tissue (Fig. 61). Some red corpuscles also escape through the walls (diapedesis) (Fig. 60, c). While inflammation involves an arterial hyperemia as its first stage and a venous hyperemia as its second stage, these two conditions are not necessarily inflammation, and may exist as entirely distinct conditions when produced by causes not leading to inflammation; also, it must be remembered that the results of venous hyperemia or infarction (e. g., extravasation) may lead to a subsequent inflam- mation. This does not make them identical. Fig. 60 Small vein in mesentery of dog, after exposure for half an hour and irrigation with salt solution: a, red corpuscles; &, leukocytes adhering to wall of vein; c, red corpuscles; d, leukocytes which have escaped from vessel; e, leukocyte in act of escaping; /, fibrous tissue. X 340. Modified from Thoma. (Green.) As the venous hyperemia of the inflammation increases, the flow of red corpuscles in the veins is increasingly retarded until stopped, when a to-and-fro motion (oscillation) begins. Finally all motion ceases, diapedesis ceases, and stasis is complete. This blood may remain fluid in the vessel for several days {i. e., without coagulation), and if the blood flow be reestablished the separate red corpuscles are INFLAMMATION 123 seen one by one to roll away from the general mass until all are in movement and stasis ceases. (Thoma.) Coagulation (thrombosis) may, however, occur in the vessels involved in the stasis, and the part be later removed through the process of resorption. (See Resorption of Clot.) With the inflam- mation fully established there are in the tissue the following elements: (1) Leukocytes and some red corpuscles and lymphocytes from the tissue lymphatics. (2) Coagulable lymph. (3) Later new embryonic cells formed by mitosis from preexisting connective-tissue cells which surround the leukocytes massed about the irritant. These are fibroblasts ready to form scar tissue — i. e., they are the elements composing granulation tissue. The disposition of these elements of inflammation is as follows: The leukocytes mass about the irritant, exert a certain amount of phagocytic activity (ferment action), and may in turn be injured, liberating fibrin ferment, which, acting upon the fibrinogen of the lymph, produces fibrin, which in turn forms a coagulum. This coagulum blocks the lymphatic vessels leading from the part involved, thus causing a retention of fluid in the tissue. In the later stages of non-infective inflammation the tissue cells undergo multiplication, forming cells larger and having more power of ameboid movement and phagocytosis than the leukocytes. These become mingled with the leukocytes in the area of inflammation. They are fibroblasts from w'hich all the connective tissues develop, and to the action of which regeneration is mainly due. Around and about the focus ^"'- ^^ of inflammation the bloodvessels are in a ^^-^...^rt-^^/''""''^"'^'''^— . condition of arterial hyperemia, and about ~^^^ '" - "^^ :'=^ s^ this is an area of normal tissue. These ^^ areas shade off into each other.^ The " ^ phagocytes cause dissolution of coagula and dead aseptic tissue, and remove them. If the irritant be thus removable it is eaten awav. If the dead tissue be super- inflammatory edema of skin. ficial, the Connection with the living tissue ,^,td S ZZ /.TxT^ beneath is eaten through and the latter (Boyd.) thrown off. If the superficial tissues . have been previously removed, the wound is covered with the exudates and leukocytes, which dry into a scab, beneath which regeneration occurs. If inflammation occur in a mucous surface, the Fig. 64 serves to illustrate these areas, excepting the fact that the central area of pus ia absent and occupied entirely by an area there termed lesser inflammation — i. e., translate lesser inflammation into simple inflammation. 124 DISTURBANCES OF THE VASCULAR SYSTEM exudate and corpuscles escape from the submucous tissue between the epithelial cells as a catarrhal discharge (Fig. 62). If the inflam- matory exudate be highly coagulable and coagulate, firm swelling is caused, apt to lead to organization of tissue, hence called fibrinous inflammation. If it be productive of hypertrophy, it is called pro- ductive inflammation. If the exudate be watery, poor in albumin, and hence not readily coagulable, the inflammation is called serous inflammation. In the later stages of simple inflammation the coagula are dissolved, the leukocytes undergo fatty degeneration, and both are absorbed, together with such tissue as has undergone liquefaction. The lym- phocytes and embryonic cells push into the area and regenerate the tissue. This is the phenomenon of resolution. Fig. 62 Acute bronchial catarrh: Passage of leukocytes through the epithelium of the bronchus between the ciliated cells. X 700. (Thoma.) Symptoms of Simple Inflammation. — These are: 1 . Redness due to the excess of blood in the vessels and in the tissue. In some cases the part may have a dusky hue. The color is deepest in the area of greatest stasis. INFLAMMATION 125 2. Heat due to the increased oxidation in the area of hyperemia about the area of stasis. It has been shown that there is no increased heat in the area of stasis. In this area chemical action is lessened. 3. Swelliny due to the excess of blood in the vessels, the exudates of leukocytes and fluid, and the multiplication of tissue cells. The hardness of a swelling is due to coagulation of the fluid exudate. 4. Pain. — The result of the pressure of the effusion upon sensory nerve terminals ; it is frequently throbbing in correspondence with the heart beat ; the impulse causes temporarily increased pressure upon the nerve terminals. Gravitation also increases the pressure and pain in a dependent part — e. g., in a hand or foot or in recumbency in case of pulpitis (which see). 5. Impaired function is an evident result of a disturbance involving such pathological phenomena as have been described. The part cannot be used owing to pain and stiffness due to the swelling, also nutrition of any part being impaired, it loses its normal function. There are no general disturbances in simple inflammation beyond a slight traumatic fever due to absorption of some aseptic material from the seat of inflammation — e. g., fibrin ferment.^ There may, however, be general disturbance due to pain, loss of sleep, appetite, etc. Shock due to widespread inflammation, as from burns, may be serious. Infective Inflammation. — If microorganisms enter the tissue through a wound or puncture or an abraded surface, or if they locate upon predisposed or non-resistant mucous membrane, their multi- plication causes irritation and inflammation of the tissue about them. This at first resembles a simple inflammation, but later becomes more severe, prolonged, and may spread into the surrounding tissue, or in some cases cause inflammation in another place in no way connected with it except by the blood or lymphatic channels (metas- tasis). Briefly the process may be described as beginning with the entrance or location of the organisms and their multiplication. An injury of the vessel walls and degeneration of some tissue occur and the phenomena, such as occur in simple inflammation, begin. There is arterial hyperemia, later retardation of the blood current; diapedesis of leukocytes occurs, and a copious exudate of coagulable lymph is poured out into the intravascular tissue. By positi\'e chemotaxis the leukocytes are attracted to the bacteria, surround them, and apparently endeavor to limit their activity, or, perhaps, to digest them. If the bacteria be few in number and not too virulent, the phagocytes are successful and the phenomena of resolution occur. If, however, the contrary be the case, the leukocytes are overcome ' Green's Pathology and Morbid Anatomy. 126 DISTURBANCES OF THE VASCULAR SYSTEM and the inflammation spreads. In case of much toxin formation, negative chemotaxis occurs and phagocytic phenomena are held in abeyance. The central or most involved area dies. It is thus seen that there may be two terminations of an infective inflammation — resolution and necrosis. Resolution. — If the phagocytes destroy or wall up the bacteria, so that they die in their own products or are killed by the protective juices of the part (alexins), the phagocytes undergo fatty degenera- tion, the lymphatics are unblocked, the circulation is reestablished, the tissue that has died is removed by resorption and replaced by scar tissue if the loss be considerable. No evident pus or externally evident necrosis is produced, and the part exhibits phenomena much like those of a simple inflammation. This is the only termination for a simple (non-infective) inflammation. Necrosis. — Death of a part may result from infective inflamma- tion, either with or without pus formation. Suppuration. — If the irritant in the tissue consists of pyogenic organisms, such as the Staphylococcus pyogenes aureus or albus, the Streptococcus pyogenes, the Bacillus pyocyaneus. Bacillus typhi abdominalis. Bacterium pneumoniae, or the gonococcus, pus will be formed, provided the germs be not killed. The Staphylococcus pyogenes aureus is most frequently the organism infecting wounds. It is practically universal. Entering a part, the bacteria distributed in the tissue act as irritants and excite the phenomena of inflammation as described. Some of the cocci are ta,ken up by the fixed connective-tissue corpuscles, the leukocytes, and the endothelial cells of the capillaries, and some lie free in the tissue. The cocci multiply and the polymorphonuclear and eosinophile leukocytes increase in number by diapedesis and surround them. The original tissue cells, including those of the bloodvessels, undergo coagulation necrosis as the result of the action of bacterial ferments and do not take up staining reagents (Fig. 63) . Coagulation of the exudates occurs. The leukocytes and tissue cells are in part degenerated into pus corpuscles by the action of the unorganized ferments of the bacteria — i. e., their nuclei are fragmented, and they undergo fatty degeneration. Some cocci die. The exudate is pep- tonized into a fluid, which, together with the cocci, dead leukocytes, and tissue remnants, constitutes pus. About this pus is a circum- vallating wall of living leukocytes, and about this again a zone of fibroblasts arranged about new capillary loops (granulation tissue). The whole constitutes, when confined within tissue, an abscess. When upon a surface the granulation tissue is upon the under side only, and the whole constitutes a suppurating ulcer. INFLAMMATION 127 While the leukocytes may overcome the bacteria, the reverse is often the case, and the pus cavity enlarges in the same manner as at Fig. 63 Miliary abscess in a case of septic embolism of the kidney, a, leukocytes advancing toward and surrounding (b) a mass of cocci, in whose neighborhood all trace of structure has disappeared; c, renal epithelium too damaged by bacterial products to take the stain; d, kidney tissue staining normally; e, vein from which leukocytes are making their way to the commencing abscess. X 100. (Green.) first by a new formation of coagulation necrosis, more circumvallation, further liquefaction of the coagulum, etc. The path offering the least vital or mechanical resistance is usually followed until the surface of 128 DISTURBANCES OF THE VASCULAR SYSTEM the body or some internal cavity is reached. The last portion of tissue overlying the forming pus is tumefied and a soft, yellow spot appears. This is called pointing. The tissue is ruptured by the internal pressure and the pus escapes. The tract from the point to the abscess cavity is sl fistula or sinus. As soon as this occurs granulation tissue springs up upon the sides of the abscess cavity and usually soon fills it with scar tissue. (See Regeneration.) If the cause con- tinues to act, as, for example, in case of a portion of dead and septic bone beneath soft tissue, a gangrenous pulp in a tooth root or infected crypts of the abscess walls, the granulation tissue breaks down, and the condition is one of ulceration or a chronic abscess with a fistula. If, in the course of abscess formation, bone be encountered by the An abscess in the skin. The horny layer has largely disappeared, and the Malpighian layer is pushed upward by the subjacent abscess (a). The mass of pus corpuscles is just breaking down to form a ca\dty (P), the walls of which are thickljf infiltrated with similar cells or the area of stasis (S). Outside is the area of lesser inflammation {LI), and still farther away are the areas of arterial hyperemia ( ff) and normality (N.T). Interpretation modified by editor. (Boyd.) pus, it may be and often is molecularly broken down into pus. (See Acute Apical Abscess.) It does not always happen that the pus finds escape either naturally or through surgical aid; the patient may die before this occurs, or the tissues around the seat of pus formation may form a boundary wall which the organisms fail to break down and thus die starved out. The abscess contents undergo changes resulting in caseation, or later the mass may calcify. (See pp. 78 and 82.) The Streptococci pyogenes may multiply laterally, follow- ing the subcutaneous cellular tissue, and produce violent spreading inflammation with but little pus formation — e. g., some forms of apical abscess and erysipelas. The products (toxins) from an abscess or infective inflammation may find their way into the blood, and a general toxemia result, or the INFLAMMATION 129 organisms themselves may enter the blood and a general infection result (septicemia).' There are various varieties of pus which have names describing the chief characteristics: Creamy pws is the erroneously called laudable pus associated with an acute abscess or ulcer which progresses, as a rule, toward a cure. It is of a yellowish-white color, creamy consistency, and without odor. Curdy pus contains flakes. Ichorous pus is thin, odorous, and irritating. Mucopus is pus containing mucus. Seropus is pus containing much serum. Sanious pus contains blood. Cause. — The cause of suppuration is the development in tissues of pyogenic organisms. The action of these causes is favored by the presence in the part of a hyperemia or simple inflammation, such as the injury introducing the organisms may cause. These as well as depraved or debilitated tissues favor the action of bacteria — i. e., act as predispositions. Symptoms. — The symptoms of suppuration are both general and local. Local Symptoms. — The symptoms of inflammation, redness, heat, pain, and swelling occur, but usually much aggravated. The pain is often of a lancinating character, sudden darts often following com- parative quiescence. On the other hand, the throbbing pain may be continuous and intense, especially when the pus is confined by bone or tense tissues, as in the case of a felon or an acute apical abscess. Recalling that around the pus area there is an area of stasis, next one of active but lesser inflammation, and about that hyperemic, then normal tissue (Fig. 64), one may judge of the degree of involvement of deeper parts by the appearance of the surface above them. Thus, for example, hyperemia at the surface indicates inflammatory action directly beneath, with a pus cavity still deeper, while inflammation at the surface, together with hardness and tumefaction, shows a more involved condition of the tissue directly beneath it — i. e., a more advanced state of inflammation or even of suppuration. The softening of the apex of the swelling gives a feeling of lessened resistance, indicating pointing or pus at the surface. In large, super- ficial abscesses the sensation known as fluctuation may be obtained by placing one finger on one side of the swelling and gently tapping upon the other. Yellowness of the apex, together with softness, indicates that the abscess is about to discharge its contents. A fistula or sinus upon the surface is indicative of a discharged abscess, and leads to a pus-forming area beneath (chronic abscess). 130 DISTURBANCES OF THE VASCULAR SYSTEM General Symptoms. — If toxemia be produced there may be chills, and, at the same time, fever as high as 104° F. A full, bounding pulse accompanies this, the patient is constipated, has a coated tongue, is exhausted by loss of sleep and often disturbed nutrition due to the pain. There may be other evidences of septic intoxication, which may become profound. (See Septic Intoxication.) Leukocytosis after surgical disease is considered pathognomonic of suppuration, the count running up to 15,000 or 20,000 per cubic millimeter. (See p. 109.) Ulceration. — The development of microorganisms upon a free surface causes tissue degeneration and death, as described under Abscess. Numerous forms of pathogenic organisms are capable of causing tissue degeneration and death of a mucous or skin surface. If infec- tion take place through a hair follicle, or if organisms develop upon an Fig. 65 Tuberculous ulcer of the intestine: a, mucosa; I, submucosal c, muscularis; g, ulcer; t, tubercle in the mucosa; t', focus caseating in the middle. X 12. abrasion, or in the epithehum in conditions of general or local debility, the epithelium is destroyed over an area, and in the subepithelial tissues the organisms multiply and cause tissue loss. If the organisms be pyogenic — and ulcerous surfaces are usually infected by these bodies — pus is formed (Fig. 65). Under some conditions, as in debilitated and neglected children, the ulcerous process may spread rapidly, as in the cheek in cancrum oris; or when specific bacilli, which excite much swelling and quick death of the tissues of the cheek, proliferate, causing the condition called noma. Prognosis. — Abscesses tend, as a rule, to spontaneous cure without marked systemic disturbance. If the pus discharge persist after evacuation of the abscess, persistence of the cause, or infection of the abscess walls through reinfection or by retention of bacteria in the crypts, is to be suspected. The occurrence of rigors (chills) and high fever is a danger signal. A fluttering, weak pulse and clammy extrem- INFLAMMATION 131 ities indicate profound septic intoxication, and are indications for local disinfection and systemic treatment. Treatment of Inflammation. — If the cause of inflammation be in evidence it must be removed ; good examples of removable causes are a splinter in the flesh, a gangrenous tooth pulp, etc. Ordinarily the pus of an abscess or an ulcer contains the cause (bacteria) within it; therefore the pus should be removed by opening the abscess, if its situation can be determined, after which the pus cavity is syringed out with germicides, which destroy the pus and the organisms. Hydrogen dioxide in 3 per cent, aqueous solution is commonly used; it is made more effective by the addition of mercuric chloride (1 to 1000). In ulceration the pus and organisms are destroyed in a similar manner, though at times sloughing tissue requires removal by the curette, caustic agents, or by digesting agents, as caroid, papoid, brewers' yeast,^ etc. Dead bone acts as a septic irritant and requires removal, and at times an abscess will remain persistently infected, requiring surgical removal of tissue. The abscess or ulcer, if protected from further infection, usually heals by formation of granulation tissue. A deeply seated abscess may require to be packed with antiseptic gauze (noso- phen), in order that it may granulate from the bottom out, otherwise a small orifice may heal, permitting a re-collection of pus beneath. Ulcers are usually dusted with antiseptic powders, iodoform, aristol, or nosophen, which cause drying of the surface and prevent the access or action of organisms. Under certain circumstances the presence of suppuration is not certain, though phlegmonous (spreading) inflam- mation is somewhat pathognomonic of it. In such cases hot, moist applications, such as hot poultices, soften the surface above the abscess and determine its direction of discharge, thus limiting burrow- ing. Counterirritants applied directly above the inflamed area also hasten in such cases. The stimulation may aid resorption (destruc- tion by phagocytosis) of the pus and resolution occur.^ The vascular engorgement in an inflamed part may be reduced by local bloodletting. Nancrede found, on dividing a vein upon the distal side of an area of inflammation, that after a brief period the flow of blood was established through the inflamed area. Local bloodletting by leeches (Gensmer) produced even more marked effects. Drugs which stimulate the vasoconstrictors (ergot), and those which paralyze the constrictors (aconite), lessen the blood pressure in the inflamed area; so that if administered in the early stages of inflammation they may modify its severity. If, on the contrary, they are administered after i Park's Surgery. 2 Ibid. 132 DISTURBANCES OF THE VASCULAR SYSTEM stasis occurs, they increase the stasis — ergot actively and aconite passively. If the flow of blood through the inflamed area be reestab- lished by local bloodletting, then the arterial sedatives are distinctly useful in lessening the flow of blood to the part. When, owing to vascular engorgement, throbbing pain is a promi- nent symptom, applications of cold are useful in lessening the caliber of vessels and in relieving pain. But if there be firm exudation and marked stasis, cold is a detriment. Heat then gives relief through inducing a more free flow of blood in the collateral circulation. Very hot applications act as do cold applications, by causing contraction of vessels, and may be used to abort an inflammation. In certain situations, as in case of an inflamed tooth pulp, sedative applications, antiphlogistics, are required. Conjoined with local measures of reducing vascular engorgement, the use of counter- irritants and general derivatives are indicated. (See Treatment of Hyperemia.) General sedatives are at times demanded for the relief of pain. Morphin used in small and continued doses not only relieves pain, but causes a contraction of small vessels. Other anodynes are also used in this connection, as acetanilid. Quinin and salol are useful as correctives of the intestinal disturbance, and mercuric chlorid in small doses is useful as a preventive of general infection. (See Acute Apical Abscess.) REGENERATION OF TISSUES Connective tissues that have been lost by inflammatory process or operation are replaced by granulation tissue arising by mitotic division of cells of the connective-tissue group. The forms of healing are by first intention, second intention or granulation, healing under a scab, and healing under a clot. Epithelial tissues are replaced only by multiplication of epithelial cells. The forms of healing are practically alike by formation of granulation tissue, the form being simply a modification (of extent) of healing by second intention. Healing by Second Intention or Granulation. — -Shortly after evacu- ation of pus from an abscess the process of repair is instituted. The leukocytes come to the surface of the wound in great numbers; some of these may degenerate into pus cells. Immediately beneath the uninjured connective-tissue cells multiply, forming embryonic cells (fibroblasts) ; at the same time the endothelial cells of the capillaries multiply at points, throwing out solid-pointed projections or buds from the sides of the capillaries (Fig. 66, b). These lengthen and REGENERATION OF TISSUES 133 join buds from other capillaries (Fig. 66, c, d, e). By mitosis the nuclei divide horizontally, lying side by side (Fig. 66, d) . Later these separate into two cells, discovering a lumen into which blood enters Fig. 66 Regeneration of capillary bloodvessels: a, normal capillaries; 6, capillary process; c, new capil- lary appearing in divided process; d, process undergoing division; e, connecting cell in which no sign of division has yet appeared. Diagrammatic. (Green.) Fig. 67 A granulating surface: o, layer of pus; b, granulation tissue with loops of bloodvessels; c, commencing development of the granulation tissue into a fibrillated structure. X 200. Diagrammatic. (Rindfieisch ) 134 DISTURBANCES OF THE VASCULAR SYSTEM from the parent capillary (Fig. 66, a', c). In this manner loops are formed, about which the fibroblasts are arranged (Figs. 67 and 68). Together these form minute red elevations upon the surface of the abscess cavity or wound, called granulations. Repeated, the process gradually fills the abscess cavity. Fig. 68 Transverse section of granulation tissue from an open wound with fibropurulent deposit: a, granulation tissue; 6, fibropurulent deposit; c, c, bloodvessels. X 150. (Ziegler.) Naturally, collapse of the walls or apposition of cut edges of a wound lessens the amount of granulation tissue necessary; hence, in the latter case, healing by first intention (with a minimum amount of granulation or scar tissue). The wound having been filled up, epithelium grows from the sides and covers the granulations (Fig. 69, e). The granulation tissue, at first highly vascular, later contracts, and many vessels are obliterated so that it becomes whiter than normal tissue — cicatricial tissue (cicatrix). REGENERATION OF TISSUES 135 The indifferent embryonic cells may have the function of forming any of the connective tissues. If cartilage is to be formed, chondrifi- cation takes place about the specialized cells. If bone is to be formed, certain cells form islets, about which calcification proceeds. Xerves require a month or more to pierce the cicatricial tissue (Eichhorst).^ In spite of this assertion the writer finds that granulations are very sensitive to touch, which seems clinical evidence of error in this observation. Fig. 69 Laparotomy wound — sixteenth day; a, a, epithelium; b, b, corium; c, subcutaneous fat; d, vessels in scar tissue of corium; e, newly formed epithelial layer; /, vessels in subcutaneous scar tissue. X 40. Modified from Ziegler. (Green.) In healing beneath a scab the exudation and leukocytes upon the surface of the wound dry into a scab beneath which granulations and an epithelial covering are formed. Later the scab falls oft'. If prematurely lost the granulations are exposed. In healing under a clot the clot is invaded by leukocytes, which have a solvent action upon it. Granulation tissue forms upon all sides of it, grows into it, and, at the same time, removes it by resorp- tion (Fig. 70). If the clot become septic the granulations may become infected and break down, as scar tissue in its early vascular stages Ziegler: General Pathologj'. 136 DISTURBANCES OF THE VASCULAR SYSTEM is of but feeble resistive power, though it does not absorb toxins. (Park.) Heahng under a clot is the form commonly seen after tooth extrac- tion. It is an interesting point that the alveolus is finally filled with bone, while the original bony margins of the alveolus are resorbed. In certain cases of abscess with contracted fistulse or openings of discharge, the orifice may close before the granulations have filled the pus cavity. If pus or an excess of exudate be now formed within the cavity, a second discharge may occur. To obviate this difiiculty, abscesses are often packed with antiseptic gauze, so that healing may occur from the bottom of the cavity, while drainage is assured. In other cases the placing of a tent Fig. 70 Or drain tube in the fistula together with asepsis sufiice for the attainment of the object. INFLAMMATION OF BONE " Active infiammatory changes may occur in the periosteum, the medullary canal, the med- ullary spaces of the spongy bone, and the Haversian canals, the compact tissue and ground substance remaining passive.''-^ The inflammation is termed periostitis, osteomyelitis, or osteitis, the terms referring to the point of location of the Absorption of blood clot. Section through the inflammation i. 6^, the pCH- margin of a clot formed among the tissues by extra- ost .^hc mcdufla, and the vasation, showing the growth of granulations by ' . , which it is removed: a, a, portions of clot; 6, b, SpaCCS the bonC being in- original tissue; c, c granulations springing from the ^oi^g^ in all (.^ggg^ Inflamma- original tissue and projecting into the clot; d, d, , wandering cells or leukocytes that seem to have tioU of boUC may bc UOn-infcC- taken red blood disks into their interior. (Section ^^y^ qj. infective; the latter is cut in gum arable and stained with hematoxyhn.) X 350. (Black.; usually due to pyogenic organ- isms — i. e., suppuration occurs. Proliferative Periostitis.— This is a proliferation of cells of the deeper layers of the periosteum combined with emigrated leukocytes. A node is thus formed which may ossify. ' Schmaus and Ewing: Pathology and Pathological Anatomy. INFLAMMATION OF BONE 137 Suppurative Periostitis. — Pyogenic organisms may enter an injured periosteum or one weakened by previous disease (e. g., by scarlet fever). The origin of the bacteria is by way of the blood, either directly or by way of the medulla (as a secondary effect of osteomyelitis), or by way of the skin. Pus forms beneath the periosteum, raises it, and destroys its connection with the bone. The vessels are stretched, damaged, and thrombosis occurs. Superficial necrosis of bone results, which may be total if other sources of blood supply are also cut off. Acute Osteomyelitis. — This is a suppuration occurring in the bone marrow, which infects the bone proper, causes much throm- bosis of vessels, coagulation necrosis of bone cells, and may rapidly cause much necrosis of medullary tissue. Occurring in large bones, much toxin is produced, which may rapidly cause death. The organ- ^ ^^° '^^ ^ . .^ isms and thrombi formed, becom- '^^^-^^-^^^'^''^^^^^^k'^^'^r^^ ing emboli, may rapidly lead to ^ ^ ^ pyemia.^ Prompt surgical inter- r /^. }, - ference is called for. - ;--> 'i Inflammation of bone may lead to its rarefaction (rarefying osteitis or . osteoporosis), its condensation (con- ,,,,,. , , ^-^ , , , T rabeculsB of bone with p(,rforiting canals densing osteitis or osteosclerosis), x )0 or its death (necrosis and caries). Rarefying Osteitis (Osteoporosis). — In the rarefying process which occurs in chronic inflammation, granulation tissue is formed, which enters the Haversian canals and spaces of spongy bone and destroys (resorbs) the bone, owing to the presence of osteoclasts. They thus form new channels between the spaces — perforating canal resorption (Fig. 71). With suppuration (ulceration) added, the granulations break down, leaving the bone as a dead, spongy, or honeycombed mass. This is caries of bone. In the early stages the inflammation may cease, and the bone not only be restored, but condensed. Condensing Osteitis (Osteosclerosis). — In chronic inflammation, of lesser degree, instead of rarefaction, construction occurs and the trabeculse of bone may increase in thickness, so that all spaces and Haversian canals become smaller. The bone becomes very compact and less vascular, and if built up in excess of its original dimensions, constitutes the condition known as exostosis; if very dense, as " ivory exostosis." Both condensing and rarefying osteitis occur about the ' Park's Surgerj-. 138 DISTURBANCES OF THE VASCULAR SYSTEM alveolar process and the roots of teeth. (See Hypercementosis and Resorption.) Fig. 72 Fig. 73 Section of bone and periosteum covering it: B, bone; c, outer fibrous layer; a, inner layer of white fibrous tissue; O, layer of osteoblasts, some of which reach the bone with their prolongations. Normal bone. (Black.) Section of bone and periosteum covering it: a, osteoclasts, cells that absorb bone; b, surface of bone, showing fibers of perio- steum penetrating it and a Howship lacuna. Lacunar resorption. (Black.) Necrosis of Bone. — Necrosis of bone following rarefying osteitis is known as caries. It is a molecular death of bone. Subperiosteal death of bone occurs from in- fective periostitis, and is due to the compression of vessels by the exudation and to throm- bosis. Nutrition ceases; death results. The dead piece is demarked by a line of leuko- cytes (phagocytes), solution of continuity or rarefying osteitis occurs at the line of union with the living bone, and the piece is thrown out as a seques- trum. New bone enclosing a sequestrum is termed an involucrum. (See Gangrene.) Resorption of Bone. — Under conditions of chronic inflamma- tion bone is often removed by neighboring tissue in one of several ways. Lacunar Resorption. — In this form the bone is excavated by giant cells into bays called Howship's lacunae, which may enlarge, or later Lattice-work figures in haUsteresis. V. Recklinghausen.) (After pnvER 139 a reconstructive action may occur and osteoblasts may fill up the bays with bone. (See Hypercementosis and Resorption of Roots.) Perforating Canal Resorption. — This has been described under Caries of Bone. The canals connecting medullary spaces are enlarged by the granulation tissue formed in them (Fig. 71). Halisteresis Ossium. — In this form of resorption the bone first undergoes decalcification and the matrix is later removed (Fig. 74). It occurs in conditions of osteomalacia as in pregnancy, senility, etc. It also occurs in the alveolar process, and is, at least in part, the cause of the cleanly symmetrical resorption of the gum and alveolar margins. (Talbot.^) Fig. 70 "^kmM Diagram of healing fracture. From a guinea-pig ten days after injury: K, ends of the bone; ia, marrow; c, periosteal callus; d, medullary callus; o, osteoid tissue. X 6. M ':'^. v'^^cf y A; p -V:"^','- V ''•• '//'/■4 ■fi .tj>-. !'0:''. The same preparation: M, myelogenous callus; P, peri- osteal callus; Ky ends of the bone; /c, osteoid trabeculae; o, osteoblasts in rows; p, thickened periosteum. X 250. (Schmaus and Ewing.) Regeneration of Bone. — Bone lost by suppuration is first replaced by provisional tissue of the connective-tissue type, in which appear osteoblasts. Calcification then proceeds under superintendence of these (Figs. 72, 75, and 76). FEVER The term fever is applied to a condition the most prominent feature of which is an elevation of the bodily temperature above the normal, ' Interstitial gingivitis. 140 DISTURBANCES OF THE VASCULAR SYSTEM 37° C. To constitute a fever this rise in temperature must continue for some length of time. Causes. — Fevers are commonly caused by the presence in the circu- latory fluids of substances which act as poisons upon, probably, the nerve centres controlling heat production. As a rule, the offending substance is a poison generated in the body through the action of microorganisms. The character and type of the fever are determined by the nature of the offending substances — i. e., the variety of infec- tion. Classes. — Fevers are divided into periodical or continued, according as to whether there is a periodical fall of temperature and a subsequent rise, or whether the fever continues practically unabated from the beginning to the termination of a disease. Fevers are classed in severity according to the maximum temperature, and, again, accord- ing to their duration. A temperature of 100.5° to 101.3° F, is called slightly febrile; 101.3° to 103° F., moderate fever; 103° to 105° F., marked fever. A temperature above 106° F. is termed hyperpyrexia. Symptoms. — The most characteristic symptom of fever is the eleva- tion of temperature; accompanying this there is an increased fre- quency of the pulse. In acute inflammatory diseases the pulse is full and bounding, the eyes injected, the bowels constipated, and the urine scanty, containing an excess of urea. On standing, the urine throws down a brickdust deposit (urates) . In fevers of a lower type, or in many fevers which begin as described, the high, bounding pulse is succeeded by a soft, quick pulse, and evidences of great debility. In fevers in which the temperature runs high there is commonly evidence of intoxication, more or less delirium, and reflex muscular action. With a persistent temperature and a pulse becoming softer and more frequent, there is increasing debility. Pathology and Morbid Anatomy. — In all cases of continued high temperature the fat of the body rapidly disappears and granular degeneration occurs in the muscles and viscera of the body. If the fever be long continued and of an adynamic type, this degeneration may become marked. Its occurrence in the muscles of the heart is common and is an element of danger. There are an increase in the amount of carbon dioxid formed and exhaled from the body, and an increased amount of oxygen inhaled. This, with the increase of urea, the product of the oxidation of nitrogenous tissues (muscles, glands, etc.), indicates that the oxidation of the tissues is largely increased; hence the elevation of temperature. As repair does not equal waste in fevers, the nutritive processes being profoundly dis- turbed, the essential elements of the tissues suffer from the increased oxidation and undergo degenerative changes. TOXEMIA 141 Prognosis. — The higher the temperature and the longer it continues, the greater drain there is upon the vital forces. As a rule, a tempera- ture of 106° F. persisting more than twenty-four hours presages death. If the vital forces flag and the heart action becomes weakened, and if there be evidence of profound intoxication, such as twitching of tendons, low, muttering delirium, and a clammy surface, the out- look is bad. Favorable signs are falling temperature, a clear eye, tongue losing its coating, free action of the bowels, free perspiration, free action of the kidneys, and a good vascular tension. Treatment, — In the light of present knowledge, efforts should first be made to discover the nature of the cause of the fever and to remove it, if possible. If not, attention should be directed to maintaining the vital forces until the body rids itself of the offending causes. As many fevers are self-limited in course and duration, this latter treat- ment becomes an important consideration. The temperature should be kept within safe limits by the administration of antipyretics, when the condition of the heart wall permit their use, and also by cool sponging or cool baths. The action of the heart should be sustained by the administration of concentrated nutriment, and by stimulants when necessary. The bow^els must be kept open. In any form of fever there is no therapeutic measure comparable with the removal of the cause, provided this be discoverable, iden- tified, and removable. TOXEMIA By toxemia is meant a more or less general disturbance of the economy as the result of the presence in the blood of substances poisonous to a tissue or the tissues. The substance may be a normal constituent of the blood which has accumulated owing to faulty elimination — e. g., urea — or be derived from the alimentary canal as the result of unusual fermentation therein. Such an effect is known as auto-intoxication. It may be due to the action of drugs of toxic character — e. g., alcohol or iodoform. This is drug toxemia. Again, it may be due to the action of the products of bacteria, which prod- ucts, absorbed from certain foci of infection, produce general effects, such as fever. Again, similar results can be produced by the intro- duction of toxic products from bacterial culture in vitro or in experi- mental animals. Septic Intoxication. — By septic intoxication is meant the absorp- tion into the blood of the products of bacterial activity, which products are produced at some focus or foci of infection as the result of tissue or tissue-juice decomposition. These bacterial products 142 DISTURBANCES OF THE VASCULAR SYSTEM produce symptoms of general poisoning or intoxication, which are mild or severe, according to the character of the poisonous body produced. The organisms do not necessarily enter the blood, hence the blood is not infectious if inoculated into another person (or experimental animal). Two varieties of septic intoxication may be distinguished: 1. Intoxication by the products of the action of specific bacteria developing upon living tissue. 2. Intoxication by the action of bacteria upon non-vital materials (sapremia). The action of the bacilli of diphtheria, Asiatic cholera, and tetanus are examples of the first class. Their toxins are virulent, but the bacteria are confined to the pharynx, intestine, and the wound respectively. Sapremia. — The entrance of putrefactive or the pyogenic organ- isms into such material as a large blood clot or gangrenous area may, by putrefaction, cause the formation of large quantities of toxins. These, if absorbed, produce rapid and profound symptoms of intoxi- cation. The symptoms vary according to the nature of the toxin and the quantity absorbed, but ordinarily occur in the following order: Malaise, rigor, fever and its symptoms, nausea, vomiting, headache, diarrhea, prostration, delirium in some cases, muscular weakness, clammy skin, feeble pulse, quick respiration, and in fatal cases coma and death. The symptoms are similar to those of septicemia, but appear more rapidly — i. e., septicemia requires time to spread. There is a putrid wound which is the source of the toxic substance. The condition is usually complicated by septicemia. SEPTICEMIA (GENERAL SEPTIC INFECTION) By septicemia is meant a condition in which the bacteria, usually one of the pyogenic varieties, gain entrance to the living tissues, enter the circulation, and are carried to inaccessible parts, where their development continues and from which point their toxins are absorbed (Fig. 77). This process requiring more time than mere absorption of toxins, the symptoms are much more delayed than in sapremia. The blood is highly infective to susceptible animals in minute amount, as it contains bacteria. Pathology. — There is a septic wound in which incubation occurs for several days. The lymphatics leading from the part and the nearest lymphatic glands become inflamed. In pronounced cases the spleen is enlarged. There is marked leukocytosis. SEPTICEMIA 143 Examination made after death due to the septic intoxication produced by both sapremia and septicemia exhibits fairly constantly enlargement of the spleen and disintegration of the red corpuscles, with staining of the intima of the vessels and heart. The lungs are congested. Death occurs through heart failure.^ Symptoms. — These are similar to those of sapremia, except that the periods of incubation about the body cause delays. Fig. 77 ®Sf>-' ^ '.i-V^ %s^ "-m* ^ a. a i'y /■ cl: Pectoral muscle beset with large numbers of the Streptococcus pyogenes, from a case of phlegmo- nous inflammation of the subcutaneous and intermuscular connective tissue, due to cadaveric poisoning (the phlegmon of the wall of the chest developed two days after the finger was injured, and the intermediate lymph vessels of the arm showed no evidences of being involved) : o, perimysium internum full of streptococci; b, transversely cut muscular fibers, still intact; c, trans- versely cut muscular fibers which are beginning to degenerate; d, muscular fibers into which the cocci have penetrated. (Preparation treated with gentian \'iolet and vesuvin, and mounted in Canada balsam. X 350 diameters.) (Ziegler.) Tieatment. — For sapremia and septicemia, the treatment is both local and general. The local treatment involves the opening and dis- infection of all wounds, even the extirpation of a part and of neighbor- ing glands being sometimes necessary for remo^'al of the cause. If possible, the part is immersed frequently in hot water, which may occasionally have mercuric chloride added to it. An antiseptic salve, consisting of resorcin, 5 parts; ichthyol, 10 parts; unguentum hydrargyri, 40 parts; lanolin, 45 parts, is to be applied to the area of infection. - Crede's silver ointment may be applied to the unbroken skin for the systemic antiseptic effect of the silver. ' Green: Pathology and Morbid Anatomy. • Park's Surgery 144 DISTURBANCES OF THE VASCULAR SYSTEM The general treatment consists in: (1) Clearing the alimentary canal by means of cathartics and maintaining its asepsis bj^ means of mercuric chlorid in small doses, salol, or other suitable antiseptic. (2) Supporting the heart action by means of alcohol and strj^chnin. (3) Supporting the strength by concentrated liquid nourishment, such as egg albumin, beef peptonoids, beef juice, peptonized milk,"^ to which diet fruit may be added.^ (4) Reducing the temperature by means of cold sponge baths or quinin. (5) Maintaining the elimina- tive action of the kidneys until the system has rid itself of the toxins. For the more profound cases. Park recommends the intravenous infusion, as an intravascular germicide, of from 500 c.c. to 1000 c.c. of a solution of Crede's soluble silver, 1 to 1000 of sterilized water at 105° F. Streptococcus antitoxin is useful. Vaccine therapy may be of value (see p. 57). PYEMIA By pyemia is meant a form of septicemia or septic infection by pyogenic organisms, which, locating at favorable spots, as in the capillaries, multiply and produce numerous abscesses known as miliar}^ or metastatic abscesses. From these foci toxins are absorbed, which produce a septic intoxication. The organisms may enter the blood from some focus of suppuration as free cells or be taken up by leukocytes, or thrombosis may occur at the original focus of infection, and portions of clot be carried in the blood as septic emboli to terminal arteries, where the results of septic infarction are set up. (See Infarction.) Symptoms. — The symptoms of pyemia are, in general, those of septicemia ; their appearance is delayed from the date of the reception of an injury or the outbreak of the primary suppuration. The onset of pyemia is usually by a chill or a succession of chills. Each fresh area of pus formation is believed to be announced by a chill and a rise of temperature. The temperature is subject to remissions, and sudden variations in its height are noted. The general symptoms are those of an adynamic fever. Local symptoms appear according to the point of lodgement of septic emboli. Pus centres may be found in the lungs, and cause symptoms of dyspnea ; collections frequently occur in joints, causing loss of mobility; eruptions appear on the skin, the swellings being apparent; typhoid symptoms become more pro- nounced, and an increasing debility ushers in a usually fatal ending. At times both septicemia and pyemia may become chronic. 'Thompson: Practical Medicine. 2 park's Surgery. THE EXANTHEMATA 145 Treatment. — The treatment of pyemia should be preventive. The carrying out of rigid antiseptic precautions has much lessened the frequency of pyemia. If areas of infection are removable, they are removed no matter what extent of operation may be necessary. The general treatment is the same as in septicemia, with much less hope of recovery. A consideration of the infective surgical processes in connection with dental and oral diseases is of the utmost moment to the prac- titioner of dentistry. Nearly all of the diseases which the dentist is called upon to treat are infective from their inception. Moreover, the saliva, holding in suspension numerous forms of bacteria, both saprophytic and parasitic, and their waste, is a highly infective fluid. It has been clearly demonstrated by the researches of ]\Iiller^ that many forms of bacteria found in specific diseases, and found inhabit- ing the intestinal tract, are more or less constantly present in the human mouth, and that the pathway in many general infections is no doubt via the oral cavity. A wound made in the human mouth is necessarily an infected wound. In the vast majority of cases the body exercises its protective function in a phagocytosis,^ or through immunizing processes, which disposes of invading bacteria or renders them innocuous. In other cases it is beyond question that this protective provision fails and infection occurs, especially if new forms be introduced. The saliva is not germicidal in any way. (Miller.) THE EXANTHEMATA Certain acute specific diseases, such as rubeola, rotheln, scarlatina, varicella, and variola are accompanied by skin eruptions generally distributed over the body, and which represent an infective derma- titis; indeed, the eruptions of many of these diseases are contagious to other individuals. Syphilis, a chronic specific disease, due to the Spirocheta pallida, produces similar effects. The special interest lying in the exanthemata is that occurring during the development of the teeth ; the latter are often profoundly affected, so that malformations, sometimes serious in character, occur in the teeth. It is to be recalled that teeth are dermoid structures, certainly in so far as the enamel is concerned. (See ^Malformations of the Teeth.) Again, after or during exanthematous diseases, notably scarlet fever, the oral tissues are much debilitated, so that abscesses about the teeth may produce much necrotic tissue or the disease itself may produce necrosis. 1 Microorganisms of the Human Mouth. 2 Hugenschmidt : Dental Cosmos, 1896. 10 SECTION II EMBRYOLOGY, AXATU.MY, AND HISTOLOGY Fig CHAPTER \1 THE DEVELOPMENT, ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH As malformations of the parts about the mouth and of the teeth are dependent upon defective development of the same, it is incumbent that certain facts concerning their embryology should be stated. In like manner, as the processes of pathology are modi- fied by the peculiar anatomy of the teeth and associated parts, it is necessary that a previous knowledge of these be acquired before the special dental path- ology can be comprehended. The embryology of the mouth begins at a very early period — before the twelfth day the future mouth may be located (His, Fig. 7S). The mouth and nasal cavity are circumscribed by parts which are developed by outgrowths from the head fold of the fetus. Those structures immediately concerned are the lateral tubercles arising from the frontal prominence (Fig. 79), which grow downward and fuse, forming the nose, the nasal septum, the intermaxillary bones, and anterior portion of the upper lip (Figs. SO and 81). From the sides of the head fold at the level of the mouth and neck appear Face of an embrj-o of twenty-five to twenty- eight daj-s (magnified fifteen times): 1, frontal prominence; 2, 3, right and left olfacton,- fossae; 4, inferior maxillarj- tubercles, united in the middle line; 5, superior maxillarj' tubercles; 6, mouth or fauces; 7, second pharjngeal arch; 8, third; 9, fourth; 10, primitive ocular vesicle; 11, primitive auditor}' vesicle. (Gray.) 148 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH certain lateral protuberances, or pharyngeal arches. The first pharyngeal arches (Fig. 78, 4) divide into (1) the superior max- FiG. 79 Sup. tubercle Lateral tubercle Sup. tubercle Lateral tubercle Head of an early human embryo, showing the disposition of the facial fissures and the superior and lateral tubercles. (His.) S.M.P.- S.M.P. NAS. Diagram illustrating scheme of union of the processes: NAS, lateral tubercles forming internal maxillary bones, INT. MAX., and nasal septum; S.M.P., superior maxillary processes forming palatal processes of superior maxillse, S.M.F.; N.C., nasal cavity; O.C., oral cavity; I.M., inferior maxillary processes united. illary processes (Fig. 78, 5) and (2) the inferior maxillary processes (Fig. 78, 4i shown just beneath the oral cavity and united in the median line), Fig 81 Complete bilateral fissures (coloboma) of face. (Guersant.) Fig. 82 Vertical transverse section through head of human embryo, about the tenth week: 1, naaa cartilage; 2, buccal cavity; 3, tongue; 4, dental ridge, lower jaw; 5, nasal cavity; 6, dental ridge, upper jaw; 7, dental ridge, lower jaw. X 30. (Broomell.') • Anatomy and Histology of the Mouth and Teeth. 150 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH The superior maxillary processes develop the palate bones and the superior maxillse. They form the balance of the upper lip. The arch itself forms the cheek. Fig. 81, from a case of arrested develop- ment, illustrates the unions and parts naturally formed, but here incomplete. Secondary processes develop horizontally toward each other, form the palatal portions of the superior maxillse and palate bones, and unite at the median line (Fig. 80, S.M.P., also Fig. 82), forming the vault of the mouth and floor of the nasal cavity. Union occurs with the lateral processes, later forming the intermaxillary bones and bear- ing the germs of the incisor teeth (Fig. 83), thus completing the formation of the upper jaw and lip. Fig. 83 07ie for nasal and facial portions. One for orbital and malar portions. Anterior Surface One for incisive portion. One for palatal portion. Inferior Suyface. Development of the superior maxillary bone by four centres, also development of inter- maxillary bones. (Gray.i) The inferior maxillarj^ processes grow forward and unite at the median line, developing the inferior jaw and lip. Fig. 86, an arrested case, shows this. The structures of the floor of the mouth and neighboring structures are formed from the second, third, and fourth pharyngeal arches and a tubercle arising near the first pharyngeal arch. The fusions of the lateral portions of the upper maxillse begin first anteriorly at about the eighth week, and progress posteriorly until complete at about the 1 Gray's Anatomy. ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH 151 eleventh. Malformations due to non-union,, therefore, date from this period, and consist of the following typical varieties : Fig. 84 Fig. 85 Cleft of hard and soft palate; rudimentary intermaxillary bone placed in advance of lips. (Mason.) Cleft of hard and soft palate. (Mason.) Fig. 86 Median fissure of the lower lip and chin. (Marshall, after Wofler.) 1. Non-union of lip on one or both sides — simple harelip. 2. Non-union of lip and of maxilla and intermaxillary bone on one side (harelip. Fig. 84). 3. Non-union of lip and intermaxillary bone on both sides (double harelip. Fig. 81). 152 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH 4. Non-union of all horizontal processes in the median line (cleft palate, Figs. 84 and 85) . 5. Non-union of halves of soft palate (cleft velum). 6. Non-union of halves of the uvula (bifid or cleft uvula). Combinations of cleft velum and cleft palate or of cleft palate and single or double harelip may exist. Figs. 81, 82, 84, and 88 show the parts in their ununited state. The failure of the inferior maxillary processes to unite is rare, but is occasionally seen (Fig. 86). The inferior maxillary tubercles develop a transitory support to the lower jaw known as Meckel's cartilage. The cartilages of the right and left side do not fuse together at the future symphysis. (Hertwig.) (See Figs. 82, and 87.) Fig. 87 Fig. 88 M.a Showing Meckel's cartilage (Af.C.) in longi- tudinal and transverse section. Osteology of harelip. (Museum of the Philadelphia Dental College.) It acts as a support to the fetal jaw, undergoes atrophy at about the sixth month of gestation, and at birth but few fragments are found near the symphysis. At birth ossification has occurred, and the bone consists of two halves united by a fibrous symphysis in which ossification takes place during the first year. The end of the cartilage in the base of the inferior maxillary process becomes the future malleus (one of the bones of the middle ear). The portion of the cartilage running from the malleus to the formed bony lower jaw becomes transformed into the internal lateral ligament of the inferior maxilla. (Hertwig.) A case of failure of development of the intermaxillary bones has been reported,^ the space between the cuspid teeth being about one-eighth inch. It is to be remembered that these processes are formed by the out- 1 Jeffery: British Dental Journal, July, 1904. DEVELOPMENT OF THE TEETH 153 growth of the mesoblastic layer of the blastoderm, and are covered by epithelial tissue springing from the epiblast. Both are concerned in the formation of the teeth. Epithelium is reflected over the face and oral cavity. All tissues between these layers of epithelium excepting the dental band and enamel organs and the nenes are of mesoblastic origin. DEVELOPMENT OF THE TEETH At about the sixth week of gestation, while the maxillary processes are but ill-defined masses of mesoblastic tissue surrounded on all sides by epiblastic tissue (Fig. 82), the ''dental hand" develops as a continuous depression of the stratum ]Malpighii of the fig. 89 mucous membrane extending from end to end of the fetal jaw (Figs. 90, b, and 91,6), over which depression is a mound of epithelial cells de- veloped from it, and called the "dental ridge" (maxillary rampart of Kolliker and Wal- deyer (Fig. 92, mr). At ten points on these bands in each jaw, at about the seventh to the eighth week, a further depression of the stratum Malpighii occurs, of a more or less definite saccular form, the sac also containing embryonic epithelial cells (Figs. 90, c, and 92, 3). This enlarges by an interiorward growth of epithelial cells, while the attachment to the mucous membrane remains constricted. At the ninth week the mesoblastic tissue beneath has somewhat condensed, evidencing the first appearance of the dentinal papilla. At this stage the cord (enamel organ) has been likened in appearance to a Florentine flask (Fig. 93, S) . The dentinal papilla pushes up the base of the enamel organ, which gradually adapts itself over the papilla, assuming first the shape of a Phrygian cap (Fig. 94), and finally a saddle shape (Fig. 95). Just before the connection of the enamel organ with the epithelium of the mucous membrane is lost (as shown in Fig. 95) ; the cord for the corresponding permanent tooth is given off from the side of the temporary cord. Fig. 95, cp, shows this after the separation. Porcine embrj-o: ep, epithelium, infant layer or stratum Malpighii; ct, embryonal connective tissue with large intercellular interspaces. 1.5 cm. X 250. (Sudduth.) 154 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH At the sixteenth week the enamel organ has developed so as to contain three distinct formative parts concerned in enamel deposition. 1. Next to the papilla the cells of the stratum Malpighii develop into nucleated columnar cells, collectively defined by an inner and an outer limiting membrane; the ameloblasts, the office of fig. 91 which is to deposit enamel (Fig. 96, e, and Fig. 97, c). 2. Those next interior de- velop into large cells nutritively associated with the ameloblasts Fig. 90 Vertical section through band from jaw of porcine embryo: ep, epithelium; b, band; c, cord; ct, connective tissue. 3.5 em. X 60. (Sudduth.) Longitudinal transverse section of the inferior maxilla of a porcine embryo: 6, band, solid at anterior portion, but divided posteriorly into band and lamina. 3 cm. X 40. (Sudduth.) and collectively called the stratum intermedium (Fig. 97, h); also shown in Fig. 96 between b and c). 3. Those in the central portion of the enamel organ are large cells rich in calcific material and polygonal from mutual pressure, and called collectively the stellate reticulum. They furnish the first nutritive material for the enamel cells (Fig. 94, 1, and Fig. 96, a). The dentinal papilla develops a reticulum of bloodvessels, nerves, and branched stellate connective-tissue cells lying in a gelatinous matrix. Upon the surface of the papilla elongated nucleated con- nective-tissue cells called odontoblasts are found, the office of which is to deposit dentin (Fig. 97, e; also Fig. 117, Od). About the enamel organ and dentinal papilla a fibrous sac develops from the mesoblastic DEVELOPMENT OF THE TEETH 155 tissue, encloses them, and is called the follicular wall (Fig. 95, c, ci), and will become the pericementum or cementum organ. The entire wall and its enclosures are called the dental follicle (Fig. 95). At the sixteenth week the cord of the temporary enamel organ gives oflF from its side a cord which will form the enamel organ of the suc- ceeding permanent tooth, and a cord is given off from the mucous membrane for the first permanent molar (Fig. 95, cp). At the seven- teenth week dentin deposition begins by the extrusion of small FiG.'J2 Section of jaw, embryo of pig, showing growth of enamel organ: 1, epithelium; 2, stratum Malpighii; 3, first stage in growth of enamel organ of temporary tooth; 4, embryonic connec- tive tissue; 5, developing bone of jaw; mr, maxillary rampart. (Andrews.) calcospherites formed within the odontoblasts, composed chemically of calcium and magnesium salts combined with albumin, a combina- tion known as calcoglobulin. A cement substance is formed within the odontoblasts, as is evident in Fig. 118. These calcospherites are evidently piled into the cement substance previously deposited against the ameloblasts, and later against each other, and around protoplasmic prolongations of some of the odontoblasts, which pro- longations remain in similarly compiled tube-like structures known as tubule walls or sheaths of Neuman, while the odontoblasts them- 156 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH selves recede, leaving behind them a portion of their substance in the tubules, and known as the dentinal fibrils. They finally persist upon the surface of the pulp (Figs. 97, 99, 105, 117). Fig. 118, a stained specimen of formed dentin, shows the arrangement of the compiled calcospherites. It is apparently almost analogous to enamel forma- tion. After some dentin has been deposited enamel deposition begins (at about the fifth month). The ameloblasts in like manner Fig. 93 Section of jaw, embryo of pig, showing growth of enamel organ: 1, epithelium; 2, second stage in growth of enamel organ; 3, embryonic connective tissue. (Andrews.) form within themselves calcospherites or enamel globules, also an amorphous substance called interprismatic cement substance. Both are calcoglobulin, and yet contain less organic matter, at least finally, than the dentinal calcoglobulin. The ameloblast first extrudes a drop of interprismatic cement substance against the dentin, and into it deposits an enamel globule (Williams) (Fig. 99, e). This is repeated, the ameloblasts mean- DEVELOPMENT OF THE TEETH 157 while receding, the result in finished enamel being a rod composed of enamel globules united in a row by intervening layers of inter- prismatic cement substance. Williams demonstrates plasmic strings which unite the ^•a^ious enamel globules to each other — probably these give the accurate relation end to end. The scheme of formation is shown in Fig. 99, and the orderly arrangement in Fig. 113. The hexagonal arrangement shown in transverse section (Fig. 114, B) is due to mutual pressure of the globules. Each rod is united laterally Fig. 0-1 Section of jaw, embryo of pig, sliowing growth of enamel organ and dentin gum: 1, enamel organ; 2, dentin gum; 3, growth of jaw; 4, tongue. (Andrews.) to its neighbor by interprismatic cement substance, which flows there during deposition of each layer of the enamel. The strise of the enamel represent periods of incremental activity. That the enamel rod is not formed by calcification of the ameloblast is proved by the fact that the ameloblast lies at an angle to the developing rod. The function of the stellate reticulum is to furnish calcoglobulin for the first enamel deposition. This is probably elaborated in the stratum intermedium and passed on to the ameloblasts, which con- struct the calcospherites and interprismatic cement substance. After 158 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH the first deposition of enamel the stellate reticulum disappears and the papilla-like structure of the stratum intermedium comes into Fig. 95 *.>">% ii^ — cjj. ''/-^Vi'j^ 5Mt i'^' \A'^yl'^^'<^< ; i ca (S cd c3 03 !>-,>>ja a >> >> >. 5 00 «5 •* (N O enamel globules united end to end by interprismatic cement sub- stance, which also unites adjoining rods longitudinally (Fig. 113). The Dentin. — The dentin is composed of tubules and their con- tents and intertubular substance. Each tubule contains a prolonga- tion of an odontoblast, also called a "fiber of Tomes," or dentinal fibril. The wall, diflFering from intertubular dentin, is called the sheath of Neuman (Fig. 116). The tubules are wavy in direction, but radiate in the crown and lie at right angles to the pulp in the root dentine. At the peripher}^ the tubules branch and anastomose freely, and some may penetrate the enamel. There are also fine anostomatic connections at other points (Fig. 116). Both the tubules and intertubular substance seem to be composed of calcospherites and cement substance (Fig. 118). The tubules are curved in outline and sometimes show a series of short, sharp curves on a general curved level at the points at which a new period of increment has occurred. They are the stripes of Schreger in dentin or "incremental lines" of Salter (Fig. 182). The Pulp.— This consists of a gelatinous matrix in which are embedded branched con- nective-tissue cells. The odon- toblasts lie upon its surface next to the dentin, with their fibrils extending into the tubules up to the enamel, and, as shown by Caush, often into it, forming organic matter in enamel, and in some cases accounting for a sen- sitivity which is, however, rare. 168 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH Fig. 112 Diagram of enamel-rod directions and tubule curves. From a photograph of a buccolingual section of a superior bicuspid. (Noyes.) Fig. 113 Section of enamel of human tooth. Photographed with Zeiss apochromatic lens and Powel and Leland apochromatic condenser. The optical parts accurately centred and the focus critical." The enamel rods are seen to be resolved into distinct sections (enamel globules), the cement sub- stance often passing entirely between the sections. X 400. (Williams.) DEVELOPMENT OF THE TEETH 169 One or more arteries enter the apical foramen or })y several fora- mina, and several veins may emerge. The arteries subdi^•ide in the central portion of the pulp and form a rich network of capillaries beneath the odontoblasts. Fia. 114 Enamel prisms: A, fragments and single fibers of the enamel isolated by the action of hydn chloric acid; B, surface of a small fragment of enamel, showing the hexagonal ends of the fiber X 350. Fig. 115 • Enamel showing both striation and stratification. X SO (about). (Noyes.) The arteries are not branches entering the foramen directly from the bone, but rather branches of arteries in the pericementum. The arteries of the pulp soon lose almost entirely their muscular coat, and their external coat is reduced to an inconsiderable amount 170 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH Fig. 116 D.C. N.Sch. Transverse ground section through the dentinal tubules of the first molar of a child, aged seven years: F, small connecting tubule. Koch's and Golgi's methods combined. X 1200. (Rose.) Fig. 117 CD.- U.D.' ,^9^mv>i 9filt? ■ T.Ii. P.C — -Od. Section of pulp, showing the relations of the odontoblasts to the dentin: Oil., odontoblasts; T.F., Tomes' fibers — odontoblastic processes; UD.. uncalcified dentin; CD., calcified dentin; PC, pulp cells. X 800. (Rose and Gysi.) DEVELOPMENT OF THE TEETH 171 of fibrous connective tissue. There is little if any anastomosis of the arteries of the pulp, so that collateral circulation is impeded, though not necessarily prevented, as pathological cases show. The veins remain for an unusual distance without a muscular coat, and are stated by Hopewell-Smith to be non-\'alvular and non-collapsible.^ These histological data have great clinical significance. (See Diseases of the Pulp.) FiQ. 118 IMain mass of dentin of a temporary tooth, stained with chlorid of gold, decalcified with acetic acid: F, F, dentinal fibers, partly vacuolated; B, B, basic substance, traversed by a reticu- lum. X 1200. (Hart.) The vascularity of the pulp decreases with age. " In young teeth there are a number of arterial trunks entering the apical foramen, which lessen in number as the passage lessens in size." Finally only one may enter. (Black.) The passage of arteries and veins through a constricted foramen has important consideration in connection with pulp diseases. It has been shown by Stein^ that the arterial supply is through the bone rather than by direct arterial continuity. (See Venous Hyper- emia of the Pulp.) The nerves enter by several bundles, and if medullated soon lose 1 Dental Cosmos, 1907. - Items of Interest. 172 ANATOMY AXD HISTOLOGY OF THE JAWS AND TEETH the medullary sheath. They are derived from the trigeminus and the sympathetic system. Those from the sympathetic are distributed to the bloodvessels as vasomotors; the others form a plexus in intimate relation with the odontoblasts. They have been found by Retzius to terminate in knob-like extremities between the odontoblasts in the mouse. These are probably sensory nerves. No direct anatomical connection has been made out between the nerve fibers and the odontoblasts or the fibrillse, although Robertson Ground section through the root of a human premolar: D, dentin; K, cement corpuscles O, osteoblasts; Ep, remains of Hert wig's epitheUal root sheath or pericemental glands of Black;' J , interglobular spaces. X 200. (Rose.) (England) has claimed to have traced the long central fiber running from the odontoblasts into the pulp into nerve bundles, and claims that they become axis cylinders. The phenomenon of sensitive and hypersensitive dentin shows an evident physiological connection. The nerves of the pulp do not possess tactile sense, so their pains are not localized, but reflected, as a rule. The pulp contains no demon- • The editor has taken the liberty of altering the interpretation. DEVELOPMEXT OF THE TEETH 173 strable lymphatics, though lymph spaces probably exist; their office is i)robabl\' performed l)y the veins, which in other parts may take up this function.^ The pulp becomes more fibrous and less vascular with age. During health it preserves the translucency of the tooth through its relation with the fibrillse and under certain circumstances renews its formative activity and produces secondary dentin. The forms of the pulps and \)\\\p cavities are shown in Figs. 123 to 132. Fig. 120 s.r>.- S. T.~ B.V. -y.f Section of a tooth pulp: B.V., main bloodvessels of pulp; C, origin of rupillaries; N.T., main nerve trunk; .V.F., subdivisions of nerve into fibrill8e;jOd., odontoblastic layer; S. D., secondary dentin; C.G., masses of calcoglobulin. X 30. (R6se_^and Gysi.) The Cementiim. — The cementum is a modified bone distributed over the dentin of the root. It meets the enamel either edge to edge, overlaps it, or is overlapped by it (Choquet). In some cases they do not meet at all, and leave the dentin exposed.- It con- tains lacunte and canaliculi, but only rarely an Haversian canal. It contains a fibrillar structure, which represents the remains of Sharpey's fibers (Fig. 121). ' Green: Pathology and Morbid Anatomy. - Hopewell Smith: Dental Cosmos, 1909, p. 1375. 174 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH The ph^^siological function of the cementum is to afford a means of attachment of the teeth to the maxillary bones through the medium of the pericemental fibers. In case of death of the pulp, and, there- fore, of cessation of nutrition of the dentin, the vital relations of the cementum and alveolar process are thus maintained and the use- fulness of the tooth assured. Whether the dentin can ever receive Fig. 121 Two fields of cementum, showing penetrating fibers: Gt., granular layer of Tomes; C, cementum not showing fibers; F., penetrating fibers. X 54 (about). (Noyes.) nourishment from the cementum after pulp death has never been scientifically shown, and the fact that it may contain dead and even putrefied material while a healthy cementum may persist, renders it extremely doubtful. The Pericementum. — {Sy7i., Peridental Membrane). — The peri- cementum is the highly organized remains of the follicle wall. As DEVELOPMENT OF THE TEETH 175 the alveolar bone and cementiim develop on either side of it, it forms also the periosteum lining the alveolus. It is, therefore, the means by which the teeth are retained in their sockets and a certain degree of motion permitted. The pericementum subserves the office of a membranous attachment not altogether unlike that found in the sutures of the cranial bones. It is considered by some observers that there are two distinct portions to the pericementum, cemental and alveolar. Photo- FiG. 122 Portion of the side of a root of a tooth, the gum and alveolodental membrane, and the edge of the bone of the alveolus. A band of fibers is seen passing over the surface of the alveolus and dividing, some passing upward into the gum, others passing more directly across to the cementum. Numerous orifices of vessels cut across transversely are seen between the tooth and the bone. (Black.) micrographs generally do not demonstrate this, and it is a matter of difficulty to imagine the pericemental bands divided into two portions. It is continuous with the periosteum on the outside of the alveolar process, as the sutural membrane is with the pericranial membrane. Its outline study divides the pericementum into three portions — a gingival, an alveolar, and an apical portion.^ ' Noyes : American Text-book of Operative Dentistry. 170 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH Fig. 123 Transverse sfclion of the peridental membrane in the occlusal third of the alveolar portion (from sheep): M, muscle fibers; Per, periosteum; Al, bone of the alveolar process; Pd. peri- dental membrane fibers; P, pulp; D, dentin, Cm. cementum. (Noyes.i) 1 American Text-book of Operative Dentistry. DEVELOPMENT OF THE TEETH 177 It is composed largely of white fibrous tissue with interlaced blood- vessels, nerves, and glands. It also contains functional cells, fibro- blasts, cementoblasts, osteoblasts, and osteoclasts. Fig. 124 Fig. 125 Fig. 12G Fig. 127 Fig. 12S Fig. 129 Fk;. 130 Fio. 131 Longitudinal and transverse sections of upper teeth, showing shapes of pulp chambers and their positions. 12 178 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH Fig. 132 Formalin-gelatin casts of pulp cavities, showing pulp irregularities. (Richards.) Fig. 133 Formalin-gelatin casts of pulp cavities compared with the teeth themselves. (Richards.) DEVELOPMENT OF THE TEETH 179 The fibrous tissue is made up of principal fibers and indifferent fibers.^ The principal fibers are grouped for the most part in bands or bundles (Fig. 123). In the alveolar portion these bundles run for the most part from the cementum to a higher point on the alveolar process. The attach- ment is secured by the penetration of the fibers into either structure. This secures to the tooth support against direct pressure into the socket and against rotary motion. Fig. 134 >liuwing the buccal surfaces of the crowns and roots in position. (Cryer.) At the apical portion the bands have a fan-like distribution. In the gingival portion the fibers are directed outward and slightly toward the edge of the alveolar process for tooth support, or outward and downward over the edge of the process to become continuous ' Noyes: American Text-book of Operative Dentistry. 180 ANATOMY AND' HISTOLOGY OF THE JAWS AND TEETH with the periosteal fibers, or outward and upward with the sub- mucous gingival tissue to aid in the support of the gum margin. Some of the gingival fibers pass from the cementum of one tooth to that of the next (Fig. 123). Fig. 135 Vertical section ofa frozen head, rear view. Shows relations of roots of molars and the maxillary sinus, and of the maxillary sinus with the frontal sinus. Wire passes from the latter through the infundibulum, the hiatus semilunaiis, and the ostium maxillare. into the maxillary sinus, establish- ing a connection. (Cryer.) DEVELOPMENT OF THE TEETfl 181 The bloodvessels of the pericementum are derived from several sources: (1) From vessels entering the membrane through the Haversian canal'-: of the alveolar process and bone, and anastomosing with branches from the descending arteries; (2) from the vessels of the outer periosteum, coming over the edge of the alveolar process. It has been shown that the destruction of main arteries as the infra-orbital or inferior dental does not cause pulp death, hence the collateral blood supply is the most important. There are comparatively few capillaries. The vessels lie mostly in the outer or alveolar half of the pericementum. Fig. 136 Diagram of glands of peridental membrane. (Black.) This disposition of the arterial blood supply insures nutrition to the peridental membrane in case of loss of the apical tissue, as in case of apical abscess, and also insures a collateral blood supply to the pulps in case of loss of main arterial trunks, as, for example, in operations upon the inferior dental canal, in which case pulps do not die.^ The arteries thus furnishing blood to the teeth are, for the upper jaw: The anterior dental branch of the infra-orbital, to the upper anterior teeth; the superior dental branch of the alveolar, to the upper bicuspids and molars and the bone about their root ends ; the descend- ing palatine and its anastomotic connection, the sphenopalatine, suppHed to the palatine side of the upper alveolar process, etc.; the alveolar, supplied to the buccal side of the upper alveolar process. •John Bethune Stein has experimentally proved this by operation of removal of the contents of the inferior dental canal. The pulps did not die, and the teeth developed as usual. Items of Interest, May, 1910. 182 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH In the lower jaw the inferior dental artery and its incisor branch supply the apical tissues of the lower teeth from the inferior dental canal. Its mylohyoid branch supplies the gums and lingual perios- teum of the lower alveolar process, the mental branch supplies the low^er buccal process anteriorly, while a branch of the facial artery anastomoses with the mental anteriorly, and the facial sends branches to the coverings of the buccal aspect of the lower jaw posteriorly. Fig. 137 Glands of Black. Epithelial structures: Ec, epithelial cord, apparently showing a lumen; Cb, cementoblasts; Cm, cementum; D, dentin. X 500 (about). (Noyes.) With the exception of those branches derived from the facial artery, all the blood comes from the internal maxillary artery. Stein has shown that the blood is supplied to the pericementum, which, by collateral circulation, supplies the pulp. The veins return the blood by similar channels. The nerves of the pericementum enter by several trunks in the apical tissue, and also enter from the alveolar wall and over the alveolar edge. While their distribution is not yet fully described, some of them possess the tactile sense, as touch upon the teeth is Fio. 138 Longitudinal section: Ep, epithelium lining the gingival space; Gg, gingival gland, so-called; D, dentin; jV, Nasmyth's membrane; Du, duct-like structure stretching away toward the gingivus from the epithelial cord, seen at Ec; Cm, cementum, separated from the dentin by decalcification. X 50 (about). (Noyes.) 184 ANATOMY AND HISTOLOGY OF THE JAWS AND TEETH fully localized. They are derived from the fifth nerve and the sym- pathetic. The Pericemental Glands. ^ — Black has described gland-like structures lying in the pericementum nearer the cementum than the alveolar wall. These are distributed over the root in a network, as shown in Fig. 136. They are convoluted cords of epithelial cells invested with a deli- cate basement membrane, and can be traced to the epithelium of the gingival space, but not to the surface. Traces of a lumen have been seen, which, if established as common, would constitute them as tubes. Their function is not definitely known, but it is presumptive that they are either secreting glands or lymphatics. The entrance of bacteria from the gingival space to deep portions of the pericementum, there to develop, may possibly be favored by their presence (Figs. 119, 136, and 137). Some consider these glands as resting epithelial cells derived from the enamel organ during the upward movement of the tooth, i. e.-, the epithelial root sheath of Hertwig. Glands of Series. — At the deepest portion of the gingival space is found a gland-like body which has been given the above name. Its function is not known (Fig. 138). The Cellular Elements. — The fibroblasts are spindle-shaped cells destined to become mature fibers. They lie among the other fibers. The cementoblasts lie along the cementum and are the cementum builders (Figs. 72 and 105). Osteoblasts are found engaged in bone construction along the alveolar wall. Osteoclasts, large multinucleated cells, lie at points along the cementum of teeth and alveolar bone. Their office is the removal of bony tissue. They remove both the organic and inorganic material, and their effects are seen upon the cementum and dentin of the roots of teeth undergoing resorption, also upon resorb'ed alveolar process. The excavations in which they lie at work are called Howship's lacunae (Fig. 73). Calcospherites are sometimes found within the substance of the pericemental membrane, and may have some significance in relation to its diseases. The pericementum in the young is comparatively large and vas- cular, and in the old becomes much attenuated, more fibrous, less vascular, and subject to degeneration. Union of alveolar bone and cementum but rarely occurs, though a mechanical attachment by fibrous pericementum may occur. (See Synostosis.) On the other hand, the union of the cementum of one tooth with that of another is not uncommon. (See Concrescence.) chaptp:r VII DENTITION: ITS PROGRESS, VARIATIONS, AND ATTENDANT DISORDERS Tpie process of teething, eruption, or dentition comprises that series of vital operations which causes the teeth to leave their crypts in the maxilla^, to pierce the gum, and to take their places in the dental arches. It is a continuation of the process of dental develop- ment, and is accompanied and succeeded by root, alveolar, and max- illary developments, which are also to be considered in connection with it. Physiologically dentition is divided into (1) the first dentition, or that of the temporary teeth, and (2) the second dentition, or that of the permanent teeth. Examination of Fig. 100 will show the state of tooth develo])ment at a period shortly after birth (a central incisor being under con- sideration). The crypt is roofed over at birth by a membranous structure. During the period from then to perhaps six months after birth about one-third of the root will have been formed. (See Fig. 104.) The root end is widely open (incomplete) and the margins are thin and sharp. A very vascular tissue occupies the space between the root and the bone, and fills the interior of the root. Meanwhile the crown cusp will have advanced from the situation shown in Fig. 100 to a point just beneath the mucous membrane, which is pressed up and stretched over the advancing tooth crown, presenting to oral view a tumefied condition more or less corresponding to the form of the crown. This is nicely shown in Fig. 139, A and B. These anatomical data serve for the consideration of the causes and process of eruption. Causes of Eruption. — It is evident that there are forces which can bring about the elevation of a tooth crown from its bed in the crypt to its position in the mouth. The consideration of these has led to the development of the following rational theories, as well as others now obsolete. 1. That crown elevation is due to the lengthening of the root — i. e., as root tissue is formed by the pulp and follicle wall lying beneath and to the side of its edges, the tooth is mechanically pushed up, the tissues lying above it are stimulated and absorbed, and as more root 186 DENTITION is formed, a further extrusion occurs. It is to be noted that the root end occupies the same level, at all stages of eruption, in the devel- oping jaw that was occupied by the cervical edge of the crown (Fig. 140). As no two bodies may occupy the same space at the same time, the root-forming pulp and follicle wall push the tooth up to gain room for more root formation. The mild continued pressure is quite competent to do this. The pressure of the soft tissues against the root end is explained by Constant to be derived from the normal blood pressure.^ That such an internal pressure exists is shown by the extrusion of ordinarily confined parts when released from the accustomed pressure. A simple accident demonstrated this to the editor. While excavating with ^^^- ^^^ a large bur the softened dentin about a decayed pulp cham- ber, the cementum was widely removed from the pericemental tissue beneath, which latter fortunately remained unbroken. It immediately protruded into >^^ '" \J^>Sh-'fn'^ "^ y^ B the perforation. Constant also ^^^^^ "^ r*"] y*--^ cites the extrusion of a tooth in pericementitis as an evidence of the influence of the blood pressure. Another evidence is the occasional rapid advance of a tooth after lancing of the gum. 2. The process of tooth development is a vital process, and that of eruption has been held also to be. (Tomes.) That cells concerned in development seem to have a predestined end or function cannot be denied; at the same time, throughout dental development, defined resistances to opposing forces seem to play a part in the' moulding of the soft and hard tissues — e. g., the depression of the enamel organ by the papilla. 3. Peirce^ holds that the impact of blows upon the jaws causes the tooth to rise toward the gum. He explains the eruption of crowns without roots upon this theory. 4. Tomes explains the eruption of teeth, after development of the root, upon the theory that the closing in of the alveolar process or contraction of the alveolus upon the pericementum (follicle wall) causes the lifting up of the tooth. That such a closure occurs about the extruding roots of teeth left after the breaking away of the crowns Lines of incision 4n lancing: A, A, over the molars; B, B, over the cuspids and incisors before eruption; C, C, C, over the molars and cuspids after partial eruption. • International Dental Journal, June, 1903. 2 American System of Dentistry. DENTITION 187 is shown by examination of the sockets of such roots. An ahnormally shallow alveohis closed by dei)osition of bone at its apex will be found in cases of small apical portions of roots so extruded. It is w^ell known that mild hyperemia is produced in pericementi which do not receive a normal resistance, which would account for both the elevation and bone deposition on the ground of blood pressure. (See Arterial Hyperemia.) Fig. 140 Diagram showing the upward movement of the crown during eruption and root development. (Constant.) The Process of Dentition. — At varying ages, according to the state of tooth development, the formed crown of the tooth ad\'ances and presses upon the follicle wall overlying it; this is irritated, and giant cells are developed, which by resorption remove this as well as the upper edge of the wall of the crypt. The mucous membrane is pushed up and moulded over the crown, thereby causing a tume- faction. The mucous membrane, at first normal in color, becomes slightly hyperemic, and then may change to an ischemic condition and whiten, owing to the removal of the blood by the pressure of the underlying crown. Resorption from beneath causes a break in the continuity of the mucous membrane, and the crown tip erupts into the mouth (Fig. 139, C). _ The rate of resorption and crown advance are equalized in perfectly normal dentition. The crown rises from the gum, is directed by the tongue and lip or cheek, and, finally, meets its antagonists of the opposite jaw. The interlocking of cusps and meeting of occlusal surfaces limit further movement of position. Meanwhile root development proceeds, and as it occurs the alveolar process is built about the pericementum, which has been drawn up 188 DENTITION from the follicle wall. By this means the roots are firmly implanted. The further development of the root proceeds until complete, and so remains until normal resorption of the temporary roots occurs, and for life in the permanent teeth. The state of formation of the roots of temporary teeth at any given age may be judged by the table of averages shown by Peirce in Fig. 104. Being but averages, allowance for delays must be made. Apart from the presence of the temporary teeth the process of eruption is identical in both sets of teeth. Periods of Eruption. — As a general rule, the eruption of the deciduous teeth may be said to begin about the seventh month after birth, and is completed somewhere about the twenty-fifth month. This rule, however, varies within wide limits; some children may be born with teeth erupted; again, the initiation of the process may not occur until the twelfth month, or even later. The incisor teeth are usually erupted in pairs, the molars and cuspids making their appearance in fours, the first molars in one group, the cuspids in another, and the second molars in a third group. The several groups require different lengths of time to complete their eruption, the time occupied in the eruption of the first molars being longer than that required for the eruption of the other groups. Between the appearance of additional groups of the teeth an interval elapses, no doubt a physiological provision, for, as will be shown later, the process of dentition is usually accompanied by evidences of more or less local disturbance, frequently by disturbances through- out the intestinal tract, and even reflex disorders of the central nervous system occur. It is believed, therefore, that the period which elapses between the eruption of the dental groups permits the organism to recover from the effects of previous disturbance before the new source of irritation appears. -* Tablei Group 1 Lower central in- Time of eruption, Duration of eruption. Interval, 2 to 3 months. cisors 7 months 1 to 10 days Group 2 Uppercentraland Time of eruption, Duration of eruption. Interval, 2 months. lateral incisors 9 months 4 to 6 weeks Group 3 Lower lateral in- cisors Time of eruption, 12 months Group 4 First molars Time of eruption, 14 months Duration of eruption, 1 to 2 months Interval, 4 to 5 months. Group 5 Cuspids Time of eruption, 18 months Duration of eruption, 2 to 3 months Interval, 3 to 5 months. Group Second molars Time of eruption. Duration of eruption. • 26 months 3 to 5 months 1 Coleman's Dental Surgery. (Stellwagen.) PATHOLOGICAL FIRST DENTITION 189 111 the above table it will be noted that the time of eruption of the lower lateral incisors is later than that of the eruption of the upper lateral incisors. The reverse course is frequently observed; indeed, it has usually been accepted as the rule of precedence in the United States. All tables, as to periods of eruption, give but the approxi- mate times; while variations are extremely common. The ages given in this table are those at about which the several teeth ma\' be expected to make their appearance. Stellwagen (the American editor of Coleman), in commenting upon this table, states that the periods of eruption in this country are from one-seventh or more earlier than the dates given. He suggests that the difference in food habit may account for the differences in time. Pari passu with the development and eruption of the teeth occur developmental changes in all of the glandular appendages of the alimentary canal ; probably the alterations in their structure, and no doubt in their physiological chemistry, are accompanied by dental provision for the mechanical subdivision of foods of postinfantile character. Symptoms of Eruption. — Slight local disturbances are so com- mon in even so-called normal first dentition as to be accepted as physiological. The resorption of soft tissue around the tip of the crown of the tooth implies a condition of mild non-septic inflamma- tion at that point. In more marked cases there is e^'idence of some irritation cognizable to the infant; the gum is of a somewhat deeper color and its temperature is elevated. Relief is afforded by pressure, which temporarily reduces the hyperemia, and the child is pleased to have its gums rubbed, to bite upon its own or the nurse's fingers, upon rings or other objects. Still more marked is the soothing effect of biting upon cold substances, such as ice, which, in addition to mechanically lessening the blood supply, causes contraction of the dilated vessels. Slight reflex disturbances are evidenced by the stimulation of the salivary glands, which produces an increased flow of saliva. Reflex disturbances of more severe character occur in pathological dentition, to be considered later. PATHOLOGICAL FIRST DENTITION The local disturbances may be exaggerated beyond that degree accepted as physiological, and may be accompanied by nervous, alimentary, pulmonary, or cutaneous disturbances. This is patho- logical dentition, and may be of several grades of severity. 190 DENTITION Causes and Pathology. — The primary cause of pathological dentition may be stated as an inequality in the rate of gum resorption and crown advance. The advancing crown pressing upon the gum tissue causes irritation; the hyperemia or mild aseptic inflammation result- ing, instead of remaining at a point favoring the development of giant cells and resorption, passes the physiological point and causes a disturbance of function. Inflammation, simple or even infective, may occur in the area. Swelling of the gum occurs, which, being distributed in all direc- tions, presses upon the crown, depressing it upon the pulp beneath the sharp root margins; at the same time the blood pressure of the pulp tends to press the tooth upward. The simple lack of resorption of the gum would be almost equally effective in preventing eruption. The sharp edges of the root must irritate the sensitive and delicate pulp tissue, which becomes inflamed and swollen, and still more strongly urges the tooth upward. Two sources of disturbance now are possible: (1) The irritated gum tissue and (2) the irritated pulp. The latter is the more likely to cause reflex disturbances. Through the intimate sympathetic relations of the fifth cranial nerve, supplied to the pulp, with the seventh, ninth, and tenth cranial nerves in and about the floor of the fourth ventricle of the brain, salivary, muscular, nervous, alimentary, and pulmonary disturbances become possible. Though the pulp is more likely to produce the reflex disturbance, a gum inflammation, if intense, is often capable of producing even prostrating symptoms. Any systemic disturbance — e. g., measles, general debihty, or lesser disturbance, etc. — which lowers the gen- eral nutritive function also in the parts associated with the teeth, may favor the production of local pathological phenomena. Again, systemic disturbance readily produces a hyperesthesia of the nervous system, favoring the production of nervous phenomena. Pathological dentition may occur in the absence of an evident hyperemic gum tissue. The tissue may be white, showing ischemia from pressure, a binding down of the root end upon the pulp being proved by the subsidence of symptoms after lancing, and sometimes by the rapid, partial eruption of the tooth immediately after lancing. Again, pathological phenomena have been noted where no super- ficial local disturbance was evident. In these cases the deeper tissues may exert a restraining influence upon the crown, but the swelling is just as probable. It is to be understood that the nervous and digestive systems of the child are in a developmental condition, and therefore in unstable physiological equilibrium, so that any added physiological work, such as unusual growth or dentition, may be more than the organism PATHOLOGICAL FIRST DENTITION 191 can endure without a definite loss of general vital potential. This may be further complicated by hereditary defects of tissue, such as neurotic, degenerative, or syphilitic taint, or conditions of hygiene or feeding tending to lower the health standard. Ottofy offers the following report, by the Bureau of Health of ^Manila, of 3250 deaths before twelve months of age: Before completing one montli 647 During second and third months 302 Various causes not dental 959 Four to twelve months due to convulsions and eclampsia 1342 Total 3250 Showing a large number of deaths due to causes in which dentition may have been a determining or complicating factor. Dr. William P. Spratley, medical superintendent of an institution for epileptics, states it as his opinion that pathological first and second dentition is a determining cause of epilepsy in children having neuropathic taint in that direction.^ Symptoms. — The symptoms of pathological dentition are both local and general. Local Symptoms. — The local symptoms are usually those of inflam- mation, red and swollen gum tissues at times assuming a dusky hue. The gums may be white, and often glistening, indicating their tense stretching over the crowns. In the gum over the erupting tooth there may exist a vesicular enlargement containing fluid. ^ Evidence of local irritability is given by the fact that the child resists the touching of the gums, seizes the breast or bottle nipple, and imme- diately releases it. The readiness with which the child will take cold substances, ice or iced water, is notable and self-explainable. Alternate, excessive flow of saliva and oral dryness are present. In the more marked cases of local disturbance evidences of bacterial infection of the mucous membrane of the mouth may make their appearance, such as ulcerative stomatitis. While, as a rule, the breaking down and ulceration of the tissue are confined to the parts overlying the erupting teeth, a general stomatitis or widely scattered patches of ulceration may make their appearance. The localized condition has been called odontitis infantum. General Symptoms. — The general symptoms ma}' be differ- entiated into mild and severe. The mild symptoms are such as are attendant upon severe and painful inflammations about the face at almost any age; thus anorexia, 1 Dental Cosmos, 1905. - Tomes: System of Dental Surgery. 192 DENTITION fretfulness, anger, restlessness, sleeplessness, thirst, mild fever, and evident desire for the upright position occur. The pain is at times parox}'smal, but may become continuous. These symptoms subside upon the eruption of the tooth or lancing, though erupting cuspids, bound by a ring of tense gum tissue or by adjoining teeth, may continue the irritation even when apparently erupted (Fig. 139, C). The more severe general symptoms are such as are brought about by reflex neuroses. The roots of the fifth cranial nerves supplied to the teeth are in intimate relation with the roots of the seventh, ninth, and tenth cranial nerves in the floor of the fourth ventricle, as well as with other cranial nerves. It may be argued upon a priori grounds that irrita- tion of the peripheral ends of the fifth in the pulp tissue may therefore readily produce neurotic results in the brain, salivary glands, skin, lungs, or larynx, intestinal canal, or muscles of the face or extremities. Taking the intestinal canal as the most complicated example, we find the following data: The stomach and intestines are under the influence of the pneumogastric nerve, which sends to its muscular coats both stimulant and inhibitory fibers. Likewise it sends vaso- motor fibers to the intestines, division of which leads to inhibition of the muscular fibers of the vessels and leads to vasodilatation and a great increase of very watery succus entericus.^ Intestinal Disturbances. — That intestinal disturbances may arise independently of teething is self-evident. They are most liable to so occur during the very period during which teething may be supposed to act as a primary cause of intestinal troubles; hence difi'erentiation becomes important. That the conditions may be associated is also evident. As a rule, intestinal disturbances arise from improper feeding, the food acting as an indigestible irritant to the stomach and intestines. Even an excessive quantity of good breast or bottle milk may, if not regurgi- tated, act as an intestinal irritant. The milk of an excited, exhausted, or debauched nurse may also act deleteriously. Fermentation due to bacteria ensues, and diarrhea and colic are a natural result. Musser^ attributes these cases to development of the Bacillus coli communis and Bacterium lactis aeriformis existing harmlessly in the normal intestine, but developing under the abnormal conditions. This occurring in warm weather when the child suffers from intense heat has a very debilitating if not fatal result. The condition may be viewed as an infective diarrhea following 1 Halliburton: Kirke's Physiology, 1896, p. G84. -' Medical Diagrnosi?. PATHOLOGICAL FIRST DENTITION 193 a vasomotor disturbance of the intestinal walls set up by reflexes primarily caused by the indigestible food. The vital resistance is lowered by the disturbed alimentation and the pain. A similar train of circumstances may be caused by teething. Peripheral irritation of terminals of the fifth nerve in the pulp may, through the tenth nerve, cause a reflex vasomotor dilatation in the walls of the intestines — i. e., hyperemia, a condition which favors bacterial invasion. Intestinal digestion is disordered, the vital resistance lowered, and an infection ordinarily resisted occurs. Diarrhea may follow. In either case alimentation is interfered with and the general nutrition suffers. The child is debilitated by lack of nutrition; moreover, toxic substances are generated in the intestine, which cause a toxemia, to which many of the general symptoms may be attributed, such' as fever, meningitis, stupor, coma, and death. The general debility also further interferes with the process of dentition. Diagnosis. — A diarrhea due to improper feeding would not be preceded by symptoms of pathological dentition, would have a history of improper feeding, and possibly of unhygienic conditions, such as unsterilized milk or milk bottles, filthy surroundings, etc. There is a catarrhal diarrhea accompanied by vomiting and constant acid, watery stools. The stools may have a chopped-spinach char- acter. There is colic due to collections of gas. Such an infective diarrhea may readily follow the reflex and debilitating effects of pathological dentition, as shown above. White^ has noted that a choleraic diarrhea may accompany and be a sign of pathological dentition. Barrett^ states that a diarrhea due to dentition will probably be followed by constipation. A symptomatic diarrhea will, as a rule, be accompanied by signs of pathological dentition at points in the jaws at which teeth should be in process of eruption. Nervous Disturbances. — ^Disorders referable to the central nervous system are the most alarming and are those indicating the higher grades of severity of irritation. The milder forms of these are faint muscular twitchings and evidences of slight cerebral disturbance. Either of these may be the result of poisons absorbed from the alimentary canal during the course of intestinal fermentation, but as cases of even convulsions have occiirred without other cause than teething apparent, and been relieved by lancing alone, the possibility of direct connection between teething and central nervous disturbance must be admitted. ' American System of Dentistry. - Oral Pathology and Practice. 13 194 DENTITION A distressing symptom, not easy to elicit on account of the age of the patient, is headache. The child is sleepless, and cries without apparent cause; it becomes quiet, partially from exhaustion, and after a period again commences sobbing. The indication of central disturbance may at times be noted in the contracted pupils of the eyes and in throbbing arteries. The usual treatment, the adminis- tration of chloral hydrate and potassium bromide, with cold appli- cations to the head, furnishes relief which is frequently not complete without attention to the dental organs. In the more severe and dangerous cases the evidences of disorder of the central nervous system become unmistakable. These appear as clonic convulsions or symptomatic eclampsia. While it is probable in many cases that reflex irritation from the process of dentition in itself is but a secondary cause of convulsions, yet evidence is sufficient to warrant its being regarded as a determining factor. In very many cases teething convulsions appear to indicate a neurotic family taint, and eclampsia may attend many disorders in children of this type, notably the mechanical and chemical irritation induced by the presence of large masses of indigestible food in the intestines. So-called teething convulsions occur usually at a time when several teeth are in process of eruption. The onset of the convulsion is rarely, although apparently often, sudden. If the child be closely observed, it is noted that a period of cerebral disturbance — ^fretful crying, evidences of headache, sleeplessness, etc. — ^is followed by a period of dulness and somnolence, or the child may lie with eyes half open. Twitching of one or more groups of muscles may be observed; the orbicularis oris and other muscles of the lips, and the muscles of the eye, notably the superior and internal recti, may contract spasmodically. A common muscular spasm ushering in con- vulsions is that of the abductor muscles of the thumb; the thumbs are drawn toward the palms of the hands. The adductor muscles of the feet contracting, the feet are drawn inward. This period may be ushered in by a sharp cry, the eyes roll upward with the lids half open, and consciousness is lost. The symptoms may disappear, the child awakening dazed and fretful; or it may sink into sleep. Unless the source of irritation be removed, or active therapeutic measures be instituted, the eclampsia may return and in severe cases be the precursor of death. Infantile paralysis of a group of muscles or even a single muscle has been recorded, lasting from a few days to months, appearing with dentition and disappearing after it. In some cases it persists for life.^ Strabismus, if produced, may also persist. ■ White: American System of Dentistry. PATHOLOGICAL FIRST DENTITION 195 Skin Disorders. — It is so common as to be almost termed the rule to find that when there are intestinal symptoms there are eruptions observable on the skin. The mildest form of these is an herpetic eruption about the mouth; in other cases papular and vesicular eruptions are observed upon the skin of the body and limbs. Occurring within the mouth infection may be added and ulcerati\'e stomatitis may occur upon the gums, tongue, lips, or inside of the cheek. Pulmonary Sy:mptoms. — ^Pulmonary irritation may be expressed in laryngeal cough attending the eruption of teeth, and disappearing thereafter. Treatment of Pathological First Dentition. — This may be divided into prophylactic and remedial. The prophylactic measures include care as to pasteurization of milk or modified milk diet, sterilization of bottles, bottle nipples and rings, the prevention of the introduction of unclean fingers into the mouth of the child, and the antiseptic care of its mouth by frequent washings with a saturated solution of boric acid in water. This last may be applied to the mouth on a soft, linen rag wrapped on the forefinger. These measures, together with the proper feeding, ventilation, and care as to clothing, which should give comfort and not be in any way irritating, tend to prevent intes- tinal fermentation and to reduce the general irritability of the infant. Remedial Measures. — To reduce local hyperemia of the gum above an erupting tooth a common domestic measure is valuable, viz., a small block of ice is placed in a corner of a clean napkin, and con- fined in place by a thread ; the infant places it in its mouth at pleasure if old enough, or the nurse permits the child to bite upon it. The mechanical effect of biting upon a hard substance has added to it a degree of cold which lessens the local vascular engorgement. Any severe local irritation about erupting teeth should be relieved by thorough lancing of the gum. It is irrational that the child should be permitted to suffer from local irritation which may develop into more serious complications. This operation is performed by dividing the gum lineally o^-er the incisors and cuspids before eruption, crucially ovev the cuspids after eruption of the cusps only, crucially over the upper first molar, and \^^th an X-incision over the upper second and lower first and second molars (Fig. 139). For severe cases Flagg advised the removal of a block of gum from over a molar. A cut is made parallel with the lingual side of the crown, a second parallel with the buccal side, a third parallel with the mesial side. A tenaculum is thrust into the block of gum, which is drawn tense, and then divided at the distal portion, prefer- 196 DENTITION ably with a pair of curved gum scissors. Lacking these latter, the bistoury may be used. The cut over the upper incisors should, if possible, be made a little to the outside of the cutting edge, that for the lower to the inside, in order that their crowns may take a proper direction toward occlusion. The instrument to be used is a sharp-pointed bistoury, as it penetrates well and permits a free draw cut. It is to be wrapped with tape or a strip of linen cloth until only one-quarter of an inch of the point is exposed. This precaution prevents accidental wounds. The child must be securely held by an assistant the least sympathetic available. Flagg's method was to place the child upon its back across the lap of the assistant, who, in one position, places his left hand over the child's eyes, securing the head; his right hand secures the hands upon the abdomen, while the legs are held against his body by the right arm. The position may be exactly reversed. The feet should be placed toward the light for the upper jaw, the reverse for the lower jav.'. In another position the child sits upon one thigh of the assist- ant, the back of the head resting upon the chest, and the hand of that side (usually the right) pressed upon the child's forehead to hold the head firmly. The other hand and forearm hold the child's hands and legs firmly. The operator encloses the gum about the part to be cut with the thumb and forefinger of the left hand, so that the bistoury cannot slip and cut lip, cheek, or tongue. Incision over the erupting tooth should be made until the knife-blade is felt to touch the enamel surface. The operation of scarifying the gums, making merely a few scratches to relieve engorged vessels, is but temporizing with the condition; the cut should be of sufficient extent to entirely remove tension from above the tooth. The little finger of the right hand may rest upon the chin of the child as an additional guard. If the child bite, a cork with a string attached for safety may be used as a prop. Mote or less bleeding follows upon the operation, and, as a rule, ceases spontaneously. A short period of bleeding is desirable, so that vascular engorgement may be reduced. Suckling by the breast or bottle usually serves to check the bleeding; the tissues about the cut surfaces are compressed by tongue and lips during suckling, and bleeding ceases. In the event of the bleeding continuing, the mouth should be carefully examined, and a piece of ice in a napkin may be given the child to suck. The child may swallow the blood and later regurgitate it. Obstinate bleeding may require the use of styptics. PATHOLOGICAL FIRST DENTITION 197 but these should he of a character to cause only coagulation of the blood, not the destruction of tissue. A little powdered tannin laid upon the cut acts promptly, as does also a small amount of powdered alum. In some cases the internal treatment may be necessary. (See Hemophilia.) Death has occurred from hemorrhage due to lancing in cases of presumably hemorrhagic diathesis; so that inquiry as to family history would be a wise precaution. Obtaining such a history, the gravity of the symptoms alone warrant the operation. In the absence of such a history the operation is to be held as trivial. If it occurs it should be treated as indicated on p. 114. The operation of lancing is warranted even when the gimi may be likely to heal over the tooth by formation of cicatricial tissue, provided symptoms demand it. It is contraindicated in diphtheria and erysipelas, owing to the danger of infection. Shock has occurred in long-continued debilitated cases, and if feared a trifle of brandy in water may be given previous to the operation. It is within the knowledge of the writer that a physician has refused to lance the gums in a case diagnosticated as cerebral meningitis, even when death was prognosticated and though the child was at an age rendering pathological dentition possible, and in spite of a history of pathological dentition in a previous child at the same age. J. Lewis Smith^ concedes the similarity of occasional symptoms of pathological dentition and cerebral meningitis, so that the above therapy was foolish, to say the least, and especially so in view of the probable death, which did occur. In many desperate cases lancing has effected marvellously rapid recoveries, aided by judicious handling of the accessory symptoms, even though all hope from ordinary therapy had been abandoned. Treatment of Stomatitis. — Should general stomatitis, with or without stomatitis ulcerosa, make its appearance, the mouth is to be promptly and freely sprayed with a 3 per cent, solution of hydrogen dioxid, followed by a spray of potassic chlorate (gr. xx to 5j), which usually affords prompt relief. Should the spots of ulceration not disappear promptly, the mouth and tissues about the ulcer are to be guarded by soft linen napkins; each ulcer is dried and touched with carbolic acid, full strength. The spraying is to be repeated at intervals of three hours during the waking period. Treatment of Skin Eruptions. — The eruptions which appear upon the skin during dentition may be a source of annoyance to the child by causing itching. As a rule, measures directed toward 1 Diseases of Children. 198 DENTITION a regulation of the intestinal functions cause a disappearance of the skin affections. If the eruption be widespread and cause much itching, a wash of phenol-sodique diluted to one-third with water usually affords relief. If the surfaces be then dried and talc powder dusted over them the condition is much alleviated. About the mouth and over excoriated surfaces an zinc oxid ointment is useful. Treatment of Intestinal Symptoms. — The fermentative material in the bowel, together with the great mass of bacteria present, should be removed by the use of a cathartic. It is indicated in both con- stipation and diarrhea. Castor oil serves well, and is readily taken by children. To lessen the irritation of the bowel, laudanum and powdered acacia may be added. The following formula may safely be used even at six months of age: 1^ — Tinctur£6 opii gtt. x Olei ricini fgiss Pulveris acacise 3ij Saccharini gr. ij AqusB cinnamomi q. s. ad fgiij — M. Sig. — Shake the bottle, and give one teaspoonful each two hours if needed. For an additional six months of age ten drops more of laudanum may be added to the general formula. In mild cases olive oil in half- teaspoonful doses may be substituted. Following catharsis, antacid sedative astringents and intestinal antiseptics are indicated : I^— Saloli 3i Bismuthi subnitratis Su Misturai cretae ad f5iij — M. Sig. — One teaspoonful every four hours. (Biddle.) I^— Tincturs opii gtt. xvj Bismuthi subnitratis Sij Misturffi cretae fSiss Syr. simp fgiss— M. Sig. — Shake well, and give in teaspoonful doses every four hours. (Barrett.) The virtues of both formulae may be obtained by including the laudanum (gtt. xii) with the salol formula. Listerine in 10-drop doses, in water, every three hours, serves as an intestinal antiseptic. The gums are, of course, to be lanced at the outset if the diarrhea be due to pathological dentition. Following the intestinal antisepsis the general debility and possible intestinal toxemia (see p. 94) are to have careful attention, and the child's food is to be properly adjusted to its needs. J. Lewis Smith claims that upon the following diet ill-conditioned PATHOLOGICAL FIRST DENTITION 199 children under his care in the hospital escape summer diarrhea and thrive; the diet is therefore here introduced. For children not nourished on breast milk of good quality, and those over three months, he recommends the following substitutes: 1. Heat barley flour in a double boiler, the water in the outer vessel to be kept boiling for five to seven days to burst the starch granules (Robinson's prepared barley flour can be bought). 2. Take of this flour one tablespoonful, add 25 or 30 tablespoon- fuls of boiling water, and boil and mix for five minutes. Cool to blood heat, add 1 dram of diastase to change the starch to dextrin and maltose. Forbes' diastase or Taka-diastase can be bought. Of the latter 1 grain will change 150 grains of starch to sugar. Pasteurize milk by heating for twenty minutes to 160° F. Cool quickly on ice and let the cream separate. To two and one-half ounces of the upper half add a little peptogenic milk powder (Fair- child's) to peptonize it. He mixes the peptonized milk with three and one-half ounces of the dextrinized gruel at a meal, and feeds the infant nine or ten times at two-hour intervals. Before feeding administer a few drops of a digestive ferment. For use in emergency he recommends two heaped teaspoonfuls of condensed milk to fifteen teaspoonfuls of boiled water, as equiva- lent to seventeen teaspoonfuls of ordinary milk. He gives the following table of quantities of food required by infants; either breast or modified cow's milk to be used. At each feeding. During the first week At the third week . At the sixth week . At the third month At the fourth month At the sixth month At the tenth to twelfth month Number of Total daily daily feedi igs. Quantity. 1 ounce 10 10 ounces. 1}4 ounces 10 15 2 8 16 3 8 24 " 4 7 28 " 6 6 36 " 8 5 40 " White, following Starr, gives the following schedule of the diet of a hand-fed infant from birth upward,^ which will serve as a suggestive and useful guide: Diet during the First Week Cream fSiiJ Sugar of milk gr. xv Whey f5ss, f3ij Water fjss, fSiJ This portion to be given every two hours from 5 a.m. to 11 p.m., and in some instances once or twice during the night. ' Diseases of the Digestive Organs in Infancy and Childhood, by Louis Starr, M.D. 200 DENTITION Diet from the Second to the Fifth Week- Milk f5ss • Cream fSiJ Sugar of milk gr. xv Water . . . fBJ This portion to be given every two hours from 5 a.m. to 11 r.M. Diet from the Fifth Week to the End of the Second Month Milk fSi. fSiJ Cream . . .• f5s3 Sugar of milk gr. xxx Water f5i. fSiJ This portion to be given every two hours. Diet during the Third Month Milk fSiiss Cream f5ss Sugar of Milk 3J Water fSi This portion to be given every two and one-half hours. Diet during the Fourth and Fifth Months Milk fSiiiss Cream fSss Sugar of milk 3J Water fSJ This portion to be given every three hours. Diet during the Six'h Month Milk fSivss Cream f5ss Sugar of milk 3J Water f§i Tliis portion to be given four times daily. Two other meals — morning and mid-day — may be as follows: Milk fgivss Cream fSss Mellin's Food 3J Hot water . . . ' fSJ Dissolve the Mellin's Food in the hot water, and add, with stirring, to the previously mixed milk and cream. In the seventh month the Mellin's Food may be increased to two teaspoonfiils and given three times daily. Throughout the eighth and ninth months five meals a day will be sufficient— at 7 and 10.30 a.m., 2, 6, and 10 p.m. Milk f5viss Cream fBss Sugar of milk 3J Water fSJ This portion for the first and last meals. For the other three meals 1 tablespoonfiil of Mellin's Food may be added, or 1 teaspoonful of "flour-ball" may be given twice daily instead of the Mellin's Food — say at the second and fourth meals. PATHOLOGICAL FIRST DENTITION 201 Diet for the Tenth and Etecenth Monthi First meal, 7 a.m.: Milk fSviiiss Cream fjss Mellin's Food 5ss (Or "flour ball" or barley jelly S'j) Water fSj To be used only when Mellin's Food is employed. Second meal, 10.30 a.m.: Eight ounces of warm milk. Third meal, 2 P.M.: The yolk of an egg lightly boiled with stale bread crumbs. Fourth meal, 6 p.m. : Same as first. Fifth meal, 10 p.m.: Same as second. On alternate days the third meal may consist of 1 teacupful (f5 vj) of beef tea containing a few stale bread crumbs. Beef tea for an infant is made in the following way : One-half pound of fresh rump steak, free from fat, is cut into small pieces, and put with 1 pint of cold water into a covered tin saucepan. This must stand by the side of the fire for four hours, then be allow^ed to simmer gently (never boil) for two hours, and, finally, ]be thoroughly skimmed to remove all grease. A further variation can be made by occasionally using mutton, chicken, or veal broths instead of beef tea. Diet from the Tivelfth to the Eighteenth Month {Five Meals a Day) First meal, 7 a.m. : A slice of stale bread broken and soaked in a breakfastcupful (fSviij) of new milk. Second meal, 10 a.m.: A teacupful of milk (f5vj) with a soda biscuit or thin slice of buttered bread. Third meal, 2 p.m.: A teacupful of beef tea (f5vj) with a slice of bread, 1 good tablespoonful of rice, and milk pudding. Fourth meal, 6 p.m. : Same as first. Fifth meal, 10 p.m.: One tablespoonful of Mellin's Food with 1 breakfastcupful of milk. To alternate with this: First meal, 7 a.m. : The yolk of one egg slightly boiled with bread crumbs; 1 teacupful of new milk. Second meal, 10 a.m.: A teacupful of milk with" a thin slice of buttered bread. Third meal, 2 p.m.: A mashed boiled potato moistened with 4 tablespoonfuls of beef tea; 2 good tablespoonfuls of junket. Fourth meal, 6 p.m.: A breakfastcupful of new milk with a slice of bread broken up and soaked in it. 202 DENTITION Fifth meal, 10 p.m. : Same as second. The fifth meal is often unnecessary, and sleep should not be dis- turbed for it. At the same time, should the child awake an hour or more before the first meal time, he should break his fast upon a cup of warm milk, and not be allowed to go hungry until the set breakfast hour. Diet from Eighteen Months to the End of Two and One-half Years {Four Meals a Day) First meal, 7 a.m.: A breakfastcupful of new milk; the yolk of one egg lightly boiled; two thin slices of bread and butter. Second meal, 11 a.m.: A teacupful of milk with soda biscuit. Third meal, 2 p.m.: A breakfastcupful of beef tea, mutton or chicken broth, a thin slice of stale bread, a saucer of rice, and milk pudding. Fourth meal, 6.30 p.m.: A breakfastcupful of milk with bread and butter. On alternate days: First meal, 7 a.m. : Two tablespoonfuls of thoroughly cooked oat- meal or wheaten grits, with sugar and cream; 1 teacupful of new milk. Second meal, 11 a.m. : A teacupful of milk with a slice of bread and butter. Third meal, 2 p.m.: One tablespoonful of underdone mutton pounded to a paste; bread and butter, or a mashed potato moistened with good plain dish gravy; a saucer of junket. Fourth meal, 6.30 p.m.: A breakfastcupful of milk, a slice of soft milk toast, or a slice or two of bread and butter. The foregoing schedule must, of course, be regarded as an average. Many children can bear nothing but milk food up to the age of two or even three years, and provided enough be taken, no fear for their nutrition need be entertained. The rule to adopt is, if a child be thriving on milk it is never to be forced to take additional food merely because a certain age has been reached. Let the healthy appetite be the guide. The following is recommended by Starr as a modified milk diet, and as a substitute for mother's milk while weaning: Pasteurized cream f5ss Pasteurized milk fgiisa Sugar of milk 3s3 Water, boiled fSJ Should this not satisfy the infant, increase the ingredients (except cream) to 6, 8, or 12 ounces. PATHOLOGICAL FIRST DENTITION 203 Hare^ recommends the following diet list followed in his hospital practice : Diet for a Child Aged Two Years Breakfast, 7.30 a.m.: Milk. The lightly boiled yolk of an egg; thin bread and butter (the bread to be one day old) . Lunch, 11 A.M.: Milk. A thin slice of bread and butter. Dinner, 1.30 p.m.: Beef tea or small piece of minced roast beef or mutton devoid of gristle. One well-mashed potato moistened with gravy. Rice and milk. Supper, 6 P.M.: Milk. Bread and butter. For drink: Boiled or filtered water. Diet for a Child Aged One Year (Five Meals a Day) First meal, 7 a.m.: 2 teaspoonfuls of grated flour-ball (prepared as directed below) in f pint of milk. Second meal, 10.30 a.m.: ^ pint of milk with 4 tablespoonfuls of lime water. Third meal, 2 p.m. : The yolk of one egg beaten up in 1 teacupful of milk. Fourth meal, 5.30 p.m. : Same as the first. Fifth meal, 11 p.m.: Same as the second. Flour-ball is to be made by taking one pound of good flour — - unbolted, if possible — tie it up very tightly in a pudding-bag; put it in a pot of boiling water early in the morning, and let it boil until bedtime, then take it out and let it dry. In the morning peel off the surface and throw away the thin rind of dough, and with a grater grate down the hard, dry mass into a powder. To use this, take from 1 to 2 teaspoonfuls of the powder, rub it down until smooth with a tablespoonful of cold milk, and add 1 tumblerful of hot milk, stirring it well all the time. Diet for a Child Aged from Six to Twelve Months (Five Meals a Day) First meal, 7 a.m.: Mellin's Food, 1 tablespoonful; or flour-ball grated, 1 or 2 teaspoonfuls (prepared as directed above) ; hot water, 4 tablespoonfuls; warm milk, enough to make ^ pint. Dissolve the Mellin's Food or rub down the grated flour-ball in the hot water by stirring, then add the milk; mix thoroughly. ' Practical Therapeutics. 204 DENTITION Second meal, 10.30 a.m., and third meal, 2 p.m.: A breakfastcup- ful of milk with 4 tablespoonfuls of lime water. Fourth meal, 5.30 p.m. : Same as first. Fifth meal, 10.30 p.m.: Same as second. Treatment of Nervous Conditions. — If nervous reflexes, great irritability, or cerebral congestion appear, attention should be directed to the condition of the bowels and the teeth. If constipation or diarrhea exist, a cathartic is given and the gums are lanced. A cerebral sedative is to be prescribed. I^ — Chloralis hydratis gr. ij Sodii bromidi gr. v Aquffi menthse piperitae . fSiJ — M. Sig. — Per orem. One dose; enlarge formula for repetition as needed. If convulsions be threatened, the clothing should be loosened and cool applications made to the head. If the child be in convulsions, it should be immersed to the waist in water as hot as can be borne, to which has been added 2 table- spoonfuls of common mustard flour, and cool water poured over its head, when, as a rule, the symptoms promptly subside. Chloroform, which children endure well, may be administered. After immersion a rectal injection of 1 dram of glycerin or a glycerin suppository will usually cause a free stool. A cerebral sedative should be administered. I^ — Chloralis hydratis gr. ij Sodii bromidi gr. v Starch paste Sij — M. Sig. — To be adtoinistered per rectum. (Atkinson.) It is well also to administer a cathartic to unload the intestines of irritating substances possibly present. After sleep, if appearances indicating dental irritation be observed, gum lancing is practised. It is wise that this operation be thus deferred, as convulsions may be precipitated by the act of lancing when the nervous system of the child is overexcited. The removal of intestinal irritants by a cathartic given iper orem is also in order before lancing. It has been repeatedly noted that when evidence of marked cerebrospinal irritation is present, for which no probable source can be assigned, and an examination of the gums shows no apparent local disturbance, yet if it be at a period when one or more teeth are in process of eruption, but are still covered or bound down by gum tissue, if gum lancing be practised relief is immediate and the lancing may even avert a threatened attack of eclampsia. It is presumed that PATHOLOGICAL FIRST DENTITION 205 these are cases of pulp irritation in which a faihire of resorption of tissue in advance of the tooth crown has caused pressure upon the pulp forming the root end. Constitutional States Modifying Dentition Children who are the victims of hereditary syphilis usually cut their teeth very early, the alveolar process being in many cases insufficient. Cases are recorded where children have been born with crowns of teeth visible upon the gum, there being no evidence of root formation, the crowns being loosely held to the gum by fibrous tissue. It is necessary to remo^-e these loose crowns to permit the infant to suckle. Children aft'ected with rachitis have the process of eruption much delayed. It is seen, therefore, that the presence of loose crowns of teeth is a condition pointing to, though by no means diagnostic of, hereditary syphilis. Long-delayed eruption of teeth should prompt a search for further indications of rachitis. Particu- larly in children in whom a history of hereditary syphilis is obtainable the process of dentition may be accompanied by rapid and frequently widespread breaking down of the soft tissues over and about erupting teeth. Local measures of treatment seem to be of but little avail, except that antiseptic treatment undoubtedly prevents complications from extraneous infection. In children classified indefinitely as strumous, which may mean the children of syphilitic or tuberculous parents, or those with no such history whose surroundings are of the most unhygienic kind, the process of dentition may not only have an untoward course, but phagedenic ulcerations may occur. It is usually in the degree of a child's debility, either inherited or acquired through improper care, that dentition assumes morbid features. The treatment of such cases must be directed to raising the health standard. As local therapeusis, no measures seem more effective than the sprays of hydrogen dioxid first; next, potassium chlorate, and, if conditions indicate it, sprays of dilute listerine, which is stimulant, antiseptic, and slightly astringent. Infantile Scurvy. — Cases are reported in which the improper feeding of children has been followed by evidences of scorbutus. It occurs usually in bottle-fed babies confined to patent foods, the nutritive element being lacking. The gums become tumid, and hemorrhagic extravasations occur in their substance; the periosteum is stripped from the margins of the alveolar walls, the soft tissues hanging in discolored, pendulous masses about and beyond the teeth if any be erupted. 206 DENTITION The child is peevish, listless, and feeble. There is apparent pain in the limbs.^ The urine may be bloody even as a first sign. The treatment is largely systemic, and consists of using fresh cow's milk modified to conform to human milk, and in the administration of fresh lemon juice, preferably boiled, allowed to settle, and the supernatant fluid used,^ or orange juice is also used. The mouth should be sprayed with sedative antiseptics, such as potassium chlorate in hydrogen dioxid (p. 197). THE SECOND DENTITION By reference to Fig. 110 it will be seen that at six and one-half years of age the twenty temporary teeth are still all in position, and that taking their places in the line of the arch are the four permanent first molars, the roots of which are still incomplete. These molars do not replace any temporary teeth, but during the "change" support the jaws with the assistance of the temporary molars until the permanent incisors are fully erupted, and with the aid of the incisors until the bicuspids come into occlusion. Their office as jaw props and organs of mastication during the change is, therefore, very important. Of their later function more will be said farther on. At six and one-half years the crowns of the permanent incisors lie in the relations shown with the temporary central roots resorbed and the lateral root partly so. Their crowns are practically complete, but the roots are unformed. The cuspid crown in its crypt lies well above and lingual to the unresorbed temporary cuspid root. The roots of the first and second temporary molars, a trifle resorbed upon the inner side, embrace the formed crowns of the first and second bicuspids. In their crypts back of the first molars lie the forming crowns of the second permanent molars. The third molars are not in evidence in the illustration, but their development is in progress. It will be seen that the permanent central and lateral incisors replace the temporary central and lateral incisors, the permanent cuspid the temporary cuspid, and the first and second bicuspids the first and second temporary molars respectively. From this age to adult age as previously the jaw undergoes constant change, enlarges by constant resorptions and depositions of bone, and changes its contour to conform to the changes occurring throughout 1 Hare. = Ibid. THE SECOND DENTITION 207 the body, and to accommodate the permanent teeth, which are in general terms larger and more numerous than the temporary teeth. It may be said that the alveolar process built about the roots of temporary teeth and the roots of the temporary teeth are all resorbed during the replacement of the latter, and that when the crowns of the permanent teeth are fully erupted new alveolar process is built up about their roots. Any subsequent change in the position of the permanent teeth is accompanied by an alteration in the alveolar pro- cess, and after extraction the latter is resorbed, but upon an implan- tation (which see) being done new process will form. Its dependence upon the teeth is, therefore, evident. The following table gives the approximate ages for the eruption of the permanent teeth: First molars 5H to 7 years Central incisors 7 to 8 years Lateral incisors ' 8 to 9 years First bicuspids 10 to 11 years Second bicuspids 11 to 12 years Cuspids, the lower usually preceding by a year or more . . .12 to 14 years Second molars 14 to 15 years Third molars 16 to 20 years and indefinitely beyond The Process of Resorption of the Temporary Roots. — After com- pletion of formation the roots of the temporary teeth remain in this state but a short time, as their successors are ready to advance to their places. Comparing the ages at which resorption begins with the ages at which it is complete (eruption of permanent teeth) (see Fig. 141), it will be noted that approximately three and one-half years are required in all cases for the removal of the temporary roots. Therefore, to determine the age at which absorption begins deduct three and one- half years from the date of eruption of the corresponding permanent tooth. The degree of resorption at any age is shown in the table. At the time the permanent tooth begins its advance it lies in a bony crypt above and lingual to its predecessor, except in the case of the bicuspids, which lie between the roots of the temporary molars (Fig. 110). Each cr;y^t has its own follicle wall enclosing a permanent tooth crown. In the follicular wall overlying the crown appear large multinu- cleated cells the origin of which is unknown, but which by some are thought to be transformed osteoblasts, by others leukocytes (Figs. 142 and 143). The latter is the probable explanation, as analogous cells are found about tissues or foreign bodies about to undergo 208 DENTITION resorption anywhere in the body. (See Resorption.) In the par- ticular situation under consideration they are called odontoclasts. The tissue between the root and crown has by Tomes been given Fig. 141 I ^A h\ lA '!ii "14 livi f'l f\h\ Decalcification of the'deciduous teeth. The numbers indicate years. (Peirce.) Fig. 142 Showing the relations of an erupt- ing permanent tooth to its deciduous predecessor. A, A, A, odontoclasts in absorbent organ. The structure of the absorbent organ, showing multinucleated or giant cells (odontoclasts). (Tomes.) Fig. 144 Jk L^ Imprisonment of second temporary molar; re- sorption of its roots, with absence of second bicuspid. (Skiagraph by Custer.) the name of the "absorbent organ" (Figs. 142 A, and 143). These giant cells have a solvent or digestive function not understood, but which is competent to remove both the organic and inorganic matter THE SECOND DENTITION 209 of cementum and dentin, and evidences of action upon enamel in other situations are not wanting. (See Resorption of Enamel.) That the solvent is acid is shown by the evidence of decalcification about the area of resorbed enamel of unerupted crowns of some permanent teeth. It is a curious fact that no evidence of decalci- fication of the permanent crown has been demonstrated to result from the proximity of the multinucleated cells in cases of physio- logical resorption of roots. In all probability the enamel is pro- tected by the presence of Xasmyth's membrane, which is resistant to acids. These cells are probably invited by irritation due to pressure of the advancing permanent tooth crown, as the resorption is almost always found at the point of approximation of the crown with the root, or, in other words, at the pressure point (Fig. 145). Fig. 145 Phases of resorption of temporary roots. (Skiagraph by Price.') Diagram illustrating the relation of a resorbed tempo- rary root and the permanent tooth, also the involvement of the pulp as a part of the re- sorbent organ. Resorption of the interior of crown of a temporary tooth. Cases of resorption of temporary roots without the presence of a permanent crown are, however, noted and explained by Tomes upon the ground that resorption is a vital act independent of the pressure exerted (Fig. 144). As resorption of permanent roots, however, has often occurred from pressure of the crown of another tooth and occurs at the pressure point in physiological resorption, localized irritation, even in the absence of a permanent crown, must be credited with a large influence in the process. It is to be remem- bered also that in the absence of the pressure resorption often does not occur, at least for twenty-five or more years — e. y., when laterals 1 Items of Interest, 1901. 14 210 DENTITION are absent and the permanent cuspids erupt to the side of the deciduous cuspids (Fig. 148). According to Tomes, redeposition of cementum occurs in pre- viously resorbed areas upon temporary roots, a fact corresponding with effects noted in permanent roots. Teeth frequently erupt lingually or labially to their corresponding temporary teeth, both remaining in the mouth. It is almost invari- ably the rule upon extraction to find that an oblique resorption has occurred, as is shown in the right upper skiagraph in Fig. 145, and generally a decided hypervascularity is seen in the pulp extending upward for perhaps a quarter of an inch. Doskow^ has shown by the prompt loss, by absorption, of a fairly firm deciduous cuspid crowned to bring it up to level and so to usefulness, that such an operation is inadvisable because of an inher- ent tendency of an absorbent organ to become established. Again, a permanent tooth undergoing resorption often remains firm until suddenly the strain becomes too great. As the root of the temporary tooth disappears the pulp continu- ousiy fuses with the absorbent organ, so that when the crown alone remains the pulp is still vital (Figs. 142 and 146). At times it seems to take up the resorbent function and resorbs the crown dentin in some cases almost entirely. In one specimen a circumscribed portion of the cementum and of enamel were removed by it at the point of junction. This constituted practically a case of perforation by resorption (Fig. 146). The tooth was at first thought to be suffused with hemoglobin, as it was of a pink color. After extraction the absorbent organ was found as a papilla attached to the gum. At times bay-like excavations in the crown dentin occur (Fig. 183, D). When the root resorption reaches the point shown in the central incisor in Fig. 110 the temporary tooth is loosened, moves about, and annoys the child, who may pick it out, or it is removed by extraction. Formation of the Roots of Permanent Teeth. — The extent of root development at any age is of great importance in view of canal thera- peutics. Incomplete roots present a mechanical difficulty of sealing the apex of the canal. The size of the pulp at the apical foramen of such teeth contraindicates the use of arsenic, and even pressure anesthesia is often unsuccessfully applied. The roots are developed in precisely the same manner as in the case of the temporary teeth, by the combined deposition of cementum by the osteogenetic cells of the follicular wall, which is drawn up on the root as a pericementum, and by the odontoblasts of the papilla, which is drawn up as a pulp (Fig. 105). 1 Dental Cosmos, 1907. THE SECOND DENTITION 211 The extent of development of any of the permanent teeth may be seen at a glance by reference to the valuable table of Peirce (Fig. 111). Fig. 147 Absence of upper left lateral incisor, with permanent cuspid in its place; two temporary cuspids retained. Man, aged twenty-five years. Fig. 148 Absence of upper lateral incisors and right bicuspid. Retention of temporary cuspids. From an adult. So graphically does this table give the desired information that explanation becomes unnecessary. 212 DENTITION Irregularities of Second Dentition. — Some temporary teeth may be retained long after adult age is reached. The teeth most subject to this are the cuspids and second temporary molars. In the case of the cuspids the permanent cuspid is delayed or takes an unusual direction, erupting lingually or labially, or at times being directed into the place normally occupied by the lateral incisors, which are wanting, or very rarely the cuspid erupts pos- teriorly to the first bicuspid. At about forty years of age the tem- porary cuspids may b.e lost by resorption of their roots, but until such time should be retained if usefully filling a space. If in inter- ference with proper alignment or eruption of the permanent cuspid they should be extracted. Tlieir late resorption is somewhat patho- logical in character, and probably due to or incited by a partial resorption of the root end during the descent of the permanent cuspid. The late enforced loss of the temporary cuspid indicates the advisability of an implantation operation (Fig. 148). The molars are retained, as a rule, because of an absence of per- manent crowns to cause resorption, although this may occur without such pressure (Fig. 144). I have ^'° 1*^ seen a case of an adult lady with eight deciduous molars in place. The question of the abnormal de- velopment or absence of perma- nent germs, or of the state of the rojts of the temporary tooth may be settled by the ^--rays (Figs. 145 and 149). The question of extraction or Retained temporary molar with bi- retention dcpcuds UpOU the diag- cuspid present. (Skiagraph by E. . f " Ballard Lodge.) nosis. A farm temporary tooth should never be extracted simply to allow a permanent tooth to erupt unless the presence of a permanent tooth in the jaw, as determined by skiagraph or other means, gives reasonable inference that the permanent tooth is held back by the temporary tooth. In most cases a reasonable delay is advisable. A patient of the editor wore a plate for thirteen years because of the injudicious extraction of an upper temporary cuspid, the permanent tooth appearing at twenty-six years of age. \\Tien the retention of temporary molars and cuspids occurs, they are apt to occupy an occlusal level lower than that of the permanent teeth (Fig. 144). They may not be in occlusion at all, as was the case with the eight molars just referred to. This proves the fact THE SECOND DENTITION 213 that the general occlusal k'\el of the permanent teeth is farther from the margin of the alveolar process than in the case of the temporary teeth. The length of the permanent crowns accounts for this. In normal replacement, howe\"er, the occlusal le\"el is ncarl\ the same for the temporary molars and first permanent molar, at least until the change is made by the eruption of the bicuspid. The correct placement of these first permanent molars seems to determine the correctness of molar occlusion, at least in the mesio- distal relation, though they may not occupy their correct bucco- lingual positions. Any slight forces disturbing the mesiodistal relation causing the upper first molar to drift anterior to its correct occlusion with the lower molar will result in an abnormal relation of the teeth to those anterior to them and to their antagonists; either upper protrusion or upj)er irregularities will occur. Fig. 150 Fig. IT)! Retained loner temporary molars, bicuspid absent. (Skiagraph by E. Ballard Lodge.) Delayed cuspid. (Skiagraph by E. Hallard Lodge.) If the reverse occur and the lower molar be placed anteriorly and the upper be placed normally or posterior to its normal position, prognathism of the lower teeth ordinarily results. If placed too far posteriorly, retrusion of the lower teeth will occur. According to Angle, the misplacement of the permanent teeth erupting early causes their inclined planes to direct other teeth from normal occlusion, or by permitting contraction of the space normally occupied, particularly in the lower jaw, permits the other teeth to assume a position in a contracted arch, thus again causing their inclined planes to cause contraction in the opposite arch, with a consequent displacement buccolingually of teeth which would other- wise normally align themselves in the arch. Once established, the cheek and lip pressure maintains the inharmony (Fig. 157). Angle divides all irregularities into three classes, with divisions and subdivisions: 214 DENTITION Fig. 152 Typical occlusion. (Cryer.) Fig. 153 Malocclusion. Class I. (Angle.) THE SECOND DENTITION 215 Class I. — The first molars are correctly occluded mesiodistally, the teeth anterior being in malocclusion, though the biscuspids may be in correct mesiodistal relation. The general characteristic of the class is that shown in Fig. 153. Class II.— The lower first molars occlude distally to the upper first molars, causing retrusion of the lower jaw. Division I is char- acterized by distal occlusion on both sides, the upper arch is narrowed, the upper incisors lengthened and protruded. The upper lip is short and functionless, while the lower lip is thickened and rests cushion- FiG. 154 Malocclusion. Class II. (Angle.) like between the upper and lower incisors, increasing the protrusion of the upper and the retrusion of the lower. There is usually mouth breathing, due to some form of nasal obstruction. Division I. — The characteristic exists on one side only, the other being normal. Mouth breathing is usually associated (Fig. 154). Division 11.^ — There is distal occlusion on both sides, but the upper incisors are retruded instead of protruded, with crowding in the cuspid region. These are associated with normal breathing (Fig. 155). 216 DENTITION Subdivision, Division II. — The characteristic is upoti one side only, normal breathers. Fig. 155 Malocclusion. Class II. Division II. (Angle.) Class III. Division I. — In this class the lower first molars occlude mesially to the upper first molars on both sides, and the lower jaw progressively protrudes anteriorly (Fig. 156). Subdivision, Class III, — The mesial occlusion is upon one side only, the other being normal, the arches crossing in the region of the incisors. Angle has formulated the law "that the best balance, the best harmony, the best proportions of the mouth in its relations to the other features require that there shall be the full complement of teeth, and that each tooth shall be made to occupy its normal occlusional relations. He also states that the best development of THE SECOND DENTITION 217 the bones of the face and throat, the size and function of its ca\ ities is dependent upon the position of the teeth. These specific causes inducing malocckision of tiic teeth as classi- fied above are: 1. Premature loss of deciduous teeth prevents the pressure of the first molars upon the teeth anterior to them, which mechanically aids in the de\elopment of the jaws and thus of the space necessary for accommodation of the permanent teeth. It also allows the first molar to drift forward and come into malocclusion, and also to close the space occupied by the deciduous tooth, thus lessening space for its successor and forcing it into buccal or lingual displacement. The same is true of loss of approximal tooth contact as the result of caries (Fig. 157). Fig. 156 Malocclusion. Class III. (.\ngle.) 2. Prolonged retention of deciduous teeth may cause a deflection of the temporary successor or prevent its eruption. 3. Through loss of permanent teeth on that side upon which the tooth is extracted, the development of the jaw will be prevented and the tooth posterior to the space will tend to tip or drift forward into malocclusion. 4. Tardy eruption of permanent teeth permits closure of the space altogether or in part, and the resistance offered causes a deflec- tion of the tardy tooth (Fig. 157). The total absence of certain permanent teeth may be placed under this heading. 5. Supernumerary teeth, by occupying space, also compel the normal teeth to take an abnormal position, and, if erupting after them, may displace them by constant pressure (Figs. 207 and 235). 218 DENTITION Fig. 157 6. Habits such as thumb and hp sucking or Hp biting will move the upper anterior teeth outward and the lower anterior teeth inward. Holding the tongue between the anterior teeth produces infra- occlusion of the anterior teeth, while the con- stantly open mouth permits supra-ocelusion of the molars. 7. Nasal obstructions occurring in the de- veloping child produce mouth breathing, and the opening of the mouth causes contraction of the muscles upon the teeth and bones, pro- ducing abnormalities of the bone of the jaw, the irregularity of Class II (Division I), an undeveloped nose and adjacent region of the face. Faught has ably illustrated these condi- tions in Figs. 158 to 165.^ The consideration of malocclusion as a general subject is properly relegated to special works, and the reader is referred to Angle's Malocclusion of the Teeth and other works on the subject. Effects of the premature loss of a deciduous second molar. Fig. 158 A B Case of adenoids. A, before operation; B, after operation. (Faught.) Disorders of the Second Dentition. — The devitalization of the pulp of a temporary tooth and proper canal filling delays, but does not absolutely prevent, resorption. Chronic abscesses upon such roots destroy the absorbent organ, but some pathological resorption may occur, as in case of permanent roots (which see). Pus has an alkaline 1 Dental Cosmos, 1908, p. 7. THE SECOND DENTITION 219 reaction which may neutralize the acid solvent. As a rule, such roots are mechanical obstructions to the permanent crowns, which are Fig. 159 Fig. 160 Diagrammatic sagittal section, .showing relation of anatomical landmarks. (Faught.) Adenoid vegetations. Compare Fig. 159. (Faught.) Fig. 161 Diagrammatic coronal section through Jiead in the region of the first molar, .showing nasal septum, uncinate process, inferior meatus, inferior turbinals, middle ethmoidal cells, middle turbinates, and hiatus semilunaris. (Faught.) deflected to one side and caused to erupt irregularly; again, the temporary root may be bodily pushed aside, its apex pressed against the alveolar process and gum tissue, which are resorbed, and the 220 DENTITION necrotic root end is seen extruded through the gum. Extraction is indicated. When temporary roots are not thus mechanically removed they are gradually extruded and decayed, or suppurative processes cause the resorption of the alveolar process about them. Fig. 162 Hypertrophy of right inferior turbinal, also deflected septum and spur. Compare Fig. 161. (Faught.) Fig. 163 Cystic middle turbinal, hypertrophied inferior turbinals, enlarged middle ethmoidal cells, and hypertrophied middle turbinal. Compare Fig. 161. (Faught.) Injudicious retention of temporary teeth may thus cause an irregu- larity. On the other hand, premature extraction by permitting the approximation of the previously erupted permanent teeth may have an equally bad effect upon an erupting tooth (Fig. 157). In anticipation of physiological resorption of temporary roots, all THE SECOXD DENTITION 221 temporary teeth should be carefully watched, cleansed, filled, and, if necessary, their roots treated so that a normal replacement by the Fig. 164 Fig. 165 Hypertrophied posterior end of inferior turbinal. Nasal polypi. Compare Fig. 159. Compare Fig. 159. (Faught.) (Faught.) Fig. 166 Right. Left. Labial aspect of bilateral sequestra apparently due to typhoid fever alone. (Cowper.) permanent teeth may occur. If pronounced di.seasej[occur just previous to the time for normal replacement, extraction is indicated. It will be recalled that the teeth are an evolution of the dermoid system, which fact possesses pathological significance in certain acute specific skin diseases. It is noted in some cases of the eruptive 222 DENTITION fevers of children, particularly when the child is much debilitated, that after the cessation of the acute disease a necrotic affection of the jaw occurs, involving the alveolar bone and its contents. As many of these cases occur between the ages of three and seven years, the temporary teeth are still in situ; these, with the partially devel- oped permanent teeth and the enclosing bone, may be exfoliated. The necrotic process may involve but one tooth, or may include all of the temporary teeth, their successors, and a large mass of bone.^ The disease with which this necrosis is most frequently associated is scarlet fever ;2 it is also found as a sequel of measles and smallpox. "The cases prior to exfoliation of the bone exhibit a stripping of the periosteum, apparently beginning about the necks of the teeth. A discharge of pus having a fetid odor is present, and the soft tissues may be raised from the bone for a variable extent;" that is, there is evidence of purulent periostitis. In the course of some weeks, six or eight, the necrotic bone and its contents exfoliate. Salter observes that the sequestra forming after severe scarlet fever are much more extensive than those which form as a sequel of measles. An interesting case of bilateral sequestra of the aveolar process due to typhoid fever alone is reported by Cowper.^ Two sound teeth were involved in each sequestrum. The administration to children of mercurials has caused such a loss of teeth and process. I have seen a sequestrum containing three undecayed teeth attributed to this cause, and others have been reported. In these cases the parts should be kept as aseptic as possible by means of hydrogen dioxid and the compound tincture of capsicum and myrrh (enough to cloud a glass of water) used as a stimulant mouth wash.^ When loose, the sequestrum should be removed. The parts heal by granulation if due attention be paid to the general physical welfare of the child. Eruption of the Molars. — The first permanent molars rarely produce more than slight rheumatic pains. The gum irritation may be relieved by an X-incision, or at times by the application of phenol-sodique and laudanum, equal parts, or phenol camphor, with the finger tip. A little alcohol or dilute tincture of iodin serves almost equally well. As some time may elapse between eruption and occlusion, the first molars do not receive a proper friction. Associated frequently with carious temporary teeth, they are frequently decayed in their sulci and fissures; to prevent this it has been recommended that oxy- 1 Salter: Dental Pathology. = Ibid. ' Dental Cosmos, 1909, p. 765. * Garretson: A System of Oral Surgery. THE SECOND DENTITION 223 phosphate of zinc be placed over these fissures without previous excavation.^ The lower second molars may cause some irritation owing to an insufficient development of the jaw at the angle, leaving an inade- quate accommodation for the crown. At about nine years of age the second molar occupies the angle of the jaw in much the same position as shown in Fig. 106 for the third molar. If held back a pathological condition equivalent to that occurring in the temporary teeth may result; reflexes producing heavy pains about the jaw or reflex effects, such as chorea, may be produced. Truman^ has prevented a threatened second attack of this sort by deep incisions in the gum over the site of the crown. The presump- tion is that such treatment relieves the tension upon the pulp under- lying the developing root. Kirk^ calls attention to the liability of chorea to be associated with reflexes from the dental region at from four to nine years of age, and cites a case from the practice of C. N. Peirce in which choreic mani- festations were permanently relieved by the removal of a deciduous molar interfering with the eruption of its permanent successor, the bicuspid. He also cites a case of repeated hysterical manifestations following nervous irritability due to each replacement of a deciduous tooth by its successor. Flagg cured a case of chorea in a boy, by the extraction of four teeth from a very crowded arch.^ The third molars frequently induce pathological conditions. The upper third molar, meeting in its descent the roots of the second molar, may be united to it by hypercementosis — the condition of concrescence (which see) ; escaping this, it may meet a dense palato- alveolar plate of bone at the tuberosity and be deflected buccally through the thinner buccal plate of bone, so that its occlusal face presents cheekward (Fig. 167). Its occlusal face may present more posteriorly or more anteriorly. Here retained food collects about it and caries occurs, or a suppurative inflammation of the cheek or free gum margin may occur. For this condition sterilization, free incision of the gum margin, and subsequent asepsis maintained by antiseptic sprays will reduce the inflammation, which, however, is apt to recur at intervals. If the cheek be irritated or the position of the tooth permanently fixed, only traction of the tooth into a correct position, grinding away of the sharp cusps, or extraction will alle- viate the condition. The extraction of such a tooth is little loss to the individual. A bit of cotton saturated with a mild antiseptic may be placed between the tooth and cheek for a time after grinding. ' L. Ashley Faught. ^ International Dental Journal, 1899. ' Dental Cosmos, 1905. * Private communication. 224 DENTITION The possibility of concrescence in such a case, as shown in Fig. 167, must be considered when extraction is intended. Individual motion is diagnostic of separate teeth, and is readily induced, when the crowns are together, by pressing a strong, thin, flat-bladed instru- ment between the teeth and turning it. • Fig. 167 Fig. 168 Abnormal eruption of the upper third Partial eruption and impaction of third molar. molar. (Skiagraph by Custer.) The pressure of an erupting third molar upon the second molar may cause neuralgic pains, and at times the teeth in general, as far forward as the central incisor, may seem to loosen up and become tender to touch and again become comfortable and tight. These symptoms may be repeated apparently in consonance with the efforts at eruption. This pressure also causes irregularities of alignment or breaks up an orthodontia. Their extraction for this reason is sometimes indicated. Owing to insufficient development at the angle of the jaw, it is almost the rule that the eruption of the lower third molar is attended with some degree of discomfort due to gum and bone irritation, and, possibly, to pressure on the formative pulp (Fig. 106). For some months prior to eruption, heavy, gnawing, rheumatic pains may be indefinitely located about the jaw and ear of the affected side. The muscles of mastication become stiff and may contract spasmodically, simulating trismus. These symptoms, if severe, may be relieved by deep X-incisions in the gum; or, if mild, by the application of non-discoloring rubefacients or sedatives to the outside of the face, over the affected parts. The massage of the parts affords some relief. Flagg recommended the following: I^ — Tinot. opii, Tinct. aconiti, Chloroformi p. seq. — M. Sig. — To be rubbed on the outside of the face. Or, ^. — Aconitinse gr. j Cerati simplicis 5j — M. Sig. — To be well spatulated. To be distended with oil of cloves or camphophenique and gently rubbed on the outside of the face, the mouth and eyes to be particularly avoided. THE SECOND DENTITION 225 Or, when the aconitine fails to produce reHef : I^ — Veratrinse gr, xx Cerati simplicis gj — M. Sig. — To be used in the same manner as the aconitine. As the tooth advances the symptoms may become progressively severe. The gum may become inflamed, swollen, and be masticated upon, the oral pyogenic organisms produce infection, presumably finding an entrance at the point proximating the second molar. The patient suffers from the pain and inability to masticate and swallow, and becomes nervous, irritable, and debilitated; the breath becomes fetid and the salivation excessive. The inflammation extends into the contiguous tissues, and pus may form, extending into them; swelling may occur in the adjacent gland, parotid, submaxillary, etc. It may also extend to the tonsil or pharynx. All mastication is pre- vented, fever is present, and the patient prostrated; septicemia and death may follow.^ Reflex pains may occur. Brown^ relates a case of noma which developed from an infection in this location. The gangrenous condition extended to the lungs. Death ensued. Results similar to these may occur when the crown is partly erupted, being covered at its distal portion by a curtain of gum which may be ulcerated upon its under surface. This curtain of gum may be thin and stretched or project rather rigidly over the tooth without stretching, as though attached to it. In these latter cases the pus, as a rule, finds egress, but occasionally it burrows into the pocket betw^een the tooth and contiguous tissue, causing much inflammation or pus formation. When gum pockets remain about teeth, food may ferment in them and cause deep pus formations which may result in Ludwig's angina, a frequently fatal disease. (See Ludwig's Angina.) Treatment. — The treatment depends upon the stage to which the inflammation has advanced. If the patient be able to partly open the mouth, the part may be sterilized by spraying it with a germicide such as a 1 to 2000 solution of mercuric chloride in hydrogen dioxid, or hot carbolized water, followed by application of tincture of iodin. (Brown.) Following this an injection of cocain solution is made into the flap of tissue, and the gum completely removed from over the face of the crown, or, if feasible, any pocket wall cut away. To accomplish this a deep linear cut is made with a sharp bistoury extending from the distolingual to the mesolingual angle of the crown. A similar cut is made from the distobuccal to the meso- 1 Flagg. and occasional reports. • 2 Dental Cosmos, 1908, p. 5. 15 226 DENTITION buccal angle. If not already free, the gum is divided at its mesial contact with the distal surface of the second molar. The block is now penetrated by a tenaculum, drawn tense, and the final cut made at the distal border with decidedly curved gum scissors. Less cutting is required in some cases. A special gum-cutting apparatus is obtainable which practically bites out a piece of the gum flap. Gum scissors. The hydrogen dioxid spray should be again applied to remove any possible pus germs present, and should be repeated at intervals of about two hours. A neglect of this simple precaution gave the editor a week of personal discomfort and inability to masticate after the removal of a trifling and apparently non-inflamed flap of gum. A cold compress should be recommended for the angle of the jaw if deemed advisable. Magnesium sulphate as a derivative may be used with advantage. If the patient be confined to his bed and unable to open the jaws, a more diflicult operation presents. The first object should be to reduce the intensity of the inflammatory symptoms. This is accom- plished by the removal of the gum block as above, if the mouth can be opened sufficiently. Etherization may be resorted to, after oral sterilization, for the purpose. A jaw separator is introduced, and operated until sufficient space is gained and the cuts- made. If no more be possible at the first visit, the lingual and buccal linear cuts should be made to insure free bloodletting, which may be increased by syringing forcibly with lukewarm water, the position of the patient being such that gravity favors its flowing out of the mouth.. Cold compresses are to be placed over the angle of the jaw and magnesium sulphate and the hot pediluvium administered as deriva- tives. Cataplasma kaolini, a compound of kaolin (Chinese clay), boric acid, methyl salicylate, glycerin, and small quantities of thymol THE SECOND DENTITION 227 and oil of peppermint/ are useful applied in quantity to the face externally. The antiseptic sprays are to be used as before directed. If, in addition, local massage over the angle of the jaw be practised, the swelling and muscular hardness usually disappear in a few days. It is well to then remove the entire block of gum to prevent re- infection. If the third molar be correctly placed, its eruption, as a rule, proceeds uninterruptedly from this point, though it may never be entirely free from some degree of overlapping by the gum tissue, owing to arrest of eruption by the occlusion of the more advanced upper third molar. Pockets are thus formed which favor food retention, which, undergoing fermentation, may either cause ulcera- tion of the soft parts or caries of the distal and distobuccal surfaces of the tooth. Grinding the occlusal face of the upper molar may assist eruption of the lower. The gum flap should be cocainized and removed by the thermocautery, or if inflamed, be sprayed with hydrogen dioxid and a pellet of cotton saturated with eugenol introduced for a short time. More marked malposition may cause difficulty of eruption, necessitating the extraction of the third molar or even of the second molar. In some cases it may be better to also extract the upper third molar, as it will probably elongate in time and allow food to pack into the interspace mesial to it. A presentation of the occlusal face of the third molar to the distal surface of the second molar is a common form of malposition. If very deep seated the third molar may at times be diagnosticated in this position by passing an explorer or thin right-angled blade down the distal surface of the second molar, or by means of a deep incision with a bistoury or exploring needle. Failing this, or prefer- ably, replacing it, the .r-rays are a Aery valuable means of diagnosis. In this situation pathological resorption of the root of the second molar may result, and irritation of its pulp be added as a compli- cation. In this case the second molar must he extracted. (See Malposition.) A more common form of presentation exhibits the distal surface of the crown above the gum and the meso-occlusal angle locked beneath the cervix of the second molar (Fig. ]()S). Caries is not in- frequently induced by this retention of food. The third molar may be removed by an operation involving the surgical removal of a portion of the base of the coronoid process followed by extraction. The pulp ' Antiphlogistin is the proprietary equivalent. 228 DENTITION of the third molar may be devitalized by arsenic applied and sealed in a pit drilled in its distal surface. After death of a portion of the pulp the pit may be made to perforate the crown from side to side, and then a dentate fissure bur mounted in the right-angle handpiece or a disk may be used to saw off the occlusal half of the crown. In the space thus gained, and between the second and third molars, a wedge of sea-tangle may be neatly fitted; its swelling causes mutual separation, which loosens the third molar somewhat by the process of resorption. It should now be quite readily extracted by appro- priate movements. Cryer recommends the removal of the occlusal section of the crown of the third molar by means of a carborundum disk, and the removal of the tooth by means of forceps or elevators. Extraction in such a case must be carefully done. The use of the elevator is dangerous unless laterally applied as there is danger of fracture of the ramus, which has occurred. (Schamberg.) The loss of a second molar may be for other reasons necessary, but such a loss in the last case described is equivalent to a loss of two teeth, as the third molar will be of little value. CHAPTER VIII MALFORMATIONS AND MALPOSITIONS OF THE TEETH Abnormalities of the teeth are found associated with position, size, form, and structure. Aberrations in form, structure, and size are inchided under the head of malformations of the teeth; aberra- tions of position are discussed under the head of malpositions of the teeth. The particular section of dentistry relating to malpositions of the teeth is by general consent made a special department of operative dentistry, that of orthodontia; but many of the phases of the subject are of great pathological interest, although the thera- peutic measures usually demanded are mechanical in character and clearly belong to the fields of operative and prosthetic dentistry. Malformations of the teeth may be macroscopic or visible to the naked eye, or microscopic, requiring special preparation for obser- vation under the microscope. The causes of imperfectly formed enamel or teeth must be sought by study of the conditions preceding their development. That modi- fications of general nutrition must modify tooth development seems to be a safe proposition. An ill-nourished child is apt to have at least poorly organized tooth material, while in one that has actually undergone an exanthematous disease the tooth form subsequently seen seems frequently to have been profoundly modified by the disease. MICROSCOPIC MALFORMATIONS Microscopic or histological defects of the teeth may affect any of the dental tissues, enamel, dentin, cementum, pulp, or pericementum. Enamel. — Defects in enamel structure range from any degree of orderliness in the even distribution of globular bodies and cementing substance in the tissue to gross aberrations in formation. The finer variations of structure are not easily recognizable. Theoretically perfect enamel should show in longitudinal section a series of squares of uniform size built into rods, the spaces between the squares and rods being marked by lines of cementing substance having a refractive index slightly different from that of the squares 230 MALFORMATIONS AND MALPOSITIONS OF THE TEETH (Fig. 113). While such a structure is perhaps never found, it is difficult to draw a line v/here aberrations from such a standard become pathological. An arbitrary standard might be assumed as follows: Regard any enamel as pathological where areas of it differ from its general substance to such an extent as to have a decidedly different refractive index. A typical form of abnormality is noted in what are known as opaque spots in the enamel, areas in which an opaque surface exists instead of the normally translucent enamel. Fig. 170 Portion of a white spot in enamel, showing lack of interprismatic cement substance. (Williams.) X 2000. Opaque Spots in Enamel. — White, brown, and corn-colored opaque areas of enamel are frequently seen surrounded by apparently normal enamel. Examined without the aid of the microscope they are seen to present a surface as smooth as any enamel, but upon this surface being broken up with a bur a chalky, granular, whitish material con- taining at times the yellowish pigment is seen sometimes occupying MICROSCOPIC MALFORMATIONS 231 the entire thickness of the enamel. These spots, if sHji;ht, are some- times without this granular character, while the pigment affects the entire thickness of the enamel. Williams submitted the enamel at the borders of such spots to microscopic examination, and compared it with enamel in the first stages of decay, finding in both a similar appearance characteristic of a lack of or a loss of interprismatic cement substance (Fig. 170). Section through human cuspid, showing sulcus and appearance of tissue in its vicinity. (Specimen by Choquet, photograph by Wilhanis.) X 75. Upon the data derived from his investigations with the develop- ment of the enamel, he concluded that these spots are due to a lack of such cement substance. This leaves, as the probable substance in the spot, unfused globules mingled with some pigment. H. A. Fynn concludes that as about 87 per cent, of children born and raised in Colorado Springs have defects in enamel, while in other close by localities these are moderately found, the cause must lie in the lack of lime in vegetable matters in that locality and hence in the milk of cows fed upon them. This lack together with the great demand of the developing osseous system for lime causes a deficiency for the relatively non-important teeth. ^ In one case of an adult lady a ' Items of Interest, January, 1910. 232 MALFORMATIONS AND MALPOSITIONS OF THE TEETH broad, brown spot was seen on a lower left lateral. There was a history of the temporary lateral having been knocked out. Enamel formation about the sulci of teeth is frequently faulty; owing to an imperfect union of the enamel segments forming the Fig. 172 *l*^» »;? f ■^M:M %.hk\h\i^ Section of human molar, showing dentinal fibrillse penetrating enamel. X 600. (Williams. i) cusps of the teeth, minute fissures exist in the enamel; these are most marked in the fissures of molars, as shown in Fig. 171. The enamel bounding these fissures has an irregular structure. The dentinal fibrillse may penetrate the substance of the enamel (Figs. 172 and 176), occupying defined channels in its substance; this is regarded by Williams as a developmental accident. He pointed ' For an interesting article illustrating this point see Boedecl Dental Cosmos, 1907. ANOMALIES OF NUMBER 265 —I. e., the occurrence of ca complete third denture. There can be but one conclusion from an examination of all the evidence thus far presented, and that is that no clear and well-authenticated cases are made out. Isolated cases of the appearance of teeth subsequent to the loss of all of the second denture are not infrequent; and, so far as clear records can be obtained, are resolvable into cases of the eruption of supernumerary or impacted teeth, though sometimes a number of teeth are reported erupted. While these cases are, at least for the present, to be held as unproved in connection with elderly persons, a well-authenticated case of multiple dentition in a child is recorded by Catching.^ Between the sixth and seventh month the eruption of one set of teeth was complete; within three months all of these had been lost. Between the eleventh and fifteenth months another period of dentition occurred, the teeth of this second denture being of such faulty structure as to crumble away quickly. At the age of two and one-half years a third dentition appeared, which caused the child such inconvenience that the teeth w^ere extracted by the mother. At the age of eleven years a fourth series erupted, incomplete through the absence of six teeth. At the age of fifteen years these teeth were sound and firm. Fourth Molar. — The molar series of man, particularly in the lower negroid races, may consist of four instead of three members. When the fourth molar appears in the white races it is usually as a stunted member, a conical or peg-like tooth, similar to that which occasion- ally replaces the third molar. There is rarely room posterior to the distal wall of the third molar for their eruption, so that they usually make their appearance in the region shown in the illustration. S. M. Hartman,2 L.D.S., of Victoria, B. C, has furnished the model (Fig. 234) of a case in which the molar form of the fourth tooth is unusually well pronounced. Supernumerary Teeth. — Any teeth in excess of the normal number of teeth belonging to any one class, although clearly cases of rever- sion of type in many instances,^ are included in the category of supernumerary teeth. Supernumerary teeth appear as simple unmodified cones, or as combinations of cones resembling the forms of teeth. The conical form is most common. Cases where these peg-like teeth appear around the third molars, singly or in number, are numerous. Their appearance in any situation is evidence that the normal number of dental cords has been exceeded. They are, perhaps, all to be regarded as cases of long reversion, not alone 1 Southern Dental Journal, October, 1886. ^ Dental Cosmos, 1891. ' A. H. Thompson: American System of Dentistry, vol. iii, and American Text-book of Operative Dentistry. 266 MALFORMATIONS AND MALPOSITIONS OF THE TEETH because they increase the number of the dental series, but because they have primitive forms, a modification of the forms found among the reptiles and fishes. Fig. 234 The fourth molar. (Hartman.) Fig. 235 Two atypical upper supernumerary teeth displacing the incisors. Guilford^ divides supernumerary teeth into those having typical anatomical forms and those having atypical forms. 1 American System of Dentistry, vol. iii. MALPOSITIONS OF THE TEETH 267 Fig. 236 Supernumerary incisors imving typical forms appear in either jaw. In the upper jaw su])ernumerary centrals and laterals both appear, the latter more fretiuently (Fig. 207). Supernumerary teeth may occupy any .position relative to the dental arch, but are more frequently seen at its lingual side. The compound cone occasionally appears (Fig. 236). In addition to molars and incisors, supernumerary bicus- pids are occasionally found (Fig. 237) ; supernumerary cuspids are very rare, but sometimes a brood of them exists, as many as seventeen fairly defined small teeth having been removed from a cyst in the location of the cuspid tooth. ^ Unless supernumerary teeth are a source of offence, either through their position or appearance, they need not be disturbed. If they are found to be so, they may be extracted. Malpositions of the Teeth. — A tooth is said to be in malposition when it is not in normal relation with the dental arch to which it belongs and to its antagonizing teeth of the opposing arch. Teeth The compound cone. Fig. 237 Case of seven lower bicuspids, two supernumeraries in place and one erupting. This patient has two supernumerary upper central incisors displacing the centrals proper, yet closely resembling them. are found in abnormal positions as the result of a variety of causes. Some of these operate prior to, during, or immediately after eruption; ' D. M. Clapp: International Dental Journal, 1900. 268 MALFORMATIONS AND MALPOSITIONS OF THE TEETH some long after the eruption of the teeth, and some because of non- eruption of teeth. (See p. 212.) Malpositions which are remediable through the application of mechanical force, applied by means of suitable apparatus, belong to operative dentistry, as has been stated. They are fully treated of in works upon operative dentistry^ and orthodontia,^ The extraction of teeth after they have been erupted, or of their predecessors, is one of the most frequent causes of acquired mal- position of the remaining teeth. The teeth move from their original positions, the anterior teeth, incisors, laterals, cuspids, and occa- sionally the bicuspids, having a tendency to drift posteriorly, some- times opening a space between the central incisors sufficiently large to create a deformity. The molars have a decided natural tendency to drift forward, and when the bicuspids are ^^^- ^^^ removed they tip anteriorly, causing malocclusion upon their distal cusps and sometimes their disto- buccal cusps' alone, with a further tendency to tip forward and sometimes inward as well. Sepa- ration of the posterior teeth may occur, and in any event the loss of mesial or distal support permits fibrous food to be packed between the teeth ; as they spring slightly apart, it is held by their springing together again. The lack of occlusion brought about by extraction of antago- nists permits elongation, and the loss of posterior Effects of premature support is apt to bring about labial protrusion loss of permanent first i • (> • rm • nt> molars. or abrasiou or upper anterior teeth. Ihis efiect is produced in youth when the first molars are lost before the bicuspids are in place (Fig. 238). The first molars are the keystones of the arches, and determine the extent of the formative process which shall occur in the alveolar bone posterior to them. They are also the teeth which, correctly placed or out of position, determine largely the occlusion of the teeth.^ If a teniporary tooth be long retained, it is sometimes raised to the occlusal level of the other teeth; again, it is sometimes left at its original level and occasionally imprisoned between' other teeth. The a;-rays should be used to determine the presence or absence of the permanent tooth germ or resorption of the temporary roots. If teeth erupt in malposition, it is held to be wise to correct as early as possible, in order to prevent further malposition of other teeth. > American Text-book of Operative Dentistry. ^ Guilford, Angle, and others. ' Angle. IMPACTION OF TEETH 269 Fig. 233 illustrates a case of malposition of molar germs which have developed in the incisal region, displacing the incisors. Impacted and Encysted Teeth. — The extreme extent of dental malposition is reached when the permanent teeth do not erupt at all. Instead of presenting in the dental arch, they may be entirely embedded in the substance of the bone, either remaining there, with or without pathological manifestations, or erupting in some unusual situation. In other cases a distinct cystic tumor forms about the enclosed tooth (Fig. 31). Impacted Lower Third Molars. — By far the most common dental impaction is that of the lower third molar. The extent of impaction varies from a partial eruption, or partial imprisonment of the tooth by Fig. 239 Right half of lower jaw, showing an impacted third molar. (.Cryer.) its bony surroundings, to its entire imprisonment in any part of the ramus. Many of the more severe cases treated under the head of pathological dentition, if unrelieved, would be included in the category of impacted teeth. In Fig. 239 is shown a lower third molar presenting the effects of a previous impaction. The irritation caused by the efforts of the tooth to disengage itself or to overcome the resistance to its eruption has caused an active formative reaction in the pericementum, resulting in an hypertrophy of the cementum. Likewise the pressure upon the bone causes a condensing osteitis, and the bone becomes dense, more obstructive, and less vascular (see p. 137). If the distance between the posterior surface of the second molar and the columns of the coronoid process be ^■ery short, it is evident 270 MALFORMATIONS AND MALPOSITIONS OF THE TEETH that upward eruption is impossible, so that the tooth may assume any direction of movement, the most common being forward, the axis of the tooth changing its position until the tooth may lie in a horizontal position or even become inverted. Fig, 240 is taken from the same Jaw as Fig. 239, but shows the opposite side; the impaction is pronounced. Fig. 241 shows another Fig. 240 Inner side of left half of same lower jaw. (Cryer.) Fig. 241 Impaction of lower third molar. Resorption of root of second molar and impingement of root upon inferior dental canal, which is deflected out of its course. (Cryer.) IMPACTION OF TEETH 271 case with different anatomical surroundings. In the first case there were evidences, both in the tooth, in its bony surroundings, and in the external cortical bone, of the results of the irritation produced by the efforts at eruption. The cementum was thickened; the outer Fig. 242 Fig. 243 Impacted lower third molar beneath gum. Second molar tipped forward. (Skiagraph by E. Ballard Lodge.) Impacted cuspid. (Skiagraph by E. Ballard Lodge.) follicular wall, the tissue designed to form the alveolar periosteum, had exercised its formative osteogenetic function, and a capsule of bone had formed about the tooth; it lay in a bony chamber. ^The pressure exerted upon the distal wall of the second molar had resulted in a pressure resorption of its root until the pulp chamber was encroached upon. These were both postmortem cases, and no records Fig. 244 Impacted biou.spid. (Skiagraph by K. Ballard Lodge.) of their clinical histories were obtainable. The symptoms produced could only be surmised by the nature of the anatomical relations and the pathological evidences. There may have been a prolonged but mild periostitis, probably a continued pulp irritation ; and in the 272 MALFORMATIONS AND MALPOSITIONS OF THE TEETH last, neuralgia of any grade of severity. The pressure upon nerves of the inferior dental canal would account for neuralgia or mental or other disturbance. Cryer calls attention to the fact that a third lower molar in its attempt to erupt, frequently causes a cellulitis, extending into the temporomandibular joint, causing acute ankylosis.^ Judging from postmortem records and recent skiagraphy, cases of impacted third molars are more common than generally believed. Instead of remaining in the alveolar portion of the bone, the impacted tooth may come to occupy a cavity in some portion of the body or the ramus of the bone (Figs. 246 to 249). The positions of the Fig. 245 Same as shown in Fig. 221, with tooth removed. (Cryer.) teeth in such cases tend to confirm Tomes' theory of the develop- ment of the jaw. The jaw being lengthened, and the ramus develop- ing through conjoined deposition and resorption of bone, the crown of the tooth appears to be either fixed in a bony nucleus and trans- ported to some distant point in the developmental progress of the jaw, or to be irregularly shifted about during jaw growth. At later periods the pressure exercised by root formation disturbs the rela- tions of the tooth with its earlier surroundings. These efforts at eruption may at late periods cause the appearance of the tooth in 1 Dental Cosmos, October, 1911. IMPACTION OF TEETH 273 odd situations. In the case shown in Fig. 248 the crown of the tooth made its way through the angle of the bone and through the Fig. 246 Wisdom teeth embedded in the rami of the lower jaw. (Tomes.) Fig. 247 muscles and skin. The opening in the skin healed upon extraction of the tooth. Impacted Upper Third Molars. — Some phases of impaction of this tooth have been spoken of under the head of Pathological Dentition. The most common is imprisonment of the tooth and its subsequent partial eruption in a horizontal position, the crown pointing toward the cheek (Fig. 167). The crown of this tooth may, in rare cases, be directed inward or backward, in the latter case being arrested by the pterygoid plates of the sphe- noid bone. It may present with an anterobuccal facing of the crown, as shown in Fig. 249, or with a posterobuccal facing. In a case recorded by Tomes (Fig. 250) the extraction of the second molar revealed the third molar in a reversed position, its roots occupying the depression between the roots of the second molar. A case has been reported of an upper molar with the roots partly embedded in the floor of the antrum, its neck carious,^ and the antrum in a state of suppuration. Wisdom tooth buried in the ramus, after Marshall.) (Tomes, 1 Possibly resorbed or decalcified instead of carious. (Editor.) 18 274 MALFORMATIONS AND MALPOSITIONS OF THE TEETH Impacted Cuspids. — In point of frequency of impaction the upper cuspids stand next to the lower third molars. It will be recalled that the upper cuspids lie high up; the floors of their crypts, in which they lie loosely, are at a higher level than those of the adjoining teeth; Fig. 248 From a wax model in the museum of the London Odontological Society. (Tomes.) they erupt at a much later period, and their crowns, as with the other anterior teeth, lie lingual to the roots of their predecessors. All of these are elements which might cause displacement of the developing cuspids. Should the advance of eruption not keep pace with the development of the alveolar bone, imprisonment is likely; Fig. 249 Fig. 250 Upper jaw, with the third molar directed forward and impinging upon the second molar. The small tooth situated high up in the ante- rior part of the jaw was forced there by the spade of the grave-digger. The artist's accu- racy in delineating all parts of the specimen has rendered this explanation necessary. (Tomes.) A second molar of the upper jaw, with the wisdom tooth inverted and embraced within the roots. (Tomes.) again, the dense bone imme- diately about the first bicus- pid and lateral incisor may offer a deflecting resistance. Examining the texture of the bone about these parts, it is evident that the direction of least resistance to the advance of a much deflected crown is into the cancellated bone of the incisor portion of the alveolar process; hence it is most usual to find the crowns of these teeth lying with IMPACTION OF TEETH 275 their cusps pointing forward (Fig. 251). Several recorded cases have the positions shown; one or both of the teeth may be impacted. Fig. 251 Abnormal jaw, showing impacted cuspids. (Crycr ) Fig. 252 . Impacted bicuspid. (Salter.) Cuspid teeth may erupt into the nasal cavity or appear in the canine fossa, and present the crowns cheekwise or lie horizontally and above the roots of the bicuspids. Glas, of Vienna, discovered a cuspid in the nasal floor associated with calcic formations in its ulcerated surface (rhinolith). The 276 MALFORMATIONS AND MALPOSITIONS OF THE TEETH patient, aged nineteen years, had frequent fetid eructations, with vomiting of green, foul-smelling masses. With the removal of the cuspid the vomiting, etc., ceased. Fig. 253 Lower maxilla, in which the right second bicuspid is placed obliquely, the root being directed backward. The crown, though exposed, does not rise above the level of the alveolar margin. (Tomes.) Impaction of Other Teeth. — While impactions are most common in connection with the teeth named, any other teeth of a denture may be imprisoned. Fig. 252 shows an impacted bicuspid whose root Fig. 254 Imprisoned central incisor. (Kirk and Cryer.) development has been normal as regards its length, but whose curve has been modified by the resistance of surrounding tissues. Fig. 254 exhibits an imprisoned central incisor, whose retention was, no doubt, determined and malposition caused by the development and IMPACTION OF TEETH 277 presence of the brood of supernumerary teeth which surrounded its crown. Upper incisor teeth have been seen in\-erted and their crowns erupted into the nasal cavity, where they have produced inflammation which later became infective.^ Fig. 255 Maxilla, in which the temporarj- cuspids (the sockets of which are shown by the dotted lines were retained, and the permanent canines developed within the substance of the jaw. The bone has been removed on the one side to show the direction taken by the tooth, which has been twisted on its axis to the extent of a quarter of a turn. (Tomes.) Sjnnptoms. — The most common symptom attendant upon impac- tion of teeth, judging from the obtainable records of cases, is tri- facial neuralgia of any degree, caused by impingement of the mal- posed tooth upon nerve filaments or trunks. Cryer^ records a case where a supramaxillary neuralgia was traced to the presence of a central and lateral incisor, and a cuspid tooth in the anterior wall of the antrum ; they were ^^°- ^^^ only discovered by an exploratory operation. A cure of the neuralgia was effected by their removal. Impacted third molars frequently give rise to heavy rheumatic pains about the side of the face and iaws, and no doubt in ^ , ^ . "' , Impacted teeth removed by such cases as depicted m Fig. 241 would surgical operation. (Cryer.) cause intractable and diffuse maxillary neu- ralgia. Salter^ records a case of long standing and intractable neuralgia, exhibiting a constant painful area upon the scalp, and in which heat and tenderness were noticed over a swelling upon the hard palate. Immediate and permanent cessation of the neuralgia followed removal of the teeth. ' Jameson: International Dental Journal, 1899. - Dental Cosmos, 1896. ' Dental Pathology and Surgery. 278 MALFORMATIONS AND MALPOSITIONS OF THE TEETH Dr. X. T. Shields^ describes a case of great pain in the region of the mental foramen, accompanied by a later appearance of fever, reaching 103.8°, with subsequent enlargement of the submaxillary gland, as cured by the surgical removal of the two impacted bicuspids and deciduous tooth shown in Fig. 257. Fig. 257 C Skiagraph showing impacted teeth. (Shields.) Symptoms of maxillary periostitis — heavy, gnawing, and dull, throbbing pain, with more or less heat and engorgement of tissues — are noted as an accompaniment of impacted teeth. Such symptoms may herald the appearance of the tip of the tooth through its bony covering and gum. Cases of maxillary abscess, in the absence of their usual cause 1 Dental Cosmos, 1908. IMPACTION OF TEETH 279 (gangrenous pull)), '"'k"^' ^^^^^ '^ prolonged iind painful course, ^ involv- ing neighboring structures, which may be vital, and after free venting be found to have arisen about an impacted tooth. The probable explanation for many cases is the partial absorption of the overlying tissues, permitting ingress of bacteria, but in some cases crown resorption may cause irritation, and bacteria in the blood may localize. Occasionally a circumscribed swelling is noted upon some aspect of a jaw, most frequently upon the palatal portion of the superior maxilla, which is attended by inflammatory symptoms, and an incision reveals an impacted tooth. If a plate has been worn the tissue between and even the bone may become necrotic. Fig. 259 X-ray photograph, showing malposcd cuspid entirely embedded in the bone and pressing upon the central. Impacted cuspid revealed by resorption of the overlying tissues. (Burchard.) Quickly forming cysts of the Jaw, upon receiving surgical treat- ment, may be found to contain the crown of an entire tooth, this evidently being the centre of irritation from which the cystic forma- tion had its origin. ^Melancholia, mania, and dementia prsecox have been relieved by the extraction of impacted teeth diagnosticated by skiagraphy.- This shows a relation between cause and effect (Figs. 260, 261, 262). The pulps of other teeth have been devitalized by the strangula- tion due to the pressure of the crown of the impacted tooth upon the apical tissue, and the production of pulp nodules in other teeth through a reflex hyperemia has been noted. The resorption of roots of other teeth has been produced by the pressure of the impacted tooth. 1 See Garretson's Oral Surgery and Salter's Dental Pathology. ^ Upson: Dental Cosmos, 1910, p. 527. 280 MALFORMATIONS AND MALPOSITIONS OF THE TEETH Hypercementosis and concrescence have also been produced by the descent of the tooth and have produced impaction. Resorption of the roots of the impacted teeth, or resorption of the enamel and dentin of the crown may occur. In one case a calculus in nowise associated with the oral cavity and divided from it by an area of pericemental tissue was found. (See Resorption of Enamel for illustration.) Even dementia has been associated with impac- tion. Any impacted tooth having association with the mouth by way of a sinus, or opening, may undergo caries with consequent pulp irritation which adds its symptoms. In all these cases diagnostic features exist, though none are com- parable to the a;-rays. Diagnosis. — The first point of observance in cases of suspected tooth impaction or of obscure supernumerary teeth is an examina- tion of the dental arches. Are all of the permanent teeth in position? Given the absence of, for example, a lower third molar from the dental arch, with a history of no eruption, and a persistent neural- gia, particularly if occasionally accompanied by or alternated with heavy rheumatic or what are known as bone pains, and finding no other evident cause of the neuralgia, an impacted tooth would be naturally diagnosticated as the source of the disturbance. Impacted teeth which lie horizontally, or nearly so, along the palatal vault frequently cause a swelling. This, taken in conjunction with the absence of a tooth from the dental arch, points to a diagnosis of impaction. In very many cases of impaction diagnosis has been a mere acci- dent, discovery being made in the course of an exploratory surgical operation. Modern sciences solves with the a;-rays the difficulties attendant upon the diagnosis of impacted teeth. B. H. Catching^ was the first to practically apply this diagnostic test in this connec- tion. The left upper central incisor of a female, aged nineteen years, became loosened, and an exploration through its pulp chamber revealed a hard body occupying a position part way up the root, which had undergone resorption to that point. The cuspid of the left side was absent from the arch. A skiagraph of the parts (Fig. 258) revealed the missing cuspid, whose crown had impinged upon and caused resorption of the central incisor. Impacted teeth may become uncovered at some aspect late in life, and the condition be discovered incidentally. Cases are recorded where the pressure of a plate has caused the resorption of tissues overlying an impacted tooth, thus revealing its presence. Fig. 259 • Catching's Compend, 1896. IMPACTION OF TEETH 281 illustrates a case where the presence of an impacted cuspid was revealed at the age of seventy years, through resorption of the alveolar bone and the gum tissue covering the tooth. As the smooth feel of enamel is a diagnostic feature when instru- mental examination is made, it is to be remembered that the enamel and dentin of an impacted tooth may undergo a true resorption Fig. 2G0 Fig. 201 Impacted lower third molar; cause of neu- ralgia. (Skiagraph by Lodge.) Cuspid tooth, unsuspected by patient; demonstrated to have been responsible for severe neuralgias. Patient, a draughtsman, had not been able to work at his business for the six months previous. The tooth was not known to be present until revealed by i-rays. It was removed from the lingual side. (Skiagraph by Lodge.) Fig. 262 Impaction of upper third molar, without local pain, cause of profound delusions and melancholia. (Upson.O with the characteristic Howship's lacunae. "Wlien partly exposed to the oral fluid caries may occur. Both these conditions produce rough surfaces, but enamel may usually be felt at some point. Treatment. — The treatment of cases of impaction is the removal of the offending tooth. Whether or not this comes within the province I Insanity Caused by Painless Dental Disease, Dental Cosmos, 1910. 282 MALFORMATIONS AND MALPOSITIONS OF THE TEETH of the dental operator depends upon the position of the tooth, and, incidentally, upon the usual range of practice of that particular practitioner. When the tooth is embedded deeply in the substance of the jaw, access to it involves the anesthetization of the patient, and the removal of the bone which obstructs the path of extraction; this may be an operation of some magnitude, and is usually done by a special surgical practitioner. When, however, it is evident that the obstructions to the removal of the tooth consist of the soft tissues and but a lamina of bone, the operation for removal is clearly within the province of the dental operator. For example, the pres- ence of an impacted cuspid is determined lying horizontally along the lateral aspect of the roof of the mouth. The parts may be injected with a cocain or eucain solution, and a cut made with a sharp bistoury through the soft tissues from the outside of the swelling to the bone. The flap thus outlined is raised from the bone, the flap including the periosteum. A large, sharp bur is then employed to remove the covering bone. When the tooth is freely exposed it may be dislodged with forceps or elevator. The parts are then washed with a hydrogen-dioxid solution, dried, the flap pressed back into place, and steresoP painted over the parts. I^ — Purified gum lac 5ix Purified gum benzoin §|- Balsam of tolu B^ Oil of cinnamon (Chinese) 5-3- Carbolic acid •■ 5 iij Saccharin §5 Alcohol Oij— M. 1 Dental Cosmos, 1S95: SECTION III AFFECTIONS OF THE ENAMEL AND DENTIN CHAPTER IX ABRASION, EROSION, AND STAINS Formed by the ameloblasts, later changed into Xasmyth's membrane, and borne upward with the crown during the process of eruption, enamel has no posteruptive source of nutritive supply from without. Its only conjectural source of nutrition is, therefore, from the pulp via the dentinal tubuli. This seems to have been proved by Caush, and later by others. (See p. 165.) Teeth do change in color with advancing age, generally becoming yellower; this is probably due to the tubes containing organic matter which are now supposed to permit a slow interchange of nutritive sap.^ The editor has a patient with a vital tooth of mahogany brown color, which she claims changes the depth of color. Changes in the color of the dentin may be transmitted through enamel, which is normally almost or even quite transparent. Such a transparency may be seen at the incisal edges of thin incisors before these edges are worn down. Another proof of transmission of color through enamel is seen in caries; a bluish-black or white appearance is caused by the decayed mass or decalcified inner surface of the enamel. Again, amalgam or gold, oxyphosphate or oxychlorid, reflects its color through enamel, and, in excavating, the shadow of the excavator may be seen through thin walls. Enamel may be stained or whitened by decalcification due to causes acting externally. Extreme polishing may also cause a new character of light reflection simulating a change in color. Talbot claims a change in color of teeth during prolonged illness, such as pneumonia, typhoid fever, syphilis, tuberculosis, and in pregnancy.2 With advancing age the translucency of teeth 1 C. Francis Boedecker: Dental Cosmos, September, 1911. - Dental Cosmos, 1905, p. 49. 284 AFFECTIONS OF THE ENAMEL AND DENTIN verges more toward transparency — apparently a sclerotic change. (See Transparency.) After implantation a tooth may somewhat change its color, but this evidently cannot be due to nutrition from the pulp, as this organ will have been removed before implantation. It would seem that it may take up coloring matter from the saHva. Enamel may suffer mechanical and chemical injury, but whether it may undergo constructive changes or retrograde metamorphosis is at present only conjectural. There is, however, a possibility that a molecular change may occur as a result of slow interchange, environment, or impact of mastication. The dentin and cementum contain about 28 and 30 per cent, of organic matter respectively, and stain deeply and permanently with great readiness. Possessed of living cells, they also undergo changes in their structure under the influence of various stimuli, their substance being added to or reduced according to circumstances. They are also acted upon by mechanical and chemical agencies, if exposed to their influence. ABRASION Abrasion is the mechanical wearing away of tooth substance. Occurrence. — It occurs most commonly upon the occlusal surfaces of teeth, but is also found upon the approximal and labial surfaces, the labial cervix, and more rarely upon the lingual surfaces. It is also seen in the temporary denture, expecially in the molars, and is found in animals (Figs. 273 and 274). Appearance. — Purely abraded surfaces present a smooth, flat, or concaved, highly polished appearance. The surface may become stained or otherwise altered in color, or subsequent caries may remove its smooth surface. Occlusal Abrasion. — Occlusal wear is very common, and occurs largely with men who chew tobacco ; the contained silex, .being gritty, acts as an abrasive. Such wear, due to the use of hard food or gritty substances, is seen in skulls of aboriginal man. Ottofy describes a peculiar form of w^asting due to chewing betel nut mixed with bay leaves and slaked lime. Xo doubt a silicious element is introduced. Some degree of occlusal wear is accepted as normal to all teeth, the act of mastication producing marks or facets at the point of articu- lation of antagonizing teeth. A tip-to-tip variety of occlusion permits free lateral movement of the lower jaw^, and a herbivorous type of articulation causing abrasion. It is also frequent in those ABRASION 285 cases presenting the first degree of prognathism. In some of these cases the labial surfaces of the upper incisors and cuspids, and the linguo-incisal margins of the lower incisors are worn. A single over- lapped lower tooth may abrade an upper tooth in this manner. The gritting of teeth is also a cause. This gritting, termed " bruxo- mania," may occur only at night or for a few minutes each day; again it may appear for entire days, weeks, and months, not ceasing even during sleep. In such cases the teeth are worn down flat. Maria and Pietkiewicz^ noted 12 cases of central nervous lesions, mostly dementia, developing bruxomania; also it has been noted in cases of epilepsy and chorea. A clay pipestem may wear a hole of its own diameter in the incisal edges of anterior teeth; other stems wear less. Upholsterers and seamstresses have peculiar abrasions (tack holding, thread biting) Fig. 263 Abrasion of anterior teeth, with loss of posterior occlusion. (W. A. Capon.) The undue loss of posterior occlusion and consequent overuse of the anterior teeth cause their abrasion after the manner shown in Fig. 263. A marked overbite, produced in any manner, may cause lingual abrasion of upper anterior teeth. Where the abrasion occurs in a fairly regular manner, four degrees of abrasion are classified: (1) Abrasion removing the cusps; (2) abrasion removing the occlusal third of the crown; (3) abrasion removing the middle third of the crown; (4) abrasion extending to the gum line or beyond. (Broca.) (See Figs. 264 and 265.) When there is a marked overbite occlusion, with a consequent lessening of the lateral movement of the mandible, the teeth do not acquire flattened contact surfaces, but their cusps increase in sharpness and pointedness. This at times becomes exaggerated, and produces an interlocking of cusps or rather worn surfaces which have very sharp edges. In the first degree of abrasion the dentin is often hollowed out in 1 Dental Cosmos, 1907. p. 525. 286 AFFECTIONS OF THE ENAMEL AND DENTIN advance of the enamel of the cusps, forming concave places in which berrj^ seeds lodge and cause annoyance. These spots are at times hypersensitive. The plane surfaces also are often sensitive upon merely rubbing the teeth together. Fig. 264 L ''^' "* *■■ IS «^-""i\' 'Mm^ ^•P The first and second degrees of abrasion. Specimens from museum of Philadelphia Dental College. Fig. 265 The third and fourth degrees of abrasion. Secondary dentin plainly visible. Specimens from museum of Philadelphia Dental College. Labial and Approximal Abrasions. — Some forms of abrasion have been attributed to too vigorous use of tooth-brushes, particularly ABRASION 287 when gritty powders are employed. There is no doubt that mechan- ical abrasion about the necks of teeth is produced in this manner, the gum Hne receding beyond the enamel border, exposing the cementum; but a careful examination will reveal the cementum and next the underlying dentin to be affected; the enamel, when abraded, shows first as a facet, then as a spot of bare dentin with thin edges of enamel around it (see the left lateral in Fig. 2S4), and later the area may be grooved. As a rule, however, the effect shown in Fig. 283, lower jaw, is the more common. These tooth-brush abrasions are quite characteristic. In well-kept dentures the gums are seen to have receded from their normal line, but may exhibit little evidences of turgescence; the roots of the teeth, upper and lower, are exposed to a greater or less extent along their labial and buccal, but not usually along their lingual aspects; and they are excavated to variable Abrasion due to employment for twenty jears of a gritty English tooth paste. At 7, gold crown abraded. (Miller.) depths, upon the bicuspids and first molars more than upon the other teeth, as here the greatest force of brushing is received. The depressions have a normal dentin color, sometimes deepened in the mouths of non-smokers, and which in smokers may be periodically blackened by deposits of carbon. If caries supervene, the abraded areas lose their normal color, and may be readily indented by sharp instruments, which they resist before the advent of caries. The bicuspids and molars, particularly, may be grooved in such manner as to require restoration by fillings. Miller^ investigated this subject very carefully, and found that the grit in many forms of tooth powder vigorously used was quite competent to wear away tooth structure, gold, and other fillings (Figs. 266 to 269). Figs. 268 and 271 show a lingual wasting ' Dental Cosmos, 1907. 288 AFFECTIONS OF THE ENAMEL AND DENTIN Fig. 267 Photomicrograph of sediment obtained by washing tooth paste, which caused the abrasion shown in Fig. 266. (Miller.) Fig. 268 A B c Abrasion of lingual surface by assiduous brushing with tooth powder. At D and E amalgam worn down. (Miller.) ABRASION 289 resembling graphic erosion. In both cases abrasion is proved by the wasting of metal, which acids could hardly accomplish. Miller Fig. 269 Artificial abrasion produced by brushing with a much-used English tooth paste with motor brush for eighteen hours. Remains of gold filling in first bicuspid. (Miller.) Fig. 270 Gradual wear of both tooth substance and filling material, notwithstanding the open bite. (Miller.) experimentally proved abrasion competent to produce the grooves known as "wedge-shaped defect" (Fig. 269). 19 290 AFFECTIONS OF THE ENAMEL AND DENTIN Calculus may be worn in like manner, either by the brush or by the festoon of a plate (Fig, 272). Miller found that among clinic patients who never used a tooth- brush the labial abrasion was wanting, and he observed that a cessation of wear followed the abandonment of the use of gritty powder and the adoption of a soft brush and mild powder, which is the evident indication in such a case. A clasp may abrade a tooth, and, if food debris be retained on its inner side, caries may follow in the abraded area. The purely abraded surface will be polished. Slight approximal abrasion may be normal as a facet, due to the rubbing of one tooth upon another at the contact point. A marked example of this was seen in the mandible of a skull of a Maori. (Museum of Philadelphia Dental College.) The third lower molars are locked beneath the distal surface of the crowns of the second molars. Some form of bone loss occurred, producing looseness of the third molars. The individual motion of the teeth produced a deep abrasion of the enamel of the second molars upon the distal surface, and an occlusoproximal abrasion of the third molars. Grit in powder may easily be detected by taking a small portion between the incisor teeth, or may be found by elutriating the powder, i, e., place in water, stir, let settle for a few seconds, pour off the supernatant fluid, and examine the sediment as above or microscopically (Fig. 267). Miller found from experiments, as to the effects of various acids acting for a time and followed by brushing with abrasives, that it depends very materially upon the nature of the acid. Those acids which rapidly decalcify (soften) the dentin, of which we may take hydrochloric and lactic as types, most readily retard the wearing away by friction (unless the friction be so great as to wear in spite of the decalcification). While those which act slowly on the dentin (oxalic, tartaric, etc.), as well as those which have a macerating effect on decalcified dentin, may be wanting in this influence. He concluded that wear could not be produced by acid alone, but that any acid or acid salt which possesses the power of extracting the calcium salts from enamel, or of breaking up the connection between the enamel prisms, may accelerate the process of wasting, provided the necessary mechanical factor works together with it. Miller found food to be a negligible quantity as to wear upon labial surfaces. The editor has a patient presenting the general characteristics of Fig. 285, who has been a brush enthusiast, and was taught in early life to use a toilet soap containing fine pumice (Bazin's poncine soap). ABRASION 291 Extensive approximal abrasion may be due to extrusive elonga- tion of a tooth in one or both jaws, causing a tooth to occlude with its antagonist with a glancing motion. In this manner specimens are produced abraded from the occluso- approximal angle to nearly the apex of the root. The festoon of a metal plate may rapidly cause abrasion of the lingual cer\'ix of a tooth. The condition is, however, rare, caries being more common. In the editor's practice a case was seen in which several teeth were so affected in a few months by an ill-fitting metal plate. The festoon of a vulcanite plate has also produced such an abrasion. Abrasion sometimes follows caries when the latter has become freely exposed to attrition. The softened surface wears away and the part assumes a polished appearance, but is discolored as the result of the stain due to the caries. (There is also eburnation, which see.) It is probable that a hyperacid condition of the saliva in con- nection with mechanical forces may be a cause of rapid abrasion. (See Erosion.) Effects of Abrasion. — These are external and internal, and most marked in the occlusal variety. The crown wears dowm until at times the gum is reached. In the process sharp edges of enamel are formed. These splinter off, leaving rough edges, or the enamel may fracture or split longitudinally, following the axis of the crown. Supported by dentin it does not further break away (Fig. 293). Sharp enamel edges may irritate the tongue, producing ulcers of a sometimes chronic type, which acquire indurated edges and simu- late syphilitic sores or epithelioma. The causal relationship between sharp edges of the teeth and lingual epithelioma appears to be quite clear in some cases. Brown^ mentions a case of tetanic spasms of masticatory muscles due to this source. Sores which have given evidence of malignancy and been diagnos- ticated as malignant growths, have been cured by rounding and polishing sharp and irritating enamel edges of teeth. The continued stimulation of the ends of the dentinal fibrillar, which are exposed in abrasion, causes them either to become hypersensitive or stimulates them to formative activity. Tubule material is built upon the inner walls of the tubule, obliterating their lumen. This is the so-called tubular consolidation or calcification (eburnation). Accompanying this, secondary dentin is often formed. As a result, most commonly the pulp chamber of the crown is filled up with 1 Dental Cosmos, 1908, p. 4. 292 AFFECTIONS OF THE ENAMEL AND DENTIN Fig. 271 Fig. 272 a, abrasion of lingual surfaces; b, of amalgam filling produced by a plate. (Miller.) Abrasion of calculus. (Miller.) Fig. 273 Fig. 274 LJ^ Abrasion of lower incisors of a horse pro- Defects resembling wasting in the teeth of a duced b.y "cribbing." (Miller, after Kitt.) sea lion. (Miller, after Murie.) ABRASION 293 secondary dentin as the abrasion proceeds, and the crown may often be worn off nntil the cervix is reached, while the pulp remains, \ital and covered (Fig. 205). In some cases the abrasion closely ap- proaches the pulp, which has failed to protect itself, probably because of atrophy of odontoblasts, and the phenomena of hyperemia, or even exposure, and its results occur. A left upper bicuspid of the second skull in Fig. 265 was in this state. The causes and phenomena of abrasion of the temporary teeth are practically- the same as in the case of adults, except, perhaps, that children are more subject to the action of rectal parasites, as ascaris lumbricoides, tenia, etc., or suffer from irritable bladder due to hyperacidity of the urine. These conditions commonly produce a reflex stimulation of the muscles of mastication, resulting in nocturnal gritting of the teeth. Same case as Fig. 263. Bite opened by bridge-work, posteriorly. Anterior teeth restored by means of Land jacket crowns. (W. A. Capon.) Treatment of Abrasion. — In the cases of cupped occlusal dentin, hard fillings of gold or, preferably, platinum gold are advisable. Whether the filling be built in or an inlay be set, it is advisable not to cut too closely to the enamel in making the cavity, for the struc- ture of such a wall is often fractured after filling when this is done. If possible the form in Fig. 276, with retention made elsewhere than near the side enamel is preferable. Inlays requiring only pin anchorage are preferable when undercutting would weaken. If nearly all teeth are present and the abrasion slight, bridge-work may be used to restore the full occlusion without attempt at restora- tion of the worn surfaces. If the abrasion of the upper anterior teeth be deep, the bite may be raised by appropriate posterior crowns or bridges, and solid platinum-gold fillings may be built upon the anterior teeth, either the uppers alone or upon both the upper and lower 'teeth. Anchor- age may be obtained in the dentin, or screws may be planted in the 294 AFFECTIONS OF THE ENAMEL AND DENTIN Fig. 276 dentin between the enamel and pulp and the fillings be built about them. Instead of malleted fillings, tips of the gold-inlay type may be made (Figs. 277 and 278). Casting the inlay is a simpler method. For those cases in the second degree, as a means of limiting the abrasion. Dr. J. C. Curry has introduced small truncated cones of unannealed iridioplatinum, which are to be cemented into holes drilled into the occlusal faces of the molars and bicuspids with an inlay drill of exactly correspond- ing size mounted in the right-angle hand piece. As many are put in as the safety of the pulp and the enamel will permit. They act upon the same principle as steel nails in a shoe heel. In other cases, after securing a proper opening of the bite and posterior occlusion with crowns or bridges, single porcelain-faced gold or platinum crowns may be made to cover each of the anterior teeth. For this purpose the crown is ap- propriately reduced to convenient form, but the pulps need not be destroyed. Fig. 279 represents the method outlined by Evans.^ There can be no objection to pulp removal in any of these cases, if for any reason a dowelled crown seem preferable. Manner of preparing the outer retaining wall of a cavity in case of cupped occlusal abrasion. Fig. 277 Fig. 278 Fig. 279 Gold tip for abraded teeth with living pTilps. (Evans.) If cast the margins are to be beveled outwardly. Gold tip for abraded teeth with pulps removed. (Evans.) Porcelain-faced crowns for teeth with living pulps. (Evans.) Land jacket crowns, consisting of a wedge-shaped platinum jacket with a porcelain facing attached by means of one of the numerous inlay bodies, may be used instead of the Evans crown. In some cases other forms of crowns may be indicated (Fig. 275) . 1 Crown and Bridge Work. ABRASION 295 There present at times cases of abrasion in which, aside from tiie wear, pyorrhetic conditions may be present, or where bridges cannot be properly inserted, especially when only a few teeth remain. If this pertain to the upper jaw only, the lower denture may be restored to usefulness, the upper teeth extracted, and a full upper denture inserted; this permits the adjustment of the bite to any desired level. If the conservation of a few teeth is desirable they may be crowned or bridged, the occlusion being raised if desirable, then a plate constructed. If the condition be transferred to the lower jaw and the anterior teeth be in good condition, a piece with the Roach^ or Morgan attachment type may be fixed upon cuspid or bicuspid crowns. It is to be remembered that in any case of opening of the bite the occlusion is to be restored throughout. The bite must not be raised by means of partial plates which strike before the natural or crowned teeth, as they tend to embed them- selves in the soft tissues and create inflammation. If the bite be only slightly raised by plates, this embedding will cause a return to the original condition. Neither must too great a strain be placed upon supporting teeth (see Overwork of Teeth). In case of hypersensitivity, Robinson's remedy, silver nitrate, nitric acid, or the actual (hot burnisher) or the electrocautery may be effective; if not, the areas should be excavated and filled, or, if necessary, the pulp should be devitalized. If the abrasion be caused by tobacco its use should be stopped. A difficult class of cases to treat is found in those highly nervous individuals who grit their teeth during sleep. It is probable and reasonable that this cause alone may serve to explain abrasions trace- able to no other source. The cure of such cases as these could only be possible through the wearing at night of some modified form of interdental splint. Arnone has described a simple vulcanite splint for the lower teeth to open the molars about one-sixteenth of an inch and the incisors one-half inch. This he calls "the insulator," and is to be vulcanized at 160° C. It is to have the upper surface rounded (Fig. 280). He also describes "the paraglossus," a double vulcanite splint made in one piece to be inserted by bruxomaniacs during sleep, or by epileptics during the forewarning "aura," if present, to prevent grinding or tongue biting.- The cases naturally indicate the medicinal use of a bromide before retiring, unless the causes can be discovered and removed. If such gritting be present in children, the evidences of irritable I Dental Cosmos, 1908, p. 17. 2 Ibid., p. 924. 296 AFFECTIONS OF THE ENAMEL AND DENTIN bladder, due to hyperacidity of the urine or of rectal parasites, should be sought and treated. The urine may be rendered alkaline by the use of potassium salts, and kept so by restriction to a largely vegetable diet. Belladonna may be used to reduce vesical irritability. Rectal parasites may be removed by the use of vermifuges, or, occasionally, by rectal injections. Fia. 280 Fig. 281 The "insulator." (Arnone.) The "paraglossus." The metal groove shown relates to another method of construction. RESORPTION OF ENAMEL Fig. 282 Definition. — Resorption of enamel is the removal of enamel sub- stance by soft tissue containing osteoclasts. Occurrence. — It occurs externally only in impacted teeth sur- rounded, at least in part, by irritated tissue, and internally very rarely after resorption of dentin by the pulpi (Fig. 282). (See Pulpitis.) Such tissue is found in dermoid cysts, and causes the resorption of teeth. (See Fig. 32.) Pathology and Morbid Anatomy. — Osteo- clasts approximate the enamel as they do cementum, decalcify and resorb it. The dentin is next attacked. There result irregular excavations (Howship's lacunae) and white or discolored areas of evident slight decalcification of the enamel. A deposition of bone into the area may occur. ^ The process is probably the result of a non-septic inflammation, as in the case of root resorption. (See Interstitial Gingivitis.) The enamel may be resorbed from its internal surface after the resorption of dentin by the pulp (see Chapter XVII), and, as shown Impacted cuspid with resorp- tion of enamel and a hemato- genic calculuc. (Miller.) ' Hopewell-Smith: Histology and Pathohistology of the Teeth. 2 Ibid, EROSION 297 by Woods, may be filled in with adventitious material of a strueture resembling cementum. Treatment. — Should the disease by chance occur upon a tooth which later has been drawn into place, the area may be filled; otherwise it has only a pathological interest. EROSION Definition. — Erosion of the teeth is a term applied to the chemical or chemicomechanical destruction of the hard tissues of the teeth in such a manner that broad, shallow, smooth excavations are made in the enamel and dentin in situations free from attrition bv mastication. Fig. 283 Fig. 284 Case described as ero.sion. (Darby.) Case described as erosion. (Darby.) Fig. 285 1 . A case of erosion (drawn from the cast) : B, silhouette from a perpendicular line through the left centrals, upper and lower, showing the loss of substance. (Black.) Figs. 283, 284, and 285 illustrate the characteristic appearance of areas until recently supposed to be due to the chemical or chemico- mechanical solution which has been termed erosion. 298 AFFECTIONS OF THE ENAMEL AND DENTIN The demonstrations of Miller with reference to abrasion of labial and lingual surfaces of teeth by means of the tooth-brush and gritty powders, and the abrasion of approximal surfaces into grooves in animals by the drawing of gritty grasses, etc., through or along the teeth, or the gnawing of bones by carnivora, etc., have cast a heavy cloud of doubt upon the chemical etiology of what have been usually considered as erosions due to the action of acid sodium phosphate excreted by the mucous glands of the lips or cheek. The appearance illustrated in Fig. 283, lower jaw, and in Figs. 284 and 285 might readily, in the light of Miller's demonstrations, be regarded as abrasion if the causes (brush and abrasive powders) he suggests be found; but the graphic outlines shown in Fig. 283, upper anterior teeth, seem difficult to harmonize with the abrasion theory. The cases of this sort are rare as compared with the others, the editor recalling but two having the peculiar undercut mesial and distal erosion borders. The spreading of brush bristles, as the brush is brought from the gum down, might account in part for this, but in one of the cases mentioned there was also an undercut at the incisal border, which would render the theory difficult of application. One case was in a man aged forty-five years, a German Jew, fond of wines, beer, etc., at meals; the other a middle-aged maiden lady of nervous temperament, with whitening hair, slightly wrinkled skin, and some evidences of goutiness. According to Miller, acids or acid salts, which can extract calcium salts, may accelerate the wasting process provided the necessary mechanical factor works with it and wears off the decalcified tissue before it becomes leathery, when wear is retarded. Kirk burnt asbestos cloth, treated it with hydrochloric acid, neutralized this with ammonia, washed it with distilled water, and again subjected it to high muffle heat. This absorbent, inorganic cloth he applied to buccal glands for twenty or thirty minutes in cases of erosion, dis- solved the mucus obtained in distilled water, dialyzed the salts out, and examined the evaporated residue under the microscope and by reagents. He found acid sodium phosphate to be the decalcifying agent in what he called graphic (hydroglyphic) erosions (Figs. 283 and 284). Head^ found by experiment with a 1 to 20,000 solution of acid sodium phosphate in water, acting in the incubator at body temper- ature, that superficial decalcification of enamel occurred after four- teen hours, and when polished off it again decalcified in eight hours, and was quite superficially decalcified in two days; that a 5 per cent., 1 Dental Cosmos, 1907. EROSION 299 2 per cent., 1 per cent., and 1 to oDO solution acted under similar conditions in seventeen hours, and points out that a solution of 1 to 10,000 and 1 to 20,000 acid sodium phosphate in alkaline saliva acted after eight and five da\'s only. He also has shown that enamel which was experimentally slightly decalcified again hardened when placed in saliva for a time. He was, however, unable to explain the result.^ Miller found the slowly acting acids to not produce such decalci- fication as to retard the abrasive action of brushing with a 10 per cent, pumice. Given, then, a decided production of acid sodium phosphate by the buccal glands in contact with the labial surfaces of teeth (Kirk) for eight hours (the period of sleeping, and Head's period of one experiment, see above), it is quite reasonable to suppose that an undetermined percentage of acid sodium phosphate dissolved in buccal mucus, which in total has an acid reaction to litmus (Tru- man, Kirk, and others), is competent to produce a superficial decal- cification, which the morning brushing will remove. This repeated for months or years may produce the effect seen. Brubaker, in 1894, immersed a tooth for a week in a solution of acid sodium phosphate, subjecting it daily to tooth-brush friction, and at the end of that time spots and grooves resembling erosion made their appearance. According to Head and Kirk, the acid phosphate does not attack the enamel so as to roughen it, but leaves it translucently smooth and white, and this mildness of the action of the acid sodium phosphate is just the action that would make smooth erosion with a minimum of abrasion. (See Miller's experiments, p. 290.) Head points out " that 1 to 500 lactic acid in water will decalcify enamel in thirty minutes, while the same percentage in saliva does not do so in fifteen days, but that the inhibitory effect of saliva is overcome when the lactic acid has a strength of 1 per cent." The inhibitory effect, therefore, seems to lie in the relative relations of the acid and alkaline elements, though Head has shown that a mix- ture of 1 per cent, solution of acid sodium phosphate with a 1 per cent, solution of tribasic sodium phosphate, which is capable of turning blue litmus red, but not of turning red litmus blue, placed the acid under control so that the mixed solution did not corrode the tooth placed in it, which a 1 per cent, solution of acid sodium phosphate in water would do. Regarding the production of the abnormal exudate from the labial glands, Kirk argues that in diseases of suboxidation (resulting in hyperacid conditions such as gout and rheumatism) the blood is » Dental Cosmos, 1910. 300 AFFECTIONS OF THE ENAMEL AND DENTIN loaded with carbonic acid as a result of faulty metabolism. In the epithelium of the kidneys the mass action of the carbonic acid upon the sodium phosphate of the blood normally produces acid sodium phosphate, which is eliminated in the urine, and sodium bicarbonate, which is returned to the blood and maintains its alkalinity (see p. 90), according to the following reaction : HNa2P04 + H2CO3 = H2NaP04 + HNaCOs. If the amount of carbonic acid be of only normal pro- duction, this action will result in only a normal amount of acid sodium phosphate in the urine and perspiration; but if in excess and not cared for by the lungs, skin, and kidneys, the buccal glands may also take up the action and excrete acid sodium phosphate in an identically similar manner. The acid calcium phosphate is also found in the saliva at times, and can be formed in a similar way, the calcium phosphate being substituted for sodium phosphate as the basic salt. . Kirk states that in the saliva of arthritics there are frequently found acid salts, such as acid sodium phosphate and acid calcium phosphate. The excessive amount of carbonic acid accounts for the excessive loss of phosphate in the kidneys seen in arthritics, as the acid sodium phosphate and acid calcium phosphate require for their production the basic phosphates, and the elimination of those con- tinuously produces a phosphaturia until depletion of phosphates occur, when their amount lessens and other salts appear. (See p. 90.) In a paper published in 1902, Kirk^ describes polariscopic obser- vations made upon saliva from a patient aiSicted with a general erosive wasting of the teeth. The patient had had attacks of inflam- matory rheumatism, and suffered from obstinate constipation, periodic attacks of migraine, headaches, and neuralgia, and his saliva was most acid at night. The saliva was dialyzed, the dialysate concentrated, and found to contain lactic acid salts, calcium lactophosphate, calcium lactate, and magnesium lacto- phosphate (Fig. 286). In view of these two classes of cases. Kirk has suggested that erosion cpses may be of two kinds: (1) A general erosion, in which all of the surfaces are uniformly involved, and in which lactic acid is the solvent agent; and (2) cases distinctly due to an exudate from abnormal buccal glands or gland, the acidity of which is due to either acid sodium phosphate or acid calcium phosphate. Talbot^ claims that the systemic acidosis produced by various diseases and by fruit eating in excess is responsible for the acidity of the buccal mucus and saliva, and for pulp and gingival degeneration and resorption 1 Items of Interest. 2 Dental Cosmos, December, 1907. EROSION 301 through a process of artery and nerve-end degeneration. A decrease in the normal acidity of the urine (below 30) indicates renal insuffi- ciency, and the difference indicates the amount retained in the system. An excessive acidity of the urine indicates excessively imperfect oxidation. This expression of the cause is quite compatible with the view of Kirk, and both are views of general malnutrition. (See p. 87, etc.) Fig. 286 •^ ^■^•t>K % ,4^^Vi^P^ ^H B^" ^m lli%/ii Kv >|hHH ^wfmi \ ^^^^1 41( / ' ■ ^ .^ '^-^^J- Crystallization of salts from dialysate of saliva from erosion case, showing two typal forms. Large crystal is calcium lactate. (Kirk.) The disease appears to affect females more than males; appears usually after thirty years of age, and often some history of goutiness, arthritis, or rheumatism can be obtained. Miller denied the presence of this disease in the gouty, but since his observation the editor has had several patients hold up gouty fingers when questioned as to a possible gout as a cause of the erosions present. Erosion Due to Extraneous Acids. — Miller^ describes a case reported by Davenport,^ of Paris, of a healthy man whose teeth were eroded and worn away by acid vapors within six months of entering a factory devoted to the manufacture of nitric and sulphuric acids. This effect was observed upon the other workmen also, and also in workmen in a dynamite factory in which these acids are used. The teeth were first set on edge. Miller suspended a tooth in a flask con- taining equal parts of nitric and sulphuric acid, and found that the vapors attacked not only the inorganic but the organic portion as ' Dental Cosmos, 1907. 2 Transactions American Dental Association, 1881. 302 AFFECTIONS OF THE ENAMEL AND DENTIN well, so that upon slight rubbing with a soft tooth-brush the tissue was worn away, leaving a hard, polished surface. Miller states that Fig. 287 Another field from the same specimen as Fig. 286, also showing two typal forms. Large crystal is calcium lactate. (Kirk.) Fig. 288 ^M ^S^^HB ^^3} ^^^■■^■■MMlB|taBr«'' ^'i^* pR^iH ^^^&^ mmH ^Bfi^ Tf'^.' -\ ) .-4,'^^^^^^^H ^H Crystallization from solution of a tooth in 1 per cent, lactic acid. Large crystal is calcium lactate. (Kirk.) the vapor is nitrogen peroxid, N2O4. Lemon juice, even in lemonade, and vinegar will produce this effect of setting on edge, which undoubt- EROSION 303 edly is due to the chemical solution of a small portion of the enamel, probably the interprismatic cement substance, leaving the enamel globules a trifle higher, this soon being worn oflF to a general level again. Guilford^ mentions a case of erosion caused by shaddock (grape fruit) eating. Tomes cites cases of erosion caused by lemon and grape sucking. The pitting of grapes has produced cases of peculiar erosion of the labial and lingual surfaces and incisal edges of anterior teeth. In one case the incisal anchorage of an approximal gold filling was almost worn away upon the tooth most used to pit the grape. Unquestionably, other fruit juices might act in a similar manner if the acid has an affinity for tooth structure, and the expo- sure to its action is sufficiently lengthy and often enough repeated to produce effects. The Effects of Erosion. — Tubular calcification and secondary dentin are produced together with atrophic changes in the pulp, due to secondary dentin formation. Gold and amalgam fillings are left as raised islands by the wasting of the tooth around them, though ^filler has shown that associated abrasions may cause their wear, which acids evidently can hardly be expected to do. Scratches shown as lines and Baume's clefts are explainable upon the theory of abrasion by brush and powders; though usually transverse, there are sometimes vertical lines. The stimulation of the dentinal fibrillse by acid or mechanical stimuli may cause great hypersensitivity; as a rule, however, this is not pronounced (Fig. 289). The anterior teeth are sometimes shortened so that their occlusion is lost. Kirk's lactic acid case was of this order. The carious process may become implanted upon an eroded area, or at some part of it, usually the cervical portion. Whether this is initiated by a decal- cifying process due to the acid sodium phosphate, or uncleanliness due to a cessation in the intensity of the brushing, ip not so clear as it formerly seemed, when it was thought due to a temporary cessation in production of acid sodium phosphate, which was regarded as immunizing the part to caries. In any event the stain of iodin is taken, showing the presence of bacterial films at the point showing caries. Diagnosis. — The presence of the peculiar excavations, the hyper- sensitivity of dentin if any, and the acid character of the mucus from the follicles, as shown upon test with litmus paper made just after rising,^ are diagnostic signs. Kirk's method of obtaining the • Lectures. 2 Truman. 304 AFFECTIONS OF THE ENAMEL AND DENTIN acid may be used. (See p. 298.) The acid reaction is not marked during the day. The existence of erosion has become a valuable Fig. 289 F C- S D EC ■^ Sagittal action of human incisor prepared by Hopewell-Smith's process, and stained with hematoxylin: E C, erosion cavity, on surface of which can be seen Baume's clefts; P, pulp tissue undergoing degenerative changes; F C, atrophic odontoblasts; S D, secondary dentin. X 45. (Hopewell-Smith.) diagnostic sign for the general practitioner in his search for the nature of masked maladies from which patients frequently suffer. EROSION , 305 Obscure gout has been pointed out through dental indications alone, where the practitioner had before been baffled in his diagnosis. Treatment. — The treatment of erosion divides itself under two heads: Prophylactic and restorative; the prophylactic is again divided into local and general treatment. The problem of eradicating the cause of the disorder lies in a correction of the morbid glandular secretion. It is evident that if the irritation and altered secretion of these glands be due to some systemic cause, a disease of suboxidation, notably an affection of the gout order, a cure of the local disturbance involves the cure of the underlying systemic cause. Talbot^ reduces the acidity to normal with sodium bicarbonate (10 to 30 grains), or sodium chlorid (45 grains), after meals; or sodium phosphate morning and evening. One-tenth grain of calomel is given each two hours, for a time, to cleanse the bowel and stimulatie the liver. Eight to ten glasses of water should be taken daily. A practically antigout diet and hygiene are suggested to increase oxidation and elimination. Local treatment of the gums is necessary. (See pages 91 and 99.) Kirk,- working to the end of reducing acid buccal secretion uses, three times a day, yi^ grain pure phosphorus in olive oil in gelatin capsules, along with a very mild laxative, and when the urine shows a deficiency of phosphates, 25 to 30 grains per diem of glycero- phosphate of lime and soda are given. Next in importance to the prevention of acid formation is its neutralization. This implies the application of alkalies or the use of alkaline mouth washes. The greatest production of acid occurring during the night, applications of adhesive masses of alkaline sub- stances are made to the teeth at night. The principal of these is prepared chalk, calcium carbonate; it is rubbed over the labial faces of the teeth and between them, before retiring. It remains in sufficient amount to neutralize any acid substances coming in contact with it. Excellent results, as to the checking of the progress of the decal- cification, are obtained from the use of magnesium hydrate held in suspension in water, or milk of magnesia. Kirk found that three hours after the use of a teaspoonful of the milk of magnesia the saliva maintained an alkaline reaction. It should be used at night as a wash, after cleansing the teeth, the residue to be left as an alkaline coating upon the teeth. The chalk and milk of magnesia may be mixed into a paste. If the preparation be disagreeable, a few drops of essential oil may be added. (See Caries.) The abrasive factor and its possibilities as causes of apparent erosions suggest the • Dental Cosmos, December, 1907. ^ Dental Cosmos, 1908, p. 811. 20 306 AFFECTIONS OF THE ENAMEL AND DENTIN avoidance of any strongly abrasive powders, or, perhaps, a confine- ment to the use of castile soap and a soft brush. It has been suggested by Ottolengui^ that in the earlier stages an impression and plaster model of the teeth be made for comparison at future dates, so that the progress of the erosion may be noted. Restorative Treatment. — If the eroded areas be excavated and filled, the erosion may proceed about the edges of the fillings. It may, however, take some time for the erosion to become as deep as the original area. If metal be used, the margins must be extended to avoid this if possible. Metal is very unsightly in the locations peculiar to erosion, so that porcelain inlays, which the locations favor, are indicated. In their place silicate cement fillings may be used, but must be constantly kept in a good condition of surface or they become unsightly. The generally distributed erosions are only amenable to the prophy- lactic treatment (except by crowning when teeth are largely wasted away), and slight erosions are best treated in the same manner. MECHANICAL INJURY OF THE TEETH The enamel is a material much more brittle and inelastic than the dentin, and, therefore, less capable of resisting a parting strain. Under ordinary circumstances, however, well-formed enamel dis- tributed over sound dentin resists all the ordinary forces brought to bear upon it. Under abnormal conditions, however, enamel appears to fracture readily in two directions: (1) Along the line of the interprismatic cement substance between the prisms themselves, and (2) along the line of cement substance between the globules. The possibility of reference of all cases into one or other class indicates that the cement substance is naturally a tissue relatively weak. Dentin may apparently fracture in any plane. Causes. — The teeth may be mechanically injured by (1) the action of abrg-sion, which mechanically wears away the teeth; (2) by the application of undue force during mastication or by the improper use of cutting, filling, or extracting implements; (3) by blows of some sort delivered either directly upon the teeth or through forcible closure of the jaws, as the result of a shock or blow delivered upon the rim of the jaw. Aside from blows or bites of sufficient force to break sound teeth, ' Methods of Filling Teeth. MECHANICAL INJURY OF THE TEETH 307 it is rare to find teeth fractured without a previously acquired weakness in the tooth itself. The causes of weakness are several. During the course of abrasion the enamel is worn to a sharp edge, which is readily fractured. Oblique splintering occurs in the line of cement substance between the globules. The enamel edges become ragged and further fracture is imminent. Thread biting produces a similar but localized condition (Fig. 293). Caries by removing the natural support of the enamel renders this brittle material subject to fracture in ordinary use. The removal of dentin from both the mesial and distal sides of a crown by caries — e. g., a bicuspid — renders the buccal or lingual section liable to fracture as the result of a strain delivered between the cusps and tending to wedge them apart. This accident is liable to occur in proportion to the lessening of the healthy dentin between the cavities or beneath the occlusal fissure. An upper incisor so decayed would naturally have its labial section fractured away, particularly its incisal half. The exposure of the dentin of a devitalized tooth to the saliva seems to weaken it. AMiile these principles are correct, it is surprising to what extent enamel undermined by caries may retain its integrity if properly supported by an adhesive oxyphosphate of zinc. The packing of cohesive gold against frail enamel walls renders them liable to direct fracture, or if packed so as to permit leakage the wall is further weakened by lactic acid produced upon its under surface. Again, the improperly prepared cavity margin may be comminuted, a condition favoring the recurrence of caries. Gold does not support enamel walls so well as oxyphosphate. If built over comparatively frail w^alls in such a manner as to protect them from direct impact, they stand fairly well. Inlays of gold serve a useful purpose in this connection. Amalgam by its attendant leakage permits gradual weakening of frail enamel walls. The use of a cement lining, as in combination fillings, is distinctly useful both as a support and prevention of leakage. Johnson^ explains fracture after filling, where the enamel walls were previously undermined but not fractured, upon the theory that previous to filling the pain attendant upon mastication brings about a temporary disuse of the diseased tooth. After filling, comfort ensues, the patient again uses the tooth, and fracture occurs. The fractures caused by blows present features of interest. An I Principles and Practice of Filling Teeth, 308 AFFECTIONS OF THE ENAMEL AND DENTIN Fig. 290 actual splitting off of one of the angular portions of a crbwn may occur, or a fracture may be seen resembling one sometimes seen in a pane of glass the result of a light blow from a stone. In the latter case the cracks radiate from a central crushed spot, and may involve only the enamel. A large section of an incisor may be fractured away and include the labio-incisal third and all the lingual section of the crown and a small, ob- liquely fractured portion of the root. This results from a blow — the exact opposite usually results from occlusal strain. Biting upon hard objects has caused the fracture of sound bicuspids and molars, the line extending mesodistally between the cusps, the fracture being oblique or through the crown and between the roots. Thus a molar or first bicuspid may be divided into two sections, each supported by a root or roots (Figs. 291 and 292). Fracture and repair of enamel after eruption is not, so far as I am aware, known. Cases of fracture and repair of dentin have occurred. A case of such repair by adventitious (sec- ondary) dentin has been recorded by Tomes,^ and Fig. 294 illustrates a fracture of the root well below the gum line. The root is girdled by the line of fracture, but the dentin has been repaired, and the attachment is firm. The line evidently indicates a repair from the pulp side. A case analogous to healing of a comminuted fracture of a central has been reported.^ Fig. 295 illustrates a peculiar fracture due to an unknown cause. In a case reported by Val. Macdonald,^ of a similar fracture, the pulp maintained its vitality in both crown and root for two years, and until the tooth was extracted. There was between crown and root a growth of soft tissue connected with both the pulp and the pericementum, and considered by Macdonald to be pulpal in origin (Fig. 290). In an experimental implantation of a dried tooth filed to fit the socket of a previously extracted tooth union of osseous nature took place, and a slight fracture of the root was reunited by osseous deposition.^ ' A System of Dental Surgery. (See Secondary Dentin.) 2 Watson: Dental Record, May, 1906. ^ Dental Cosmos, January, 1908. * Mendel Joseph and Dessonville: L'Odontologie. (See Cosmos, 1906, p. 1060.) Fracture of two years' standing with pulp vital and a lateral tissue growth resembling granulation tis- sue covering the root face, would explain how the case. Fig. 294, occurred. MECHANICAL INJURY OF THE TEETH 309 Longitudinal cracks in the enamel of otherwise fairly sound teeth occur, the line running from the labial edge of the gum to the incisal edge of an incisor (Fig. 293), or from the fissure of a bicuspid along the enamel to the summit of a cusp, or from the cervical margin of an approximal cavity to the gum margin. Fio. 291 Fig. 292 Oblique fracture. Fracture involving the bifurcation of the roots. These lines probably indicate that force has been applied sufficient to cause a parting of the enamel cap without loss of continuity in the more elastic dentin. Dryness from mouth breathing may be a possible cause of cracks, and the contact of excessively hot or cold substances has been advanced as an hypothesis, but mostly they are found in cases of overworked teeth. In some cases the enamel cracks may be very numerous. These cracks take up stains, and at Fig. 293 Fig. 294 Abrasion associated with fracture of the enamel. Root fracture and reattachment by adven- titious dentin. (From a specimen.) times in the preparation of cavities cause annoyance by centring the chisel and perpetuating a defect necessitating the removal of much tooth tissue or the risking of future caries. Treatment. — The treatment of fractures involves considerations purely operative, and depends upon the nature of the case. Rough- 310 AFFECTIONS OF THE ENAMEL AND DENTIN ened, abraded enamel margins are best rounded with carborundum stones or coarse sand-paper disks, and should be polished. Some- times a deep serration must be filled; corners are to be neatly rounded or restored to contour by fillings or inlays, or at times the entire incisal edge is to be ground away and the tooth drawn down and retained until firm. In case of an uncompleted tooth root, and the pulp not quite exposed, a pure gold all-metal crown is to be adapted with or without grinding, according to the future requirements, and the root com- pletion awaited. If necessary, the capping of the pulp may be attempted as well for the same purpose. After root formation the pulp may be destroyed if desired. If conservation of the pulp be not possible, the pulp may be prepared for removal by pressure anesthesia or cocain injection, and the root filled. (See Root Fillings.) Fig. 295 Fig. 296 Fracture with dovetails for amalgam. (Evans.) Fig. 297 Fracture of portion of upper cuspid, cause unknown. (Skiagraph by E. Ballard Lodge.) Oblique fracture of root, with pin and amalgam for restoration, ready for crowning. Artificial Crown and Bridge-work. (Evans.) Fractures involving the cementum demand either the removal of the loosened piece and the construction of a special crown retaining a portion of the natural crown as a base, or the removal of all of the natural crown and the mounting of a substitute upon the root, or the parts may be banded, or in case of molars an all-metal crown may be mounted. In some cases screws or a staple must be placed in the roots and the parts restored with amalgam (Figs. 297 and 298). If the loosened portion be retained, thin oxychlorid of zinc is to be introduced into the joint after appropriate sterilization, and before the gold crown or holding device is set. It distributes itself by capil- larity if the joint is slightly opened once or twice. Should the pulp MECHANICAL INJURY OF THE TEETH 311 be vital at the time of fracture, it will become inflamed, and should be removed by the pressure method if possible. To accomplish this the parts must be lashed together and an occlusal opening made. After devitalization the parts may be given a dove-tailed form, and be temporarily held together, internally, by amalgam, or a circular band may be inlaid in a trephined groove by Cigrand's method (Fig. 300^). The cuspid root shown in Fig. 298 had an amalgam filling in its mesial side until after the cap and band were constructed. A temporary crown caused the wall to fracture out, so the plan was devised of drilling holes in the root side, tapping them with the How Fig. 29S Fig. 299 Screws placed into a fractured root to enable the building up of amalgam around a waxed pin attached to a gold cap. This root is one of four piers of a nine-tooth bridge. Staple used to unite portions of a fractured root. (Evans.) Fig. 300 Cigrand's method of trephining a root faoe and inlaying a metal ring; also u-seful to prevent fracture when plain dowel crowns are used. tap and placing iridioplatinum screws on both sides of the pulp canal groove. The pin and cap were then waxed slightly, placed in posi- tion, amalgam built in and when hard the wax was melted by heating the cap and pin, which were withdrawn. After thorough hardening the bridge- work was proceeded with. Fortunately the root received its strain from the lingual side, w^hich was largely intact. The requirements vary, and must have due consideration. 1 For certain crowning devices in cases of fracture, see Evans' Crown and Bridge-work, and Goslee's Principles and Practice of Crowning Teeth. CHAPTER X STAINS OF THE ENAMEL AND DENTIN Certain stains are found upon the surface of the enamel and some- times penetrating its substance. The calculus sometimes located upon the enamel is not included in this consideration, though the calculus itself sometimes becomes stained. So far as they have been observed, stains may be divided into those of metallic and non-metallic origin. METALLIC STAINS Metallic stains are those which are caused by the direct depo- sition of minute particles of metal, inhaled by workers in the metals, in the organic collections upon the surfaces of the teeth, or taken into the mouth in various solutions of drugs. Copper. — Miller found that "workers in copper, brass, or bronze all presented a green stain upon the upper teeth, showing every shade of green and bluish green up to bluish purple. The latter color pre- dominated in rooms where phosphor-bronze was worked." Attention is called to th« fact that "trumpeters very often show a discolor- ation of the teeth." Similar discolorations are sometimes noted in proximity to copper amalgam fillings. The presence of copper was demonstrated in scrapings from some of the stained teeth, imparting a characteristic green color to a Bunsen flame. Iron. — "Workers in iron presented stains of a brownish color." As pointed out, "the green salts of iron under the conditions found in the mouth would become oxidized and brownish in color." The administration of iron salts, medicinally, is believed to produce black discolorations, iron sulphid being formed. "Iron deposits are usual in the border-line between carious and normal dentin." It is usually believed that the brownish spots frequently seen in connection with incipient or arrested caries of the underlying enamel are due to the formation of iron salts. Manganese. — Manganese was found in the dark colored deposits upon the teeth of herbivorous animals, but as yet not upon those of man. The investigator stated " that alkaline saliva may be necessary to the production of these deposits." Manganese stains may occur METALLIC STAINS 313 from the use of potassium permanganate, manganic oxid being formed. Mercury. — In cases of prolonged mercurial administration the deposits (black) upon the teeth may give the reaction for mercury, " If mercury and potassium iodid are given together, the green iodid of mercury might be present upon the teeth." It is probable in these cases that another discoloring substance may form. There is in mercurialism more or less gingivitis; the gums are swollen and spongy, bleeding readily. "More or less putrefactive decomposi- tion of the albuminous matter present upon the teeth occurs, and hydrogen sulphid is formed. Reacting upon the oxyhemoglobin of the blood, sulphomethemoglobin is formed — greenish red in concen- trated, green in dilute solutions." Miller ascribes the discoloration found in conditions of gingivitis from various causes, with lack of hygienic care, to a probable reaction between hydrogen sulphid and oxyhemoglobin. Lead. — Hirt (quoted by Miller) found in cases of lead poisoning discolorations upon the teeth: dark brown at the necks, light brown on the crowns, with sometimes a trace of yellowish green. Miller's tests (limited in number) showed no lead reaction from the dental deposits in lead poisoning. Nickel. — Some of the salts of nickel are green. Metallic nickel attacked by fluids of the mouth and mixtures of bread and saliva pro- duce greenish salts. The entire root of a tooth containing a nickel retaining screw has been stained a uniform apple green. Silver.— The dentin of pulpless teeth containing amalgam fillings is sometimes stained black, owing to the formation of silver sulphid. The use of silver nitrate as a wash may cause the albuminate of silver to precipitate salts of silver upon the teeth. If a cavity be touched with silver nitrate and an amalgam filling be introduced, the salts of silver will be instantly fornCied at any point where the silver nitrate and amalgam combine. If this be upon the enamel, the latter will receive a somewhat lasting black stain. The nitrate of silver applied to dentin causes the dentin to assume a light yellowish green tinge, and the albuminate of silver is formed ; later metallic silver is precipitated, the tissue becoming black. Gold. — Gold chlorid stains may be formed during the bleaching of teeth containing gold fillings by the chlorin methods. The dentin becomes first pink, then violet or purple, then black. ^ ■ Kirk: American Text-book of Operative Dentistry. 314 STAINS OF THE ENAMEL AND DENTIN NON-METALLIC STAINS Green Stain. — This most common of green deposits upon enamel occurs upon both the temporary and the permanent teeth, particu- larly of young persons. The deposits usually have a crescentic form, are mainly upon the labial faces of the anterior teeth,, and may be but a narrow line or may cover one-half the labial face. It is unusual for the deposit to extend far into the interproximal spaces, their tendency being to follow the edges of the approximal surfaces. While green stain undoubtedly does form upon adult teeth (Figs. 301 and 302) where clearly the enamel cuticle has long been absent, it is only very common upon young teeth where remnants of Nasmyth's mem- brane persist about their necks. The color of these deposits varies from light green to greenish black. Fig. 301 Extension of green stain on the approximal surface Extension of green stain on the lingual of the incisors. (Miller.) surface of the incisors. (Miller.) If an instrument be passed over the portion of enamel affected, more or less roughness of the surface is evident. If the deposits are subjected to friction with abrasives, they disappear slowly and the enamel beneath may be found roughened. This has led to the belief that these deposits cause decalcification of the enamel.. It is found upon adult teeth that when an area of cervicolabial enamel has become roughened through slight decalcification, a green stain is likely to form upon the rough surface if proper hygienic care be not exercised. It is also found that if the stain be removed by means of abrasives, the roughened enamel may be readily polished — i. e., the decalcification is very superficial. If cases be observed early enough in childhood, it will be noted that green stain is usually preceded by a lack of oral hygiene; collections of food debris are not removed from about the necks of the teeth, which implies that prior to the formation of green stain the affected NON-METALLIC STAINS 315 enamel surfaces have been subjected to the action of fermenting food debris — that is, to acids. These facts liave led to an acceptance of the view that the roughness or decalcification has preceded the green deposits. " If teeth be placed in a 10 per cent, solution of hydrochloric acid, in from two to four minutes the enamel cuticle begins to loosen, and in from five to ten minutes is isolated. It is found that the entire stain comes away with the cuticle." Nature of the Coloring Matter. — The coloring matter is found to be insoluble in water, glycerin, alcohol, ether, chloroform, and oil of turpentine. Mineral acids, hydrochloric, nitric, and nitrohydro- chloric act but slowly upon the coloring matter; even hydrochloric acid requires some hours to completely destroy it. Tincture of iodin, commonly believed to act as a solvent of green stain, was found to affect it but slightly. Both chlorin and nascent oxygen destroy the coloring matter rapidly, the cuticle being bleached in a few minutes by a 10 per cent, solution of hydrogen dioxid. Thick, dark green deposits were incompletely bleached after eight hours' immersion in the 10 per cent. H2O2 solution, pointing to a lack of uniformity in the composition of the stain. The belief that the green coloring matter is chlorophyl is contra- dicted by the fact that it is not soluble in ether. Miller^ regarded the association of the green discoloration with sulphomethemoglobin, or some allied substance, as the most probable explanation, though he found a micrococcus in a deposit of green stain which produced a grayish-green color in glycerin agar. Miller did not find any definite connection between a milk diet and green stain. Goadby^ has found Bacillus liquefaciens fluorescens motilis present in several cases of green stain. It deposits in its culture medium a fluorescent blue-green pigment. Other mouth bacteria produce a greenish pigment — e. g., Bacillus pyocyaneus and Bacillus fluorescens non-liquefaciens.^ The deposits of green stain are considered to be secondary to enamel decalcification rather than the cause of it, when found in connection with it. In case of roughened enamel, green stain appears at times to have been taken into its substance, rendering removal without bleaching difficult. Black Stain. — A peculiar black stain occurs in the mouths of appar- ently healthy individuals, both men and women, and smokers and non-smokers, and even with those also who drink neither tea nor coffee. It occupies the general position described for green stain, 1 Dental Cosmos, 1894. = Mycology of the Mouth, s Ibid. 316 STAINS OF THE ENAMEL AND DENTIN but may cover much of the surface of the teeth. It occurs in some- what unclean mouths, though the teeth may have been regularly brushed. As a rule, those teeth having the deposit are comparatively free from caries. Its etiology is not worked out, but it may be due to a formation of iron sulphid in place of sulphomethemogiobin. It is very readily removed, and does not, as a rule, affect the enamel. At times a superficial caries is found associated with it, and at some minute spot the enamel may be penetrated. Whether this cavity is a result of the action of the film is not certain. Tobacco Stains. — Smokers have characteristic black deposits upon both the teeth and calculus deposited upon them. The stain is most marked upon the lingual surfaces of the teeth, and a pipestem held well back in the mouth may cause a thick deposit upon some of the posterior teeth. Tobacco juice itself stains exposed dentin and cementum, and enters cracks in the enamel, producing brown discolorations very difficult or impossible to remove. Red Stain. — A peculiar red stain occurs upon the necks of some teeth, but is not generally distributed. It is probably due to chromogenic bacteria, as it is only found on unclean surfaces. According to Goadby,^ Bacillus prodigiosus. Bacillus rouge de Kiel, Bacillus mesentericus ruber. Bacillus roseus, Sarcina roseus. Micro- coccus roseus, and other micrococci produce a red pigment in at least some of their media. Sarcina lutea and Sarcina aurantiaca produce yellow and orange- colored pigment respectively.^ The exact relation of chromogenic bacteria to stains is not worked out. DENTIN STAINS Exposed dentin may be stained as enamel is. In addition it may take up certain stains like tobacco. Metallic fillings, such as amalgam, containing mercury, silver, copper, or cadmium metals which combine with sulphuretted hydrogen to form sulphids, may cause staining of dentin. Metallic posts containing silver, copper, or nickel, or made of steel or iron wire, may produce sulphids in the same manner. The dentin may also be stained pink by hemoglobin entering the tubules during the progress of venous hyperemia. This finally develops iron sulphid. 1 Mycology of the Mouth. 2 Ibid. TREATMENT OF STAINS 317 The dentin may also be stained by iron sulphid formed during putrefaction of the pulp, by the action of ammonium sulphid upon the iron contained in the hemoglobin of the blood undergoing decomposition. TREATMENT OF STAINS Enamel stains are best removed by mechanical means, after the removal of calculus from the teeth. (See Salivary Calculus.) For this purpose brush wheels and rubber cups charged with pumice and revolved in the dental engine are used to remove the accessible por- tions of the stains. Next a wood point, made by sharpening an orange-wood stick or hickory shoe-peg to a wedge-shape, is charged with the pumice and rubbed by hand over all the surfaces not reached by the brushes and cups. For the more inaccessible situations the point is to be mounted in a Jack or other porte polisher. A very fine linen tape, a German silver strip, or flat floss silk charged with pumice will remove the stains at the contact points. A very small finishing bur or dull ordinary No. 1 or No. ^ bur is useful upon lingual surfaces or in grooves. The powdered pumice used is best mixed with glycerin to prevent the flying of the pumice during the rapid revolution of the wheels. Saturation of the stains with tincture of iodin followed by a douche of water renders them more visible, and also brings to view the associated bacterial films upon the teeth. Register recommends the use of 1 per cent, hydrogen dioxid, to be forcibly sprayed upon the gums and deposits both before and after the use of tincture of iodin. The brush and pumice will then rapidly remove the stains and bacterial films upon the accessible portions of the teeth. Tobacco stains in cementum need not be removed to their full depth. Head^ has suggested the removal of deep enamel stains and the deposits in irregular depressions and joints of inlays, inaccessible to the stick, by the use of nascent oxygen derived from 25 per cent, ethereal pyrozone, or a paste of sodium dioxid and water, made by dissolving the latter in distilled water at about 32° F. These are applied to the part on cotton, and nascent oxygen liberated with a hot burnisher. The face and gums are protected by the securely placed rubber dam and by oiling the face. 1 Items of Interest, 1902. 318 STAINS OF THE ENAMEL AND DENTIN The method is also appHcable to the bleaching of obstinate stains of the dentin, especially near the cutting egdes. In the joints of inlays fresh cement is to be rubbed — preferably the silicates — in order to prevent a rediscoloration. If beneath green stains decalcification be discovered, the decal- cified area should be removed, the enamel polished, and the patient urged to careful prophylaxis. After the removal of calculus and stains from the teeth the mouth and teeth should be kept in as cleanly and aseptic a state as possible by the employment of correct prophylactic measures. Dental caries and pyorrhea alveolaris are thus also largely prevented. (See Pro- phylaxis of Dental Caries and Pyorrhea Alveolaris.) The stains found in the dentin are also divisible into metallic and non-metallic. The former are best removed by transforming the insoluble metallic salt into a soluble one. The most frequent and practicable course is to form soluble chlorids through the action of nascent chlorin. Copper, nickel, gold, and iron stains should be subjected to the chlorin method of bleaching, followed by repeated washings with chlorin water, 50 per cent., and hot distilled water to remove the chlorid formed.^ Silver stains are converted into silver chlorid by the chlorin method, or iodid by the use of tincture of iodin, and dissolved out by the use of sodium hyposulphite followed by hot distilled water.^ For mercurial stains Kirk recommends the use of aqueous, ammo- niacal solution of hydrogen dioxid after the chlorin method, and a saturated solution of potassium iodid after the iodin method, in either case followed by washing with hot distilled water. Manganese stain is removable by the use of 25 per cent, aqueous solution of hydrogen dioxid saturated with oxalic acid crystals and followed by washing with hot water. The non-metallijc dentin stains are removable by the use of chlorin evolved from chlorinated lime by the reaction with dilute acetic acid, or of nascent oxygen evolved from hydrogen dioxid or sodium dioxid. In either case the color molecule is destroyed by the indirect or direct oxidizing effect. The hydrogen dioxid may be used in the form of the 25 per cent, ethereal solution (25 per cent, pyrozone) applied for a time or sealed within the tooth for twenty-four hours, or the 25 per cent, aqueous solution may be driven into the tubuli by the aid of the cataphoric current. 1 Kirk. 2 Ibid. TREATMENT OF STAINS 319 Sodium dioxid should be employed in saturated solution in distilled water (made at about 32° F.). The dentin is first desiccated and then saturated with the solution. ^Yeak sulphuric acid (10 per cent.) is used to liberate the nascent oxygen. Kirk recommends a second application, omitting the use of the acid. As with metallic stains, all the by-products should be washed out with hot distilled water. ^ A further description will be given under the caption of Moist Gangrene of the Pulp. • For a complete description of the bleaching process, see Kirk's article in American Text-book of Operative Dentistry. CHAPTER XI DENTAL CARIES: HISTORY; EXCITING AND PREDISPOSING CAUSES Definition. — Dental caries may be defined as a disease of a tooth characterized chiefly by the production of a locahzed cavity, con- cavity, or area containing decalcified tooth structure and due to a combined acid fermentation and liquefaction. History. — Examinations of crania show the disease to be certainly as old as semicivilization, and when more data are obtainable it will, no doubt, be found even older. The skull of a mummy in the British Museum, dating 2800 B.C., exhibits well-marked caries and other dental diseases. Caries appears in the teeth of the skulls of all peoples, no matter what their degree of civilization, provided their dietary included cooked, starchy foods. Causes. — These may be divided into exciting and predisposing. Prior to the investigations of Miller,^ published in 1882, a vast amount of labor was expended in the effort to determine the cause of dental caries. The deductions made were partly speculative and partly based upon scientific investigations. From 1754 to 1835 caries was regarded as an inflammation or gangrene of tooth structure; Boudett, Jourdain, Hunter, Fox, Bell, Fitch, and Koecker advancing one or the other theory.^ In 1835 Robertson,^ of Birmingham, England, advanced the opinion, based upon his observations, that it " is to chemical and not to inflammatory action that the destruction of the teeth must be attributed." The author pointed out forcibly the errors and fallacies of previous writers. He stated that "Particles of food retained in fissures and imperfections of the teeth and in the spaces between the teeth undergo a process of decomposition and acquire the property of corroding, disuniting, and therefore destroying the earthy and animal substances of which the teeth are composed." John Tomes, a little later, was the first to record microscopic examinations of carious dentin. He described the transparent zone 1 International Dental Journal, 1884. 2 For an interesting and exhaustive exposition of their views, see American System of Dentistry, Section on Dental Pathology, by Black. ' A Practical Treatise on the Human Teeth, second edition, Philadelphia, 1839. HISTORY AND EXCITING CAUSES 321 lying between the carious and non-carious dentin, and observed and pointed out also the dentinal fibrillse. He announced the very significant fact in relation to caries, that if blue litmus paper be applied to a carious cavity it is at once reddened, which furnishes evidence of the presence of an agent capable, if unresisted by the vitality of the dentin, of depriving the tissue of its earthy constitu- ents, leaving the "gelatin to undergo a gradual decomposition favored by the heat and moisture of the mouth." Tomes first established the essentially chemical character of some features of caries. The character of the acid and its localization were, however, not ascertained. In 1807 Bridgman promulgated the theory that the crown of the tooth and the gum were of dift'erent electrical potential, and that being bathed in the oral fluids the conditions of a battery were set up. Acid substances were said to be set free at the positive pole (the crown), causing decalcification. S. B. Palmer, in 1874, claimed that after filling recurrent caries was caused by the conditions of a battery being set up — i. e., the differ- ence of electrical potential between the filling and dentin in the presence of saliva or of the fluid of the dentin as an electrolyte caused liberation of acids, producing decalcification of the tooth or disintegration of the filling — e. g., oxyphosphate. Miller, in 1881 and 1900/ experimentally examined these assump- tions. He ground the enamel away from the crowns of freshly extracted teeth and filled cavities made in them with gold and gutta- percha. These he placed in separate flasks containing a physiological salt solution (0.75 per cent, sodium chlorid). This, in the presence of electric currents, should produce hydrochloric acid by liberation of hydrogen and chlorin, and decalcification should occur. After four years there was no decalcification. Similarly filled teeth were suspended in dilute lactic acid. The decalcification was exactly similar to that in the unfilled pieces used as a control. Had electrolytic currents been generated between the metals and dentin, the latter would have been acted upon more vigorously than in the unfilled pieces. In 1868 Watt- advanced the theory that free sulphuric, nitric, and hydrochloric acids were generated in the mouth during putrefactive processes and caused the different varieties of caries. ]Magitot^ pointed out that the essential phenomena of caries, as they were then understood, were the same in natural teeth mounted upon plates as in the natural organs in situ; proving that caries is 1 Dental Cosmos, April, 1901. 2 Chemical Essays, 1868. ^ Treatise on Dental Caries, Experimental and Therapeutical Investigations. 21 322 DENTAL CARIES intrinsically independent of existence of vitality. By immersing teeth in solutions of sugar undergoing fermentative changes he found that decalcification occurred. Teeth immersed in solutions of sugar in which fermentation had been prevented by boiling the solution and sealing, or by additions of sufficient carbolic acid, remained unaffected. Leber and Rottenstein, in 1867, first called attention to the probable causative association of bacteria with some phases of dental caries. By staining carious dentin with iodin the dilated dentinal tubules were shown to be filled with granular bodies, which they recognized as bacteria, identifying but one of the many forms of oral bacteria — the leptothrix. They deemed an initial exposure of dentin a necessary preliminary to the invasion and growth of the leptothrix, which in conditions of lessened resistance gained access to the tubules and in* some undescribed manner caused their dilatation. The question of the recognition of the presence of bacteria directly resolves itself into the subject of special staining. Prior to the work of Koch, presented in 1881, no means of isolating specific bacteria by special cultures and staining were known, and it is remarkable that in the same year the essential features of dental caries were first made out with some degree of clearness. Miles and Underwood (World's Medical Congress, 1881) pointed out clearly and at length the different appearances produced by simple decalcification of dentin and those by dental caries. Speak- ing of Magitot's experiments, they say: "We assume that two factors have always been in operation: (1) The action of acids and (2) the action of germs. When caries occurs in mouths it is always under circumstances more favorable to the action of germs than to the action of acids." They believed that the acids necessary for the decalcification were excreted by the germs, which utilized the dentinal fibrillse as a food supply. It will be seen that the invasion and multiplication of organisms in the tubuli were held as the antecedent of the process of decalcifica- tion. The deductions of these gentlemen were drawn from data not derived from the methods of modern bacteriology — i. e., special stains and special cultures. Moreover, they were made before the physiological chemistry of bacteria was even partially understood. In 1882 W. D. Miller, of Berlin, announced, as the results of experiments conducted by him, that he believed the first stage of dental caries to consist of a decalcification of the tissues of the teeth by acids which are for the greater part generated in the mouth by fermentation. This, it will be seen, is a position in agreement with that of Robertson. EXCITING CAUSES 323 Miller's observations and experiments established the following basal facts in connection with dental caries: 1. That in all cases of dental caries microorganisms may be seen under the microscope in the tubules of the carious dentin, and that bacteria exist in great numbers in the mouth. 2. That the invasion of the tubules is always preceded by decalcification of the dentin — i. e., an area, sometimes rela- tively large, of decalcified dentin may be seen in advance of the organisms. 3. Analysis of the softened dentin proved that a large part of its lime salts were removed — i. e., decalcification had occurred. 4. Test with litmus paper gave the acid reaction in nearly every case, so that the inference that decalcification was due to an acid was warrantable. 5. The food substances taken into the mouth are of all classes. Carbohydrates (sugars and starches), hydrocarbons (fats), and nitrogenous (albuminous) materials. The carbohydrates are fermented with acid reaction by many mouth bacteria, commonly producing lactic acid; the albumins ferment with an alkaline reaction. It was inferred from this and other experiments that caries was due to the acid fermentation of carbohydrates and not directly to the fermentation of albuminous substances. 6. That oral fermentation is the result of bacterial action his following fundamental experiments show: (a) A small tube was filled with a solution of starch and fastened to a molar tooth on retiring. The next morning the contents of the tube had a strong acid reaction. A tube of the starch solution with saliva added was incubated at blood temperature. After four or five hours the mixture became acid. (b) The mixture of starch and saliva was kept at 100° C. for a half hour, and incubated. It did not become acid — /. e., the exposure to this temperature killed the ferment. (c) The saliva was boiled for a half hour and then added to the starch solution and the mixture incubated. No acid was produced — i. e., the ferment existed in the saliva, not in the starch. (d) The ptyalin of the saliva was destroyed by heating the mixture for twenty minutes at 67° C; the incubated mixture still became acid — i. e., ptyalin did not act as the acid-forming ferment, but the fermentation must have been caused by some other ferment not destroyed by exposure to this temperature. (e) To the mixture of saliva and starch carbolic acid was added as an antiseptic. No acid was formed, but the ptyalin changed the 324 DENTAL CARIES starch to sugar — i. e., the acid forming-bacteria were inhibited, the ptyahn not. (/) A number of tubes were each supplied with a small quantity of the saliva-starch solution and sterilized ; a third of them were infected from the mouth, a third by carious dentin, and a third were left uninfected as controls. The infected tubes became acid; the controls did not. {g) The first of a series of tubes containing sterilized saliva and starch solution was infected with carious dentin; when this became acid a fraction of a drop was carried from it to a second tube. After that became acid a third was infected from it, and so on indefinitely. Conclusion. — Carious dentin contains a ferment or ferments capable of reproduction — i. e., living organisms are present in it. 7. The nature of this living ferment was determined by infecting a culture medium with carious dentin taken from the deeper layers. The bacteria cultivated were distended into pure cultures by carry- ing through a series of cultures and examining microscopically during the process. The same morphological characteristics were exhibited in the last tube, as shown by the germs in the deeper layers of carious dentin itself, and was identical with that of Bacterium acidi lactici. These germs may be found in the sediment of a culture tube, and consist of cocci and micrococci, either single or in chains. These cocci possess the power of forming lactic acid from glucose. The organism is a facultative anaerobe (Fig. 303). 8. A sound bicuspid was sawed into sections, and an equal number of these sectiens placed in each of two test-tubes. Upon these was poured a 2 per cent, aqueous extract of beef (albuminous). To one tube a minute portion (0.2 per cent.) of cane-sugar was added. Both tubes were sterilized, and after cooling infected with a pure culture of the germ obtained from the deeper layer of carious dentin. The sugar-containing solution became acid in a few hours; in a week the dentin was softened; in two weeks thin sections were completely decalcified; in three weeks cavities were found in the dentin exactly similar to cavities formed in teeth in the mouth and presenting under the microscope other phenomena of caries to be described later. A more prolonged fermentation resulted in the complete disintegra- tion of the slabs of dentin, a proof of the fact that one organism may comiAetely destroy dentin. In the tube containing only the extract of beef no acid was pro- duced, and no decalcification of the dentin occurred. From these facts Miller argued that putrefaction does not initiate the process of dental caries, and may not be essential to the destruc- tion of either the inorganic or organic dental elements. EXCITING CAUSES 325 9. That the acid produced was lactic acid Miller demonstrated as follows: Starch and saliva were mixed and fermentation induced. This was then checked by sterilization with heat. A quantity of material being collected in this manner, the whole was concentrated by evaporation, and tested w^ith a solution of methyl violet, which would turn first blue and then green with an inorganic acid. Not so reacting, and not distilling off during the concentration, the acid present was pronounced a non-volatile organic acid. The concen- trate was shaken with a quantity of ether, which dissolved the organic acid present. When the solution was clear it was filtered and the ether partially distilled off, when the partially concentrated solution was further concentrated over a water bath and then mixed with an excess of freshly prepared zinc oxid. The w^hole was boiled, water Fig. 303 Fig. 304 „ J 5 6 7 12345-1 \d « o ^% being added as needed, until the solution became neutral, when it was set aside to crystallize. A drop placed upon a slide under the microscope showed the forms of crystals of zinc lactate (Fig. 304). By testing the molecular weight of the washed and dried crystals it was determined clearly that the substance was zinc lactate. In practically a similar manner lactic acid was obtained directly from carious dentin. While Miller demonstrated the ability of one organism to produce all the essential phenomena of caries, including liquefaction of the dentin, he did not claim that only one or two organisms are involved in the process, but that "any germs possessing the power of producing acid fermentation of food may and do take part in the first stage of caries, and that all those possessing a peptonizing or digestive action upon albuminous substances may take part in the second stage; 326 DENTAL CARIES and that those possessing both properties may take part in both stages."^ He was of the opinion that it is not the presence of this or that kind of bacterium, but rather the joint activity of the total flora as expressed in intensity of fermentation in food particles which deter- mines the extent of caries. Out of eighteen mouth bacteria examined, Miller found ten that produced lactic acid in sugar-containing solutions.^ He also found acetic and butyric acid to be by-products. Hinkins and Acree,^ in experiments upon pure cultures of a number of oral bacteria in various artificial media, found lactic, butyric, valerianic, formic, carbonic, and hydrosulphuric acids as either principal or by-products of the fermentation. It is quite clear from Miller's demonstrations that bacteria, or at least one bacterium, are the exciting causes of dental caries; and that for their function as such they require carbohydrate material as food. Their action upon these substances has been studied. The carbo- hydrates introduced into the mouth as food are monosaccharids, disaccharids, and polysaccharids. (1) The monosaccharids or glu- coses have the general formula C6H12O6, and are represented by dextrose and levulose, found in seeds, fruits, roots, honey, and in many forms of candy, such as peanut brittle and glaces, and galac- tose formed from lactose or milk sugar by hydrolysis. These ferment directly into lactic acid without formation of gas. C6H12O2 + bacterial ferment = 2C3H6O3. A certain proportion of the glucose, etc., is appropriated by the bacteria as food. (2) Disaccharids or saccharoses have the general formula C12H22O11. The principal one is saccharose, found in sugar- cane, the sugar-beet, sugar-maple, and maize. This is inverted by the ferment of the bacteria into glucose and levulose through a process of hydration : C12H22O11 + H2O + bacterial ferment = C6H12O6 + C6H12O6. Two other disaccharids enter the mouth or are formed therein: lactose and maltose, both Ci2H220n (H2O). Lactose exists in milk and by hydrolysis is changed by bacteria to galactose, 2C6H12O6, and then ferments like other monosaccharids. Maltose is an intermediate product in the formation of glucose from starch, and is produced by 1 Microorganisms of the Human Mouth. ^ Ibid. 3 Dental Cosmos, 1901. EXCITING CAUSES 327 the action of ptyalin. It is also directly fermentable by some bac- teria (Goadby). (3) Polysaccharids or amyloses with the general formula (C6Hio06)n. Starch, cellulose, glycogen, and gum. Starch was found by Miller not to undergo direct fermentation by mouth bacteria — i. e., culture media containing starch but not sugar when infected by bacteria did not ferment into lactic acid unless ptyalin was present.^ When saliva was used, however, the acid reaction occurred, owing to the formation of glucose through the action of ptyalin. In oral fermentation starch is first changed by ptyalin to maltose by hydration, and the maltose to glucose. Then the bacteria changes this to lactic acid. 2C6H10O5 + 2H2O + ptyalin = daHzzOnCHaO). Starch. Water. Maltose. Ci2H220u(H20) + ptyalin = 2C6H12O6. Maltose. 2C6Hi206 + bacterial ferment = 4C3H6O3. In a serial of seven papers in the American Dental Journal, beginning November, 1910, J. Oxford Keller, D.D.S., endeavors to establish the claim that dental caries is produced by causes existing in the saliva apart from organic acids produced by microorganisms. The causes ascribed are: 1. Neutral salts — a chemical combination of acid and base, as potassium phosphate. 2. Neutral salt acid or neutral salts with excess acidity. 3. Neutral salt alkaline or neutral salts with excess alkalinity. These by chemism are supposed to extract the salts from tooth structure. After making the assertion that lactic acid has never been discovered even in trace in human saliva, he states that such acids as lactic, sulphuric, muriatic, acetic, oxalic, phosphoric, malic, and carbonic may be contained in saliva in combination or association. (Compare with Miller's deter- mination of lactic acid in carious dentin. — Editor.) He states that lactic acid does not develop in the mouth in sufficient strength to cause caries; that full digestive fermentation necessary to produce lactic acid requires from three to six days, and any found would be neutralized by the alkaline saliva. (Compare with Miller's Experixnent, No. 6, a. — Editor.) The editor has carefully read these papers, but can see no reason to disturb the text of. this work on their account, for the reasons that: 1. The microbic plaques are always present in enamel in incipient decay, and should protect against the access of saliva to enamel. Certainly it would have to contend with them, but when the carbohydrate element in it is considered, it is probable it furnishes them their pabulum. 2. That acid may exist in a cavity while the saliva is alkaline, and can be often noted in food masses collected on teeth, and can be demonstrated to patients by the aid of litmus paper. 3. That caries is clinically noted in the exact locations in which plaques are found is demonstrable with tincture of iodin, whereas if salivary salts are alone responsible, there is no reason why clean spots should not be affected. 4. That where saliva is most abundant decay occurs least, as a rule. ' 5. Because the author has by no means shown how the salts of saliva produce decay, as his experiments with concentrated saliva, which disintegrated teeth after two or three years may have contained concentrated acid, and as compared with Miller's experiment No. 8, seems uncon- vincing. 6. Black has shown that the plaques formed by saliva in formation of calculus are the habitat of bacteria after twenty-four hours, hence their agency is hard to exclude. 1 American System of Dentistry, vol. i, p. 805. 328 DENTAL CARIES According to Goadby^ a few bacteria found in the mouth can pro- duce the change direct from starch to maltose and thence to acid. This is of no practical consequence, however, as ptyalin is always present in the mouth. (See- Miller above.) Glycogen, CeHioOg, or animal starch, is fermented to glucose by liver cell ferment, and probably exists in the oral epithelium in certain states as well as in the saliva in others, hence a systemic state may introduce gliicose (in diabetes). (See Glycogenic Infiltration and pages 95, 334, and 338.) Miller has demonstrated that bacteria produce acid from starches and sugars in about equal proportions, provided the starches are cooked. The cooking of starchy foods bursts the starch granules and renders them more adhesive to the teeth, as well as more fer- mentable. The following synopsis of experiments^ made with food mixed with saliva in definite quantities speaks for itself: Material. Duration of experiment. Acid formed, in units. s Bread, starch, potato, maccaroni, rice, corn, and other cooked starches 12 and 30 hours. 20 to 25 and 42 to 110 Raw starches, potato, spinach, etc. 12 and 30 hours. Cane-sugar and grape-sugar . . 12 and 30 hours. 17 to 20 and 37 to 41 Meats, fish, eggs, etc 12 and 30 hours. or alkaline The table shows that albuminous materials and raw starches produce no acid and are not concerned in caries except in so far as meats, etc., act as culture media perpetuating bacteria which later may produce an acid reaction in carbohydrate materials. The fats maj^ be fermented with production of fatty acids. Goadby has found these of no importance in relation to caries, but Miller has shown that the acids found in dermoid cysts, among which are fatty acids, can produce decalcification; as other acids, as oxalic, were present, the relation of fatty acids is not quite clear. Miller asserts that fats deposited upon the teeth, as well as calculus retard decay, and that fat mixed with saliva will give an alkaline reaction.^ Milk contains a carbohydrate (lactose) and often lactic acid bacilli. It therefore may supply both the bacilli and their food. This, however, only has relation to caries after plaque formation or by retention of acid milk against the teeth. That such a result may occur has been shown by Bennett. That alkalies do not produce tooth disintegration in the mouth is ' Mycology of the Mouth. ^ Microorganisms of the Human Mouth. ' An acid unit equals the amount of acid necessary to neutralize 0.1 c.c. of a 0.5 per cent, solu- tion of potassium hydrate— e. g., if in an indefinite quantity of acid material 25 of such alkaline units are necessary to neutralize the reaction, there were 25 acid units present in it. « Dental Cosmos, 1904. EXCITING CAUSES 329 shown by the fact that a tooth is not affected by alkaline solutions which are not strong enough to injure the soft parts. The influence of carbohydrate diet in the production of caries is well shown by tables compiled by Mummery and quoted by Miller.^ The races consuming a fish and meat diet almost exclusively — e. g., the Esquimaux — are recorded as having about 3 per cent, of caries in skulls examined, while those using a mixed or vegetable diet have from 10 to 40 per cent, of caries. A most convincing example is that given by Miller of two related tribes living on either side of the Andes, in the Argentine Republic, and Chili respectively. The former, a cattle breeding and meat eating tribe, were practically free from caries, while the latter, living on mixed foods, and consuming sugar, had 19 per cent, of caries. While the fermentation of carbohydrate food debris into acid is conceded to be the active exciting cause of dental caries, the modus operandi of the inception has not been satisfactorily settled. Miller held that as he was able to find bacterial plaques upon many sur- faces of teeth, even in the mouths of immunes without caries beneath, the plaques had no relation to the inception of caries of enamel, but that the carbohydrate food collecting at favoring spots undergoes acid fermentation, with production of enamel decalcification, after which the bacteria enter. By experiments he determined that the plaques rather hindered the action of acids experimentally used as a decalcifying agent. Black, on the other hand, claims that the bacteria produce a gelatinoid material and are left upon the teeth in the form of a plaque or zooglea mass, and that the plaque is a thin, transparent, slightly yellowish film not seen without close inspection. (It can be stained by iodin. — Editor.) Williams found a film of bacteria over the decalcified area in almost all cases of superficial caries of enamel, and that it has sufficient resistance to permit grinding in situ (Figs. 320 and 321). Goadby frequently found on the opaque white patches of softened enamel a coccus to which Williams called attention, which would cause a plaque deposition upon teeth suspended in its culture, and that when acid-producing bacteria were mixed with the coccus and a carbohydrate medium used, superficial decalcification of the enamel under the plaques was produced in from a week to ten days. Miller also showed that in the immune with unclean teeth the putrefactive reaction was the dominant one, and that the collection, if persistent, could act as a protective against the access of acid- producing material. 1 Microorganisms of the Human Mouth. 330 DENTAL CARIES In the above data we find that the plaques are almost universal, even on immune surfaces (Miller), so that their presence on a decal- cifying surface is probably true, as claimed by Williams. If, then, they are a protection against the acids produced from carbohydrate they should protect, but they do not. Secondly, experiments with formed acids are not conclusive, as they may even be germicidal and the dead film might be a relative protection against decalcification by the acids. Thirdly, the bacterial films, if containing acid-pro- ducing bacteria, can easily take up any carbohydrate food collected against them, form acid from it, which they then pass to the enamel in a nascent state, hold it against it, and permit it to abstract the calcium salts, which they then pass out as lactates, etc., or allow to remain in situ. This latter conclusion in the main is the theory of Black, and while the decalcifying ability of infected carbohydrate food without the intervention of the plaques is a possibility, it seems a reasonable conclusion to admit the activity of the plaques. Kirk has shown that the precipitation of mucin from saliva rich in mucin content by lactic acid produced by lactic acid bacilli plays a part in the development of the plaques, or by binding the bacteria together creates a bacterial plaque. The frequent disturbance of the plaques by monthly cleansings (prophylaxis) also prevents dental caries in large degree, so that they must have some relation to the inception, though it is only fair to state that a constant warfare against any species of bacteria doubtless vastly reduces their number in the mouth. Noyes^ claims that in well-cared-for mouths the confinement of acid under the plaques is great, while in uncared-for mouths, though much acid is formed, it may be dissipated in the saliva and the teeth not be much attacked. This argument, however, does not take into consideration the idea of Miller that stagnant materials take on a putrefactive reaction after the acid production is exhausted (see p. 341). The Predisposing Causes of Caries. — The causes of the predis- position to caries are local and general. Local Predisposing Causes. — So invariably does caries begin in sulci or pits upon approximal surfaces, about defective fillings, and upon unclean surfaces, that faults of form or retentive nature of approximation, defects, and faulty position of the teeth must bear a relation to the difficulty of keeping the parts free from accumulations of bacteria and carbohydrates. These local predisposing causes, as they are called, are simply 1 Items of Interest, 1909, p. 750. PREDISPOSING CAUSES 331 conditions favoring the formation of the bacterial plaques upon the teeth and the retention of carbohydrate food. Faults of Form. — Deep pits or sulci in the occlusal surfaces of bicuspids or the occlusal or buccal surfaces of molars, or in the lingual surfaces of incisors, and occasionally cuspids, or pits upon the cusps of bicuspids or molars, or in other unusual situations, are not sub- jected to a cleansing friction, and so permit bacteria to form plaques in these locations (Figs. 306 to 319). The nature of the approximal contact has to do with the inception of caries. Teeth are seen in which the approximal surfaces are well rounded and their buccal and lingual angles free from approximation. Such teeth are usually relatively narrow at their cervices, so that these also recede well from the line of contact. A V-shaped space is formed which the gum festoon normally nearly fills. Such per- fection of contour is also, as a rule, associated with a perfect organi- zation of the enamel structure, in virtue of which the surface is smooth. While such teeth may decay approximally, there is much less tendency to caries (Fig. 322). Opposed to this, approximations exist of a broad nature. Broad approximations are very common, and not infrequently are asso- ciated with a certain degree of enamel opacity and an unevenness of enamel surface plainly visible to the naked eye. The fluid exuded by the gum is normally alkaline in character, and probably neutralizes the products of acid fermentation. In view of this fact, the first-mentioned form of contact evidently affords more of this immunizing principle. The extension of cavity margins beneath the gum has been strongly indicated by experience as good practice, and probably is explainable upon the same ground. There is also some evidence that the gum has some cleansing action (prob- ably phagocytic) upon metal placed beneath it, as it is noted that when unclean gold crowns are removed the portion extending beneath the gum is usually quite clean. With the narrow approximations saliva is readily forced between the teeth and neutralizes the acids formed, or washes away soluble carbohydrates, the food for the bacteria. With the broad approxima- tions such a result is less likely to occur. Stagnant saliva retaining carbohydrates probably will develop an acid reaction. (Miller.) A depressed approximal surface may decay, but frequently does not. An acquired fault of form requires notice. Anatomically the gum covers the cementum and the enamel margin. When recession of the gum occurs, the cementum is left 332 DENTAL CARIES exposed and food debris accumulates at the angle formed by it with the gum. Owing to the cementum being less smooth than enamel, microbic plaques readily collect, hence decay of the cementum frequently occurs, and is apt to progress rapidly, owing to the natural low percentage of inorganic matter. (See Figs. 312 and 316.) Arrangement and Position of the Teeth. — The overlapping of one tooth upon another creates a form of contact producing a tendency to decay at that point. Angle^ claims to have observed a comparative freedom from caries of very irregular teeth (Fig. 319). The presence of a supernumerary third molar lying at the buccal side of the interdental space between the second and third upper molar, or an inlocked bicuspid, very frequently causes approximal caries at the contact points. The upper third and lower third molars frequently stand in bad relation to the cheek or the gum. Food collects upon their buccal surfaces, or they are not subjected to the friction of the tooth-brush, and decalcification of a broad area of a buccal surface frequently results. Defects about Fillings. — Under the caption of Recurrence of Caries will be found a list of the causes which perpetuate caries about fillings. Defectively cemented bands are also a cause. I believe the abundance of these and a lack of oral hygiene to be, in a large degree, the measure of a tendency to persistent caries. A patient has a large number of cavities due to a period of negligence with consequent intensity of oral fermentation. If these are obliterated in the best manner with physically perfect fillings, and oral hygiene be exact, the tendency to caries is largely obliterated. If, on the other hand, a large number of even slightly defective fillings are made, not only is recurrent caries induced, but the caries ferment is continuously active, and exact oral hygiene is an impossibility. The number of cleansings a day is no guarantee of perfect hygiene, even with perfect teeth, as nothing is more common than to see unclean embra- sures easily taking the stain of tincture of iodin even in the anterior part of the mouth (in less degree than shown in Fig. 305). Unques- tionably food debris may even be swept into the interdental spaces by brushing alone. Miller^ has shown that a mixture of bread and saliva may become decidedly acid in one hour, and superficially decalcify sections of dentin in five hours. With this going on, day after day, in cases of soluble teeth and without other aid than brushing, and often this not thoroughly done, the persistence of decay is not surprising. This, however, does not prove the absence of systemic susceptibility or immunity as an added cause of caries 1 Dental Cosmos, 1903. 2 Ibid., 1905. PREDISPOSING CAUSES 333 or its absence. A condition similar to a defect about a filling is that of the presence of an orthodontic appliance which may afford convenient nooks for caries, fungi, and food. Other Local Predisposing Causes. — Acids taken in excess into the mouth may act as predisponents by causing a roughness of the enamel, which invites the formation of the bacterial plaques. A course of tincture of ferric chlorid has a bad reputation in this con- nection. In the cases observed by the editor the hydrochloric acid in the tincture seemed to have formed roughnesses between the teeth, and many large ca\ities of not unusual form were later pro- duced and evidently due to the carious process. Morjenstern^ describes experiments that show that acid iron waters or tinctures have a decalcifying action, ferrous iodid and ferric chlorid being particularly injurious, while reduced iron, saccharated solution of iron, and albuminate of iron produced no ill effects either local or through systemic action. The acid vomitus of pregnancy and seasickness have an analogous effect. It is not likely, however, that during a transatlantic voyage large cavities can develop. The probable explanation of the presence of such cavities directly after the voyage is that they existed before the voyage was begun. Cavities are frequently left or overlooked. (See Prophylaxis of Caries.) Since the advent of medication by lactic acid preparations and those containing lactic acid bacilli, such as sour milk, analogous effects have been observed, and therefore the mouth should be washed out with alkaline antiseptics after such remedies are taken. ^ Miller found that the saliva has no antiseptic quality as a whole and contains no antiseptic substance, and though he found the saliva of immunes to develop a little less acid than that of highly susceptible individuals, the difference was not constant and not sufficient to account for the marked difference in susceptibility. IMiller found that carbohydrate foodstuffs mixed with an alkaline saliva became even more acid than when the reaction of the saliva was intensely acid and the chance for caries was about the same with either reaction at the start. Under conditions of oral irritation, such as catarrhal stomatitis, or even the presence of many cavities of decay, a stringy, mucinous condition of the saliva may result. This may be due to a partial coagulation of the mucin by the acid present in the mouth, and the coagulum may entangle food masses and cause their adherence to the teeth. • Therapeutische Monatshefte, 1908. 2 Vanel, Dental Cosmos, 1910, p. 694. 334 DENTAL CARIES The contention of Lohmann that the carbohydrate element in mucin was the cause of caries Miller examined experimentally and found it untenable, but that the explanation here given of its entang- ling action is the probable one. Nevertheless, as shown by Kirk, the presence of such a soluble carbohydrate is a fact, and may furnish the pabulum for the lactic acid bacilli after the plaque is localized. He states that very small amounts of lactic acid precipitate the mucin and thus enables the bacteria to become fixed to the teeth as plaques. Miller has noted that some immunes have had exceedingly ropy saliva which could be drawn out into long threads, while much caries was noted in the mouths of some almost absolutely free from mucus. Miller could find no antiseptic quality in the saliva nor any prin- ciple corresponding to alexin, and found that bacteria developed in the saliva of immunes almost as readily as in that of those susceptible to caries. Fig. 305 Caries of enamel about the cervices of many teeth, due to tenacious films collected upon them; at first probably neglected, later impossible to cleanse with brush alone. (Model by W. A. Capon.) He also pointed out that the mucus may readily undergo putre- factive fermentation with alkaline reaction, and, again, the carbo- hydrates entangled in it will ferment with acid reaction,, causing any caries which might be attributable to mucin fermentation. It is possible that the secretion from the gum may in some cases be acid and favor the production of caries by decalcifying the enamel about the cervix (Fig. 305). Cook has shown that glycogenic infiltration of the oral mucous membrane may be produced by the use of irritant or astringent washes, which may possibly permit a change of this substance by bacteria into acid about the necks of teeth, accounting for a certain form of cervical decay long thought to be due to an acid mucus. (See Glycogenic Infiltration.) PREDISPOSING CAUSES 335 Structure. — While the structure of the enamel has no relation to the inception of caries, that is, teeth of poor structure may not decay, a roughness of the enamel surface, which often accompanies teeth of opaque appearance, may act as a favoring condition, and after inception of caries inferior structure and possibly the presence of Caush's tubes may permit more rapid disintegration. (See p. 165.) An interesting examination of 16,000 mouths made in Sweden by Forberg (Stockholm) and others by Rose in Baden and Thuringia seem to show that there is a relation between the color (structure) of teeth and the presence of caries, the following averages of all ages being observed : White teeth, 14.3 per cent, of caries; yellowish- white, 16.4 per cent.; yellow, 20 per cent.; grayish blue, 24.3 per cent. According to these observers,^ in the regions in which the water was rich in calcium salts the individuals examined had the yellowish- white teeth. Miller's observations confirm this. Gautier^ found that in young pigs deficient osseous development corresponded exactly to the lack of calcium salts in their drinking water. Black^ made analyses of so-called hard and soft teeth, and deduced from them the opinion that the hardness and softness of teeth have nothing to do with the inception of caries. Touching this point, Black^ instances the case of a man whose enamel had always been chalky and as easily cut as a slate-pencil, yet who had little caries of the teeth. That some teeth of apparently poor structure and defective form do not decay is also a fact of common observation, but, as a rule, they go together. These observations, together with the foregoing data, regarding the inception of caries, point to the now conceded conclusion that the caries of teeth is entirely due to the environment of the teeth, and in no sense does it arise from within the tooth, and that in so far as the cause is active it is a question of the localization of the exciting cause or its factors on the one hand, and the solubility of the teeth on the other; and that no amount of cause is sufficient to produce it unless permitted to exert its effect upon special points upon the teeth; in other words, it requires localization and time to act, though it may in some cases be broadly localized. There appar- ently remains only to be considered the effect produced by systemic states upon the development of the bacterial causes or whether any material is introduced through the oral juices, saliva, mucus, etc. 1 Dental Cosmos, 1901. 2 L'Odontologie, October, 1910. See Cosmos, 1911, p. 242. ' Ibid., 1898. * Ibid. 336 DENTAL CARIES Systemic Predisposing Causes. — Some individuals seem to suffer much from caries; others in less degree. In either case periods of immunity or comparative immunitj^ may be established, and may be again followed by a period of susceptibility and a succeeding immunity. These facts point to the conclusion that a period of caries is due either to a temporary lack of oral hygiene with a corresponding intensity in oral fermentation — i. e., the exciting cause is active — or that it is due to some systemic condition which changes the consti- tution of the oral fluids, permitting the formation of the microbic plaques upon the teeth, or increases the fermentation by supplying some element nutritive to bacteria or depriving it of some element inhibiting the growth. Black has shown that caries fungi are always present in the mouth, but do not always form the plaques. Cases also exist in which caries has begun during some period of susceptibility and a number of new cavities have been started. Later a period of immunity has followed and the cavities have not progressed. So far as classed, systemic conditions influencing susceptibility and immunity may be placed under the four headings: Heredity, Prenatal and Postnatal Influences, Age, and Bodily Condition. Heredity. — ^Black^ records observations on certain families as showing a tendency to caries of certain teeth at a given age, or in certain positions upon the teeth, e. g., occlusal pits. In certain cases the hereditary tendency persists. This tendenc}^ must be due either to an inherited cell physiology, or diet tendency influencing the oral fluid, or to transmitted faults of form or, possibly, of structure of the teeth. Prenatal and Postnatal Influences. — It is quite probable that the systemic condition of the mother during gestation may pro- foundly modify the anatomicophysiological condition of the body cells of the child; nutritional processes maj" suffer and the postnatal tooth development proceed irregularly, structure being affected; moreover, the altered biochemical function of the cells may stand in close relation to the constitution of the oral fluids, and these in turn may favor the development of caries fungi. If, therefore, the mother is not properly nourished the teeth ma}' not be well con- structed, especially if lime be lacking in her food. The same line of argument may be applied to bottle feeding of recently born infants, or to other conditions profoundly affecting general nutrition. In an examination of school children, Th. Frick^ (Zurich) found a 1 Dental Cosmos, 1904. - Ibid., 1901. PREDISPOSING CAUSES 337 much greater percentage of decay in children that had been bottle- fed at between three and six months of age. He performed an experi- ment on a Htter of six dogs, feeding three on cows' milk and bouillon; one of them died and the others had poorly developed teeth. The controls were normal. Forberg and Rose^ have shown that the individuals who drink water rich in calcium salts have a smaller percentage of caries than those drinking soft waters. Ferrier has observed a coincidence of caries and the drinking of boiled water which has been deprived of calcium carbonate. Whether this effect is due to a better develop- ment of tooth structure or is a post-developmental effect is not stated in either case. The point brought up by Head,^ who has shown the apparent rehardening of teeth in saliva after partial decalcifica- tion by a weak acid opens up the question here as to whether the use of calcareous waters after tooth eruption can increase the density of enamel. Enamel can be dried, why then not infiltrated by calcareous solutions? The question cannot now be answered. Another view might be that some of the calcium salts in drinking water come back to the saliva eventually, and if abundant may neutralize the acidity in plaques either through their alkalinity or by combining with the acids formed. Degeneracy must be considered as a factor possibly influencing the body cells, thus also the body fluids. Age. — That the age has an influence upon caries was noted by Flagg. He recorded the ages from five to eight, twelve to twenty, thirty to thirty-five, forty-five to fifty, sixty to sixty-five years, and senility as periods of decay, while the intervening periods were intervals of comparative exemption. Black has noted that caries is a disease of youth, most intense before adult age, at which time immunity is established, provided the teeth have been well and promptly filled and the mouth otherwise cared for. In view of this fact he aims at establishing this immunity by close attention to the teeth during youth. He records fluctuations in susceptibility not unlike those recorded by Flagg, and also points out that some persons pass through the ordinary periods of susceptibility and first develop caries in middle age. In old age general recession of the gum is common, and in the conditions of debility associated with old age much caries of cemen- tum occurs. The patients are often either unwilling or unable to keep the cementum cleansed. Repeated examinations of the mouths of school-children show a deplorable amount of caries which may, perhaps, be attributable to 1 Dental Cosmos, 1S99. 2 See p. 299. 22 338 DENTAL CARIES several causes, such as the induction of a lessened systemic resistance due to confinement, study, etc., and also to the inhalation of vitiated air, which presumably also contains acid-producing bacteria. More- over, bacteria of caries may be directly transmitted by kissing, common use of drinking cups, pencils, etc. Michaels,^ of Paris, has observed that "the saliva of adolescence contains a dextrinic principle (glycogen) susceptible of fermentation under the influence of ptj^alin in the presence of earthy salts. Lactic acid is formed." Bodily Condition. — It is a matter of observation that such con- ditions as pregnancy, typhoid fever, anemia, leukemia, diabetes, dyspepsia, nervous exhaustion, and debility are frequently accom- panied by or followed by a development of cavities of decay, but whether the diseases themselves or a coincident lack of oral hygiene act to permit the formation of the gelatinous plaques has not clearly been made out. If oral and dental prophylaxis be practised during typhoid fever and convalescence therefrom, the production of cavities is much limited, but this does not prove anything. The same is true of pregnancy, which introduces an exciting cause (the vom- itus), and of glycosuria, which introduces glucose. Black contends that periods of susceptibility are noted both in apparent good and ill health. That apparent health may really not be true health is a matter that must be considered. This bodily condition is seemingly the key to any change which can occur in saliva, or mucus, or oral phagocytosis, to one of which must be attributed any possible systemic effect upon caries bacteria, which can aid or inhibit their growth or localization. It matters very little whether the bodily condition is due to heredity as a general modification of cell physiology, to age, or some period of stress, as the "change" of the teeth, puberty, growth during adolescence, business or family anxieties, the degenerative tendencies of advancing age, or to some more acute systemic condition, as typhoid fever, diabetes, etc., except in so far as these conditions may introduce into the oral fluid a substance which may act either (1) as a direct decalcifying agent (an acid) or (2) as an indirect decalcifying agent by furnishing a food material for the bacteria hbm which they may manufacture acid (a carbohydrate), or (3) furnish a substance in the saliva which may glue the germs to the teeth, or (4) take from the saliva some substance which normally inhibits plaque formation. It was shown under the caption of Erosion that a very weak acid may decalcify more rapidly than a stronger solution, and it has ' Sialosemeiology. See Dental Cosmos, 1900. PREDISPOSING CAUSES 339 been noted that in systemic conditions inducing general acidosis (as chronic nephritis or diabetes) there is a tendency to deep decalci- fication of cervices of teeth, beginning particularly upon the cemen- tum. While by no means proved not due largely to fermentation of carbohydrate food by bacterial plaques, as a result of defective hygiene, there is, nevertheless, a strong suspicion that the acidosis expressed as acidity of saliva has produced the decalcification. There is also a probable reduction in the amount of normal sodium phos- phates as the result of the general acidosis, and this also found in the saliva reduces the controlling quality, which Head has shown to exist when a certain percentage of basic sodium phosphate is present in solutions having an acid reaction. (See p. 299.) On the other hand, in such a condition as diabetes there is not only a general acidosis, but also the possible transudation of a glycogenic principle into the saliva which can undergo acid fermentation by oral bacteria. Michaels^ states that the constitution of the sali^•a changes with the establishment of various diatheses, and that a physiological saliva with the biochemical principles in a state of equilibrium is probably very rare. He states that the most active dental caries is found in the mouths of hypo-acid individuals, in whom saline chlorids predominate over the acid elements of metabolic waste, reducing the acidity of body fluids below normal, and inducing a lessened resist- ance to development of infective causes, and that caries is least active in the hyperacid individuals, in whom sulphocyanid of potassium is more abundant in the saliva. Under the auspices of the Xew York State Dental Society its Committee on Scientific Research has conducted experiments which tend to show that individuals having marked tendency to caries have but relatively small amounts of potassium sulphocyanate in the saliva, while those with little caries have an abundance. It is argued, from observations, that saliva in which it is abundant causes the solution of the mucoid substances necessary to form bacterial plaques or prevents the bacteria from forming them. It w^as shown that smokers, photographers who use potassium cyanid in removing silver nitrate stains from the hands, those to whom hydrochloric acid has been administered for a time, and those to W'hom potassium sulphocyanate has been administered in f-grain doses per diem have an abundance of potassium sulphocyanate in the saliva, with lessened tendency to caries. It is argued that its natural entrance into the saliva is lessened in carious subjects, 1 Dental Cosmos, December, 1900. 340 DENTAL CARIES through some fault in the economy, and it was found that its admin- istration (also as sodium sulphocyanate^ in ^-grain doses in tablet form per diem would reestablish its regular formation, for some time even after its administration ceased. When large quantities of mucoid substances accompanied the presence of ordinarily sufficient sulphocyanate caries was not inhibited, and in a few cases low findings did not render the individual suscep- . tible because some unknown ingredient seemed to cause a solution of the mucoid substances. The test supplied by the committee is as follows : Take 2 c.c. of saliva, to which add 2 c.c. of distilled water, and shake thoroughly together. Add 5 drops of iron perchlorid, and shake again. The presence of sulphocyanate naturally in the saliva is determined by the color. A straw color indicates little or none. A brick color indicates a sufficiency. A wine color indicates abundance. The Committee on Scientific Research of the National Dental Association have devised a colorimetric scale^ which consists of two tubes. In tube A 1 c.c. of saliva is placed. In tube B 1 c.c. of a 1 to 2000 solution of sulphocyanate of ammonia. To each add 2 drops of a 5 per cent, ferric chlorid solution from the same pipette. Add distilled water to be in definite quantities until the color matches that of the saliva. Calculation of the dilution of the standard solution will give the amount of sulphocyanate in the saliva. While the observatioas have not produced finality in this direction, the observations are introduced that others may continue the line of thought. The Committee has concluded that its presence retards caries, renders teeth less sensitive, assists in softening the stains on teeth, aiding prophylaxis and changes the character of the saliva and oral fluid in general. It also finds that the administration of potassium sulphocyanate not only furnishes it immediately to the saliva, but restores the metabolic activity temporarily in abeyance which pro- duces it. The use for a few weeks is to be renewed when the test shows its need.^ Potassium sulphocyanate is described as a nerve tonic safe in even 10-grain doses. It must not he confused with potassium cyanate, which is a virulent poison. Kirk has succeeded in altering viscid saliva to a more limpid condi- tion by reducing the ratio of carbohydrate to proteid diet, first cutting 1 Parke, Davis & Co., sodium sulphocyanate. 2 Dental Cosmos, 1908, p. 1365. 3 Ibid., p. 469. PREDISPOSING CAUSES 341 out carbohydrates almost altogether, then adding them gradually to the diet. He cites observations upon asylum children kept upon well-balanced rations as having large numbers of arrested caries.^ Black^ believes that the condition of the system alters the oral fluid so as to permit the bacteria in it to produce a gelatinoid material as a by-product in one case and not to produce it in another, and that when produced plaques adhere to the teeth in sheltered spots, while when not produced no plaques adhere, though a general acidity of the oral fluids may be produced. Miller,^ some years ago, pointed out that filthy mouths often do not contain carious teeth. He offered the rational explanation that the unchanged food particles, once their acid-producing capacity is destroyed, can even act as a protection in so far as caries is concerned. In experiments on artificial production of caries, Miller found that the pabulum of the bacteria needed constant change, otherwise putrefaction resulted and decay ceased. The fact that fairly cared- for mouths often contain carious teeth is rather an argument in favor of the local etiology of caries, as teeth unbrushed after a meal, or, rather, not thoroughl}' cleansed, as is the rule in a vast majority of mouths, contain every necessary factor of caries, including a renewal of fresh carbohydrate food for the bacteria. 1 Dental Brief, 1907. 2 Dental Digest, 1907. 3 Lecture at the University of Pennsylvania. CHAPTER XII DENTAL CARIES: PATHOLOGY, MORBID ANATOMY, AND CLINICAL HISTORY PATHOLOGY AND MORBID ANATOMY It is a fact of common observation that caries begins only at spots protected from friction or uncleansed. These are in order of frequency: (1) Pits, grooves, and fissures in the enamel; (2) approxi- mal surfaces just above the contact point; (3) smooth surfaces which Fig. 306 Fig. 310 Fig. 317 Fig. 308 Fig. 309 Fig. 311 Fig. 312 Fig. 315 Fig. 318 Fig. 313 Fig. 316 Fig. 319 from any cause are habitually unclean; (4) necks of the teeth at or near the junction of the cementum and enamel (Black) (Figs. 306 to 319). In these situations Williams has demonstrated the fact that the oral bacteria, protected from friction, attach themselves to the PATHOLOGY AND MORBID ANATOMY 343 enamel, forming microbic plaques which are sufficiently adherent to permit their retention during the grinding of the specimen for microscopic examination. (See Figs. 320, 321, and 322.) Carbo- hydrate food debris lodges at the points at which retention is favored, and either ferments directly against the enamel or through the medium of the microbic plaque. The bacteria in the plaque require food and obtain it from the carbohydrate and albuminous materials which come in contact with them. From the carbohydrates lactic acid is produced as a waste Fig. 320 Section of normal human enamel, showing thick, felt-like mass of microorganisms slightly raised from the surface of the tissue by pressure of the cover-glass in mounting. X 250. (Williams.) product. (See Chapter XI.) Williams states that it is "highly im- probable that the enamel is affected, except in rare and special instances by any other acid than that which is being excreted by the bacteria at the very point at which they are attached to the enamel." This thick mass of fungi also prevents the excreted acid from being washed away, so that it exerts its full chemical power upon calcific tissue. The lactic acid produced attacks the inorganic matter of the 344 DENTAL CARIES enamel, following first the interprismatic cement substance between the prisms, later dissolving the transverse cement substance between the globules. The effect is to produce an irregular, roughened sur- face of the enamel and to bring into view the structure of the rods (Fig. 327). Fig. 321 -V Microorganisms of caries attached to enamel on approximal surface of tooth. (Williams.) The gradual loss of cement substance unbinds the enamel globules, which are in turn dissolved and washed away, leaving a depression or cavity. In the process of enamel dissolution the bacteria may enter the crevices formed by solution of the interprismatic cement substance, and by repetition of the process gain access to the dentin (Fig. 330). The form of the enamel may be retained until and even after decalcification has reached the dentin. Clinicallv this is seen as an PATHOLOGY AND MORBID ANATOMY Fig. 322 345 Superficial approximal caries of enamel with tilms; also shows slight approximal abrasion. (Miller.) Fig. 323 Budding of spores on the stems of Leptothrix racemosa. (Williams.) 346 DENTAL CARIES opaque white or discolored spot, resisting the instrument until some force is used, when it rapidly breaks down (Fig. 322). A central cavity, or several minute openings, leading to or almost to the dentin, is sometimes seen in the general decalcified area. It signifies the loss of the organic matter of the enamel by unbinding or Fig. 324 Thick growth of Leptothrix racemosa fructification heads from approximal surface of tooth, under high magnifsdng power. (Williams.) peptonizing actions. The extraction of an approximating tooth permits the film to be rubbed off or prevents the retention of carbo- hydrate media, so that the bacteria cease to be active, and this spot may remain indefinitely at this point — e. g., the disease is arrested. It may cease spontaneously to develop further, owing to the estab- lishment of an immunizing systemic change, even though the teeth PATHOLOGY AND MORBID ANATOMY Fig. 325 i 347 >-/ \ A form of streptococcus found abundantly in mouths where very rapid decay of teeth is in progress. X 750. (Williams.) Fig. 326 Scrapings of microorganisms from the approxin.al surface of a deraying tooth: -sliows the Lepto- thrix buccalis maxima and the Bacillus bucoalis maximus of Miller. X loOO. (Williams.) 348 DENTAL CARIES remain in approximation, and strict prophylaxis will usually arrest the advance of the process. It is also noted clinically and microscopically that the decalcifica- tion is deepest at a spot just above the point of contact, and less deep at points buccal or lingual, occlusal or cervical, to this spot, and still less at points more buccal or lingual — i. e., it shades off to zero lingually, bucally, occlusally, and cervically (Fig. 331). The dentin may in such cases be deeply affected. Bacteria growing in the spaces from which the interprismatic cement substance has dis- appeared causes detachment of masses of partially decalcified rods (Figs. 330 and 332). Fig. 327 Section through human enamel, showing first stages of caries, i. e., solution of interprismatic cement substance. To be compared with Fig. 170. (Williams.) When the entire thickness of the enamel is penetrated and the dentin attacked there is a change in the mode of progress of the decalcification, which proceeds along the line of union between the enamel and dentin, as well as directly into the dentin (Fig. 331); in this way the enamel is attacked from its dentinal side (backward caries) "(Fig. 329). PATHOLOGY AND MORBID ANATOMY 349 In the ultimate breaking down of the enamel the rods first separate; the outlines of the several globules of which the rods are composed are brought into plain view; next, the calcified plasmic strings noted in enamel formation become evident; and finally, the bead-Hke masses upon these strings are left as the ultimate granular detritus of the enamel. In cases of rapid enamel dissolution Williams found streptococci almost invariably present; and suggests tentatively that the variety of organism may be the factor governing the rapidity of dissolution (Fig. 325). Fig. 328 Section of human bicuspid, showing commencement of caries: a and a', appearances caused in enamel and dentin by the acid of decay; b and b'^, shreds of a felt-like mass of bacteria raised from the surface of the enamel; c, a cavity. X 12. (Williams.) These are probably the Streptococcus brevis of Goadby (Micro- coccus nexifer of Miller). Williams found Streptococcus pyogenes albus and aureus and Sarcinea lutea to be acid producers. The large cocci and diplococci shown in Fig. 333 were always found in the secondary decay of enamel. " In the direct caries of enamel the cavities are lined with leptothrix and thread-like forms." 350 DENTAL CARIES "The Leptothrix buccalis maxima and the Bacillus buccalis maximus of Miller are nearly always found, the latter more spar- ingly" (Fig. 326). Fig. 329 Section of carious tooth, showing appearances of decay in enamel and dentin at the line of union of these tissues; the dark spots shown in the enamel and dentin are masses of microorganisms X 250. (Williams.) Fig. 330 Penetration of bacilli between enamel prisms after solution of interprismatic cement substance. (Miller.) Some of these bacteria are not acid producers, and it may be that if a film is composed entirely of these they may occupy a field and really protect it by excluding acid-forming bacteria. PATHOLOGY AND MORBID ANATOMY 351 "Beneath the felt-like masses of thread forms and lying in contact with the decomposing enamel in direct decay, and also in deep cracks and fissures in secondary decay, there is invariably found a short, thick bacillus, usually constricted in the centre." (Williams, also Goad by.) Caries of Nasmyth's Membrane. — Miller^ demonstrated that the enamel cuticle may act as a breeding ground for many forms of bacteria which occupy it, forming a matrix which may retain minute particles of food, which in turn aid in acceleration of the progress of decay (Fig. 335). Fig. 331 Decalcification of enamel without loss of form: a, film. X 35. (Miller.) Caries of Dentin. — The bacteria after penetrating the substance of the enamel attack the dentin. This presents a different anatomical and chemical structure to be acted upon. Beneath the enamel the first layer of dentin is of a composition which permits the bacteria to rapidly spread laterally along this zone. They also enter the tubules of the dentin, and penetrate by multiplication toward the pulp. A wedge-shaped area of decay is produced (Figs. 331 and 337). 1 Microorganisms of the Human Mouth, 1890, and Dental Cosmos, 1900. 352 DENTAL CARIES In all cases decalcification precedes these invasions. At the periphery the tubules communicate freely by their lateral branches (Fig. 336), and the lateral spreading of the bacteria by multiplication is readily explained. It is seen clinically in caries that a portion of the dentin is abso- lutely destroyed and removed, leaving within the tooth a "cavity of decay" bounded by dentin and enamel undergoing disintegration; Fig. 332 Cover-glass preparation from scrapings of wiiite, opaque, decaying enamel: the cement sub- stance between the rods is seen to be dissolved away, and the crevices thus formed are filled with round and oval forms of micrococci and bacteria. Stained by the Gram method. X 450. (Williams.) beneath this lies dentin less affected, and beneath this, sound dentin (Fig. 337). These phenomena require explanation. The tubules of the decalcified dentin become packed for a distance with bacteria (Fig. 338). These act upon the organic matrix of the decalcified tubule walls. The internal pressure due to multiplication distends them so that the lumen is enlarged. At the same time the PATHOLOGY AND MORBID ANATOMY Fig. 333 ,t,. «w *-. <4 M^-y •^' m r^ > ■r, v^ ~^>^. -- „x . X %/ .J 353 Various forms of micrococci and bacteria from decaying enamel. Photographed by Mr. Andrew Pringle from Williams' cover-glass preparation. X 1000. (Williams.) Fk;^ 334 Cover-glass preparations of scrapings from decay of enamel; shows Leptothrix buccalis maxima and Bacillus buccalis maximus of Miller. Stained by Gram method. X S30. (Williams.) 23 354 DENTAL CARIES bacteria excrete a ferment or ferments which cause the wall at first to thicken. The dilatation and thickening together cause the com- pression of the decalcified intertubular substance, and the tubules assume an hexagonal shape owing to the mutual pressure (Fig. 339). The phenomenon is not a vital one, as it occurs in artificial caries. (Miller.) Fig. 335 Enamel cuticle permeated by bacteria. (1100 to 1.) (Miller.) Fig. 336 Carious dentin, stained with fuchsin to show microorganisms. The section shows the con- dition of the tubules as filled with microorganisms along. the junction of the dentin with the enamel at o. The tubules are very much enlarged. (l/lO immersion objective.) (Black.)' The bacterial ferment possesses a digestive or peptonizing power analogous to trypsin, and begins to liquefy the inner surface of the PATHOLOGY AND MORBID ANATOMY 355 tubule wall. As it does so the lumen is further increased and the bacteria fill the acquired space. Taking up carbohydrates lactic acid is produced, which combines with the calcium salts of deeper tubules and intertubular substance and prepares a path of dccalci- FiG. 337 Longitudinal ground-section through the crown of an inferior molar of a negro: E, enamel; D, dentin; C, cement; p, pulp chamber; a, large decay, from the occlusal surface; 6, small decay, from the mesial surface; c s, cone of septic invasion and discoloration; e, partially decalcified and discolored enamel around the carious cavity; z, dark cones; z', clearer cones; z'p. oldest cones where putrefaction of the tooth cartilage begins; c, outer transparent zone, or zone of Tomes; s d, secondary dentin, caused by irritation; s' d', secondary dentin deposited by normal physiological process, recession of the pulp. This figure is drawn from a ground and polished section mounted in Canada balsam. (Gysi.) 356 DENTAL CARIES jQed tissue for bacterial advance (Fig. 340). This decalcified tissue, to all intents and purposes, becomes a culture medium. Fig. 339 Cross-section of decayed dentin: the tubules through reciprocal pressure have assumed the shape of five- and six- sided prisms. (Miller.) This combination of the acid with the calcium salts disposes of or neutralizes the acid, which, if accumulated to the strength of 2 per cent., would cause the destruction of the bacteria, by their waste products. (Miller.) Calcium lactophosphate, calcium lactate, and magnesium lactophosphate are produced. Carious dentin, showing in- vaded tubules and uninvaded but decalcified intertubular sub- stance. (Miller.) Fig. 340 Section of decalcified dentin partly invaded by bacteria: a, uninvaded zone. (Miller.) Miller experimentally found that the calcium carbonate does so neutralize the acid formed by formation of calcium lactate, but PATHOLOGY AND MORBID ANATOMY 357 the calcium phosphate does not, as it develops calcium lactophos- phate, setting free phosphoric acid, which maintains the relative Fig. 342 ^ Liquefaction foci. (Miller.) Decayed dentin showing a mixed infection with cocci and bacilli. X 400. (Miller.) acidity. Experimentally the addition of calcium phosphate to a solution of lactic acid did not reduce the decalcification in pieces of dentin placed in it, for the reason named. The bacterial ferments continue to digest the wall of the tubule, and a time arrives when they have penetrated its substance. The intertubular substance is then removed in like manner. The same process occurring in adjoining tubules as well, the entire dentinal substance in the particular area at the cavity surface is destroyed — i. e., liquefied and washed away (Fig. 337, a). Occurring at a point beneath the general cavity surface, the bacteria in several adjoining tubules destroy their walls and the intervening intertubular substance, forming what Miller has called a "liquefaction focus" (pi. foci) (Fig. 341). This action proceeds until the enamel is undermined and the pulp is exposed. A decalcified area always exists in advance of the tubule invasion, sometimes large masses being found, though it lessens in quantity as the pulp is approached. As the enamel is undermined by the carious process the bacteria and their acids decalcify its inner surface, the process proceeding 358 DENTAL CARIES from within outward and termed "secondary caries," or "backward caries," of enamel. The enamel is thus weakened and at the same time deprived of dentinal support, and breaks down under stress of mastication. Any interglobular spaces in the dentin being filled with transi- tional or uncalcified material like the tubule walls are rapidly invaded by the bacteria during their progress along the tubules (Fig. 343). The character of the organisms in the tubules and the nature of the liquefaction seem to depend upon the particular germs present. Miller has shown that in the deeper portions of tubules micrococci appear to predominate over the rod forms, which are also present; although one tubule may be filled with cocci and its neighbor with rod forms (Fig. 342). It is only in the more superficial layers that the thread forms are found in numbers. Goadby^ has done much interesting work in this direction, and offers the following classification of bacteria found in decayed dentin : Bacteria of Dental Caries Acid-forming Bacteria Streptococcus brevis B. necrodentalis Staphylococcus albus Streptococcus brevis Sarcina lutea Sarcina aurantiaca Sarcina alba (Eisenberg) Staphylococcus albus . Staphylococcus aureus Deep layers of carious dentin. > Superficial layers of carious dentin. Bacteria which Liquefy Dentin ( Decalcified) None isolated as yet .... B. mesentericus ruber .... , B. mesentericus vulgatus . B. mesentericus fuscus B. fervus B. gingivae pyogenes .... B. liquefaciens fluorescens motilis B. subtilis Proteus Zenkeri B. plexiformis Deep layers of carious dentin. Superficial layers of carious dentin. Goadby states that his experiments show that the bacteria which dissolve blood serum also digest decalcified dentin, while those which only liquefy gelatin do not digest decalcified dentin. His experiments also indicate that of the bacteria found in the superficial layers of carious dentin some produce digestive enzymes, others acid fermentation, and others have both functions. 1 Mycology of the Mouth, and Dental Cosmos. PATHOLOGY AND MORBID ANATOMY 359 Choquet' has confirmed the observation of Miller, \'ignal, (iallipe, and Goadby that the deeper the portions of dentin examined the fewer species of fungi are found in the tubules, and explains it upon the ground that the anaerobic or facultative aerobic organisms in the outer layers advance into the deeper dentin because they are better suited to the conditions. Fig. 343 '^^ Si^^^iS^i' 7//, Interglobular spaces filled with bacteria. (Miller.) These exact findings are interesting as bearing out the general demonstrations of Miller; at the same time, Miller's experiment showing absolute dissolution by a single bacterium in pure culture is to be recalled. Choquet- has shown that dental caries may proceed under fillings against sound dentin by the following experiment : Artificial cavities were prepared in the incisors of a sheep. In these was securely sealed with cement a small particle of a gelatin culture of caries fungi applied on a sterilized platinum cap. Nine months later the dentin had become yellow, slightly decalcified, and the tubules penetrated by bacteria. This softened dentin was used to inoculate a portion of the medium originally used, and the species again cultivated. Milled estimated the relative loss of inorganic and organic matter in dentin during the process of caries by weighing and analyzing equal volumes of carious and sound dentin from the same teeth. The carious dentin had lost about seven-ninths of its weight, which was due to the loss of twelve-thirteenths of its original calcium salts by decalcification, and two-fifths of its original organic matter by liquefaction of its substance. Tube Casts. — In the zone of decalcification in advance of bacterial invasion of the tubes are found rod-shaped bodies or shining granules, ' Microbes of Dental Caries, Dental Cosmos, 1900. 2 Microorganisms of the Human Mouth, •Ibid. 360 DENTAL CARIES first described by J. Tomes. They occur in both natural and artificial caries, hence it must be inferred that their presence is not the result of a vital process. The rods do not dissolve in organic acids, but dilute sulphuric acid quickly dissolves them. They are unaffected by alcohol or chloroform, a proof that they are not composed Fig. 344 of fat. IMillcr regards them as probably calcic formations against the tubule wall as a cast of the wall, and which become loosened when en- largement of the tubule occurs. They have a tubular structure, are brittle, and may contain a central thread-like filament which may possibly be the remains of a dentinal fibril. Bacteria may surround them, but do not enter them. The granules are probably broken rods.^ The data Tube easts. point toward a probability that the rods are composed of calcium lactate and calcium lacto- phosphate, the result of a combination of lactic acid with the calcium salts of the dentin. The resultant salt is probably deposited as a tube cast, as suggested by Miller. Polariscopic experiments should be competent to settle the question. The Transparent Zone. — x\round the zone of decalcified uninfected dentin appears a zone of dentin more transparent than the surround- ing normal dentin. The zone extends from periphery to periphery around the cone of carious dentin (Fig. 337, c). The tubules in this area contain granular matter not seen in normal dentin, nor in the dentin of dead teeth in the same situation. ^ Tomes and ]\Iagitot both regarded the transparency as an attempt made by nature to impede the progress of caries. Walkhoff regards it as due to a sclerotic action, the fibrillse upon stimulation producing intercellular substance (tubule wall) at their own expense and primarily of their offshoots. Black once regarded it as the earliest stage of decalcification, but has discarded this idea. Miller advanced the following data:^ 1. Transparency indicates increased homogeneity as opposed to the heterogeneity of normal dentin — i. e., the coefficients of light refraction are brought nearer together. 2. It occurs in living dentin only and is not found in natural teeth mounted on plates and decayed in the mouth, nor in secondary caries of dentin from the pulp cavity to the periphery, and is, therefore, a 1 Miller. "^ Ibid. ' Microorganisms of the Human Mouth. PATHOLOGY AND MORBID ANATOMY 361 result of vital action. (Compare Figs. 337 and 347 with Figs. 345 and 346.) 3. The tubules have their lumen lessened in diameter in the trans- parent areas, an agreement with the position of Walkhoff. 4. Secondary dentin may accompany the process in contiguity with the area; moreover, secondary dentin is translucent. It indi- cates a constructive excitation of the odontoblasts, of which the dentinal fibrils are prolongations (Figs. 337, Sd). Fig. 345 Section from a lower incisor worn on a plate, extensive decay without increase of transparency. X 15. (Miller.) 5. Chemical analysis proved that no lime salts had been lost, and it was pointed out that a gain in the percentage of salts was unneces- sary, as new dentin is necessarily composed of organic as well as inorganic matter, wherefore the analysis would not necessarily varj' from that of normal dentin. 6. It is found in connection with abrasion of human teeth in which the activity of acid may possibly be an open question, and it also occurs in the worn teeth of dogs, the saliva of which is strongly alkaline. Miller states that opacity may follow or be associated with trans- parency.^ 1 Dental Cosmos, April, 1903. 362 DENTAL CARIES The natural conclusion is that the transparency is a form of tubular calcification, and that it impedes the progress of caries; that it does not succeed, as a rule, is due to the overwhelming action of the bacteria. In cavities from which the walls are broken away, freely exposing the carious dentin to mastication, the carious dentin and its con- tained bacteria may be removed by friction (Fig. 355). In the transparent area the tubules become obliterated ; a polished, discolored surface results resembling in degree an abraded surface. Fig. 346 Secondary caries of dentin advancing from pulp chamber and therefore occurring after death of the pulp. Absence of transparency. X 15. (Miller.) This process is called "eburnation," and is really tubular calcifica- tion (which see). In the same tooth a more sheltered border of this spot may be undergoing the carious process. Miller records cases of badly decayed teeth in which the process ceased spontaneously and the dentin became hard and smooth. Pigmentation in Caries. — Pigmentation occurs in caries possibly from extraneous substances entering the carious area, possibly from the substances formed during putrefaction. The slower the progress of the decay the greater the discoloration. PATHOLOGY AND MORBID ANATOMY 363 The colors vary from light yellow to reddish l)r()wii, dark brown, and black. The color is, as a rule, darkest upon the outside of the carious dentin, but the pigment may extend through large masses and be found staining dentin beneath the caries hard enough to leave in situ. As a rule, this is not the case. Black suggests the possible formation of sulphids. Miller has found iron almost constantly present in carious dentin. The dis- coloration of dentin does not seem to be necessarily due to the carious process, as it may be seen in areas of abrasion. In a specimen Fig. 347 Transparency resulting from cracks in the enamel at a and b. X 20. (Miller.) possessed by the editor a limited cervical caries caused a growth of secondary dentin and an area of tubular calcification. From the pulpal surface of the secondary dentin to the area of caries extends a sharply defined area which has a flesh-rose color (Fig. 348). Many areas of secondary dentin due to abrasion are stained a dark brown. Artificial caries produced in teeth placed in a mixture of bread and saliva and the mixture constantly renewed was white. If putre- faction was allowed to occur, discolorations ensued (Miller). The discolorations of carious dentin may be due to the action of chromogenic bacteria. Miller isolated from the mouth an organism 364 DENTAL CARIES which he named Bacillus f uscans, and " which, cultivated on the surface of nutritive agar-agar, in a few weeks imparts to the medium a yellowish-brown color, which gradually darkens and extends deeper into the substratum as the age of the culture increases." It is significant that the three acid-forming organisms found by Goadby in the deep layers of carious dentin do not form pigment in their artificial media. Caries of Cementum. — Caries of cementum occurs when the gum has receded, exposing the cementum to the fluids of the mouth. As a rule, a triangular depression exists bounded by the thickened gum margin, the cementum, and the enamel. This favors the collection of the bacterial plaques, and caries follows. The gum may be much receded, yet no caries occurs. As a rule, however, recession and uncleanliness frequently assure its presence. Especially is this true in cases of general recession in aged or debilitated persons. Fig. 348 ■• Fig. 349 Cervical caries associated with secondary Caries of cementum and dentin com- dentin. Area pigmented. pletely encircling the tooth. The path of bacterial invasion after decalcification is by way of Sharpey's fibers to the lacunae and canaliculi; later the dentin is invaded as in the crown. Frequently the form of the cementum is largely retained, while the decalcification is deep. CLINICAL HISTORY OF CARIES The clinical history of dental caries records the observable phe- nomena associated with its inception, progress, and termination. Inception of Caries. — Caries begins, after the manner described in the pathology, at favoring spots. As a rule, in molars the occlusal fissures are first decayed, being often carious in this situation before fully erupted. Uninformed parents usually consider the first perma- nent molar a temporary one, and frequently neglect it. It moreover CLINICAL HISTORY 365 has often seriously defective fissures which afford lodgement for microbic plaques, which seem to be readily formed because of the unhygienic state of the temporary teeth, which are frequently carious, and the permanent molars are unbrushed during eruption. Not infrequently a cavity is produced on the mesial surface of this tooth by a carious condition of the distal surface of the second temporary molar. In other mouths both teeth are affected alike, owing to the nature of the approximation. The relative liability of the various surfaces of the different teeth to caries may be averaged for a great number of persons, but tables drawn from clinical cases may have little application to a particular individual, as peculiarities of local predisposing causes and personal habits modify the inception. Nevertheless, such tables are exceedingly interesting as showing a general relative liability. Charts have been made by Black which explain themselves (Figs. 350 to 353). The figures given for the buccal surfaces of the third molars seem rather lower than those I would feel warranted in giving; certainly after adult age caries frequently occurs. The lower anterior teeth are the last of all to be affected, and it is common to see the six lower anterior teeth free from caries years after all of the other teeth have been lost. This is attributable to the constant motion of the saliva, the presence of calculus, and to the mechanical effects of tongue movmeent, lip movement, and mastication. In the temporary set the molars decay much more frequently than the incisor teeth, partly because longer retained and partly because of the width of their approximations. The pulp is readily exposed because of its relatively larger size. Approximal cavities are frequently more broad than deep, and present problems of anchorage. The Progress of Caries. — The rapidity of progress of caries depends upon the intensity of the action of the exciting cause, the structure of the tooth, and the nature of the vital resistance offered. The exciting cause will act most intensely in mouths ill-cared for, and containing much carbohydrate debris, and these conditions being equal, enamel of poorer organization and presenting a greater degree of solubility, in teeth presenting broad approximations, will be the more rapidly destroyed. Caries does not begin or spread under the gum. Williams has expressed the opinion that, as a rule, the process of enamel destruction occupies a considerable period of time, a fact which may account for the general lack of caries in the temporary teeth until about four or five years of age. 366 DENTAL CARIES Fig. 350 O n 3 SB H >2 €0 3rd. MOL^R ^- /— 2nd. Molar ^ /^ 1 M ST. OLAR ^ /— 2nd Bicub »id V. ^ 18T. Bicuspid ^ ^■ Cuspid ~s /— LATERAL Incisor -\ ^— Central Incisor ] MESIAL BUCCAL GRINDING PALATiNfc DISTAL MESIAL BUCCAL GRINDING PALATINE DISTAL MESIAL BUCCAL GRINDING PALATINE DISTAL MESIAL BUCCAL GRINDING PALATINE DISTAL mesial BUCCAL GRINDING PALATINE DISTAL mesial BUCCAl INCISIVE PALATINE DISTAL mesial BUCCAL INCISIVE PALATINE DISTAL > 1 > i - < 2 m 2 1 M • 1 J ■■■■ " ■ ' - ! J ' ! ■ t ' i- _,iU: — i ; i 1 - -" — 1 ■ — ' '■■ i 1 \~' J -1 -. , - ~ -- i n1 1 1 — _^ I'll ~- 1 ' - .. 1 1 i — j ^ 1 - . 1 --- ~ — 1 ' [ 1 , .^, , , ' — r- -i ^-- ~ 1 ' * i j ^^ ^ _l '' ■ !■ 1 ' ;^^^ _ Ei .^ 1 ■ ! ; 1 1^ ^ i P 1 " ■ : 1 1 S 8 i i i ; 1 ■ ; ! ^^ j ; , i K, ■ ^ > 1 1 ' ^1 # - k M ^ 1 , 1 . ' ' 1 i 1 ^ tSS« _j 1 ^ e 1 ^ 1 1 j ^ i 1 ' ! i i 1 5^ .f ! > i ! L-- H s^ ' 1 1 ■ 1 ' ' 1 ^ III I ! i 1 1 i ; 1 i 1 1 1 1 1 i V" \ . ':■ 1 i i 1 ■ ; 1 ; 1 1 ! ! '■€ ' 1 i 1 ! 1 ! ! i i 1 ^i\ 1 1 1 1 1 1 1 1 1 H 1 1 U, p b C •<» N < 0, iu !;; c, b 1 J b b p p ■SI b ^ d b p 0- b- Cj b- b C b- Co b 0, b- <> Co b Co |0 b- V C, Co b- These charts represent the number of carious cavities observed in one hundred persons, and the position of these canities on the individual surfaces of the teeth. There are five columns of squares devoted to each tooth of one .side of the mouth, representing the five surfaces as shown on the left hand. The number of cavities in the surface represented is shown by the number of squares darkened, so that the efJect of the diagram as a whole gives a striking picture of the frequency of decay in the individual surfaces of the several teeth. On the right the percentage, or the number per hundred persons, is given in figures calculated to the first decimal point. On the left the per- centage of cavities in the individual teeth for all surfaces is given in the same way. The cavities occurring on one side of the mouth only are represented. And only one decay in an individual CLINICAL HISTORY Fig. 351 367 o r I L Z 5 o r 3rd. Molar -^ ^ 2nd. Molar ^ 1st. Molar ^ ^ 2no. Bicuspio ~N ^ 1st. Bicuspid ^ c USPIO ■"s ^ Lateral Incisor ^ Central Incisor ^ MESIAL BUCCAL GRINDING LINGUAL DISTAL MESIAL BUCCAL GRINDING LINGUAL DISTAL MESIAL BUCCAL GRh-IDIiNG LINCjUAL DISTAL MESIAL BUCCAL GRINDING LINGUAL DISTAL MESIAL BUCCAL GRINDING LINGUAL DISTAL MESIAL BUCCAL INCISIVE LINGUAL DISTAL MESIAL BUCCAL INCISIVE LINGUAL DISTAL BUCCAL INCISIVE LINGUAL DISTAL 2 > '$ % ^ ^A \ : mJ ■ 1 '. T rb 1=^1 -i- ~'"H J L4- ' ,' ■ |_ ! "■_i- 1..^ _ ;_ J_.. ■ ^^^ = — — i j 1 J , l« - - — !- i —1 - ' 1 k> ~ -- =j_._ ■t ! 1 -J !^ ' \ t u- i 1 1 ! ! 1 1 . 1 \ i ^ 1 i '. : i : ! j i ! 1 O ~ 1 1 i i 1 1 i i ''\"'' . j — 1 j 1 i J i <-. t I I 1 ^, t : ^ ! • • , ! 1 i ; : i M '— ! j 1 1 lit! j i N, -t^^- 1 , , ■_1 J ' ^ , 1 I : ; 1 i ^ i 1 1 1 , i t,. !^ I o 1 i ^ : i ' ^ 1 U, l\) O O Cu lo -v •^ Co c- o b b C, b b-s» bbbCjCcbviCiC, bb covjb-^bCjC,C|Cobuvjb surface is counted; that is, if two or more pits are found decayed in the grinding surface of a molar, but one is counted; and the same rule is followed with all of the surfaces. Charts Nos. 1 and 2 (upper and lower jaw) are made up from my records of fillings for 628 persons of all ages, and, therefore, repre.sent what is seen in practice rather than the actual number that may occur. Charts Nos. 3 and 4 (upper and lower jaw) are made from 100 of my own patients between the ages of ten and twenty-five years, for whom I have filled all cavities and know the condition at present. They represent the actual number of cases in which the individual surfaces have decayed m these 100 persons. (Black.) 368 DENTAL CARIES The decalcified enamel may retain its form for a time after dentin decalcification has begun. An opaque spot, often discolored, is seen upon the tooth, and is readily broken down by an instrument before dentin decalcification occurs. If the approximating tooth be Fig. 352 O c I 3 > ,!^ =D 3 ^ 1? ^ ■■-?*- u ■-JJ3. 3rd. Molar 2nd. Molar -- ^ M ST. OLAR ^ /- 2nd. Bicuspid -N /^ 1 Bic o ST USPID ^ /-' Cuspid -N Lateral Incisor ^ /- Central Incisor o H > > > H o z m c > s > D H > r > > H m o 2 > > r > > O to c > > r o H > > > 5 o z c > 2 > > > > O z c > 3 > > > > 2 < C o > 2 > > > > < c > S > g > -□ > > z o m ID 3 > ' I. -J — • £. - -- ^ ' - „- : - L ^ v Jiv^ \ :)i^ %-~ » ^v ^^ ^ - ^ - ■^ ^ \s\ - ^' ~ - - - - - - - In' « 1 ^<"^ c^ ^ 1 ^^ ^ ^ ■■ ■■' 1 N ^ #! ^ bbC>CbO,ciCf,C, bo bC\C^bbbbC,d bbC,bO,CbbbC, bbCiC>C>OibC,C,pi CLINICAL HISTORY 369 extracted the carious process may cease, owing to the removal of the bacterial plaque or a lack of food supply (retention). This result may not follow if the dentin has been invaded before the extraction. After enamel destruction at a limited area, caries progresses along Fig. 353 O /^ /^ 3rd. Molar ^ /^ 2 M ND. OLAR 1 M ST. 3LAR ^ 2nd. Bicuspid ^ 1st- BlCUSFID ^ CU£P = ^ /^ Lateral Incisor ^ Central Incisor ^ > z > z CI c o > > 1 1 2-1 en 1 z H c r- > Z z o > s > > z c > 2 r- "^ O 1- •- > o z n 2 > > > r; 1 o z ? r . z c 1 c 2 2 > > z c > < CD c > 2 > > z o c > 2 > 2 > D H > z 2 CD 2 2 > Co ■" "Z - n i .L_ ~ J ; .... 1 — ! - 1 i _„ o, ■" 4v. ! I i : . i - - - s 1 ^ - ^_ > \ - f» k^ '^ 1 -^ - - - ^ L 1 _ 1 U. Lijk, t\) t^iu'oL^, vio-co^ <.r,.s,s •^K.s^ ..'J.V-'...^^...V' bb bbCnC. b bbC.i>^ibC,bb Cibbi^b bbbbCr,i^booO,ucc ot^oc oo o 24 '0 DENTAL CARIES its inner side and penetrates the dentin. The enamel is undermined. The extent of cavity orifice is no certain guide as to the depth of penetration. The under surface of the enamel then decalcifies. This is backward or secondary decay of enamel, and causes an opaque appearance of the undermined enamel. Cases are frequently observed in which the only external evidence of caries, in a molar or bicuspid, is a white or bluish-black line marking the fissure, and yet the dentin may be deeply and widely penetrated (Fig. 355, .4). Fig. 354 Caries undermining enamel: a, masses of bacteria lining the cavity. X -50. (Miller.) As a rule, however, as the cavity in the dentin enlarges the enamel at the orifice becomes disintegrated, so that the orifice is enlarged and more food debris enters to accelerate the process (Fig. 337). A deep and wide cavity may thus be formed before the patient is objectively or even subjectively aware of its existence. After a time the occlusal enamel boundary of the cavity breaks down and food is even more readily admitted. It has been noted that if the enamel break away in such a manner as to expose the carious dentin to the friction of food masses which CLINICAL HISTORY 371 are not retained and to the access of saliva, the progress of the caries is delayed and in some cases ceases altogether. The process of eburnation is set up. (See Transparent Zone and Tubular Calci- fication.) (Fig. 355, B.) The process is sometimes seen in certain cases in which caries has followed the dento-enamel junction, the enamel chipping off as undermined, ^ ^ so that almost the entire superficial portion of the dentin may be subjected to this pro- cess and remain of original form and dis- colored and eburnated. This is "spreading caries." In other cases the tubules are followed and the pulp is rapidly approached. This is "penetrating caries." Caries may progress rapidly for a period, and then receive a check to its progress. Teeth previously free from the disease may suddenly fall victims to its rapid and widespread progress. No doubt, in many of these cases there are removed from or added to the local oral conditions, constitutional influences which deter or favor the local development of caries producing bacteria. The editor has the models of the jaws of a boy, aged fourteen years, with every tooth but three decayed to the gum, and the three teeth contained six cavities. Secondary dentin is less readily decalcified than primary dentin. The dentin of pulpless teeth is more rapidly invaded after enamel decalcification than that of vital teeth, owing to the absence of vital resistance. This condition does not necessarily apply to the enamel of pulpless teeth. While caries appears at all ages from childhood to old age, its ra\-ages are most pronounced and its progress most rapid during the period of adolescence and early maturity. Its effects are most marked between the ages of eight and twenty-five years. As a rule, a denture which remains at twenty-five years unaffected by caries, remains unaffected or but slightly affected to an indefinite age. To be sure, this implies two conditions: (1) That the active causes of caries have been in but slight evidence, and (2) that the denture is of the highest order. The classes of dentures which escape are per- fectly formed and symmetrically arranged teeth, in the mouths of patients who lead sanitary lives and care for the teeth, who masticate vigorously, and who escape other diseases. Very filthy dentures may escape, owing, as stated, to putrefaction. Caries beginning at the junction of the cementum and enamel of the teeth has a somewhat different clinical history from that noted when its occurrence is in other situations. Its progress is subject to 372 DENTAL CARIES great variations. In any of the catarrhal conditions or atrophic conditions of the gum which lay bare the neck cementum, caries usually occurs. It occurs also as a process secondary to labial abrasion and erosion of the teeth. Teeth affected by erosion, however, at the ended area are commonly exempt from dental caries. The Terminations of Caries. — After the pulp is exposed it sooner or later becomes inflamed and hypertrophies or dies. In the latter case putrefaction results, which for a time may exert a restraining influence upon decay, but not for a long time. Masses of food freely enter the pulp cavity and caries proceeds in the dentin from within toward the periphery. This is "secondary caries" of dentin, and as it occurs in dentin without vitality, no transparency results (Fig. 346). Notwithstanding, caries at this stage proceeds rather slowly, particularly if the crown be much broken down. The result of secondary caries is a hollowing out of dentin of the root, and finally a decalcification of the cementum, which may persist for some time as a thin, elastic wall. Finally this is destroyed either at the occlusal periphery or caries causes pene- tration to the pericemental tissue. This may occur laterally or through to the bifurcation of the roots. In either case it is called "perforation by caries." Into this perforation the pericemental tissue may become protruded by hypertrophy, and the condition of hyperplastic or fungous gum be established. Following the breaking down of the crown, the blood pressure in the pericementum begins an extrusive process, the pericementum becomes thickened, and the tooth is somewhat loosened. Decay of the root face and interior and breakage of the cemental margins proceed simultaneously with the extrusion until finally but a small discolored bit of the root end lies upon the surface of the gum, from which it is removed by some slight force or is extracted. The entire process of caries in a tooth may thus extend over a period of from ten to twenty years. At times the extrusive force pushes a root up sidewise, particularly when the tooth has been tipped over before the loss of the crown. It may thus be retained in position and attached upon its under side for some time. The upper side may be polished by abrasion. The exposed end of a root undergoing extrusion is also sometimes made smooth by abrasion. A bit of root left in situ after breakage during extraction usually undergoes the same process of extrusion, but may not decay until it comes under oral influences. Usually a sinus leads to such a root, but very rarely the gum may heal over it. Such a root may at any time become the source of apical abscess or of an intractable neuralgia, the cause being only determinable by radiography. CHAPTER XIII DENTAL CARIES: DIAGNOSIS, SYMPTOMS, AND PROGNOSIS HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS Diagnosis of Dental Caries The diagnosis of dental caries is made through both objective and subjective symptoms. The signs are the existence of cavities and of softened areas, directly visible or made evident through instru- mental means. The symptoms are pains of several degrees of inten- sity. The nature and intensity of the pains furnish a guide to the depth of the carious invasion, and but an indirect indication of the location of the disease. Diagnosis by Objective Symptoms. — The presence of the markings of superficial decay, decalcified surfaces, or cavities may often be detected at a glance or be seen reflected in a mouth mirror. Opacity of enamel is usually due to its superficial decalcification or caries beneath it, though at times a malformation may exist. The dis- coloration or opacity about a fissure should excite suspicion of caries. In the routine examination for cavities, sharp, finely pointed explorers bent at various angles are to be passed over all the surfaces of the teeth. If the enamel at any point admit the point of the explorer, caries is usually present. Fissures are sometimes deceptive in this respect. A good rule is to adjudge the presence of caries when the point catches slightly as removed. It is well to remember in this connection that an unsuspected adjunct fissure will often contain beneath it caries deeper than the central point judged defective. In the search for approximal caries great care is required, explorers with very short points being often necessary, as long points will not turn into the cavity owing to the close contact. Frequently a cavity may only be discoverable from one point of access, so that the approximal surfaces should be examined both from the labial and lingual sides. In the absence of evident cavities, some force should be applied to detect softened spots of enamel. The catching of the explorer upon both teeth, after it has passed through the interspace, often simulates the catch in a cavity. 374 DENTAL CARIES Kia -Arte Fig. 357 Explorer for cari> (Jack.i) Dow electric lamp for mouth illumination, with reflectors. Reflector A is jointed to vary the angle of reflection. KcHector B is for illumination of the fauces. Reflector C is for lateral illumination. (Jack.2) Unwaxed floss silk passed over carious surfaces indicates a rough surface by fraying. It may, however, at times pass readily over a cavity easily detected by instruments; so that it is not absolutely reliable as a test. The strong light of an electric mouth I lamp transmitted through the teeth ex- hibits a cavity as an opaque spot outlined upon a pinkish background. It not only permits an easy diagnosis, but also affords evidence of the depth of penetration. Mechanical separators or wedges are at times necessary to press apart contiguous teeth sufficiently to admit exploring in- struments. The necks of the teeth should be examined with sharp points to note any softness of the tooth tissues. The mar- gins, particularly the cervical and neigh- boring margins, of every filling should be explored to test the integrity of the junc- tion of filling and tooth or any excess or deficiency of filling material. The examination should be conducted by one of two systematic methods. In one method the occlusal faces of all the teeth are first examined in one survey, then the interproximal spaces, and lastly, the ' American Text-book of Operative Dentistry. 2 Ibid. HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS 375 buccal and lingual surfaces of the teeth. In the other method every portion of each tooth is examined, beginning with a central incisor or terminal molar, before passing to the adjoining tooth. Any cavity or condition found should be noted upon a diagram for refer- ence at sittings. Diagnosis by Subjective Symptoms. — Complaints by patients that cold or hot, salt, sweet, or acid substances taken into the mouth cause unlocalized or partly localized pain indicate exposed and hypersensitive dentin or pulp exposure. Such complaint is to have due consideration. Pain beginning without the application of special stimuli is like- wise ordinarily connected with caries or its sequelae, and should be taken into account. Pain produced upon mastication has either the same significance or is a symptom of pericemental irritation. Prognosis of Caries If existing caries be promptly treated in youth and a proper sys- tematic prophylaxis be employed, its recurrence during youth may be largely prevented. At about adult age a fair degree of immunity may be expected. In the absence of treatment or prophylaxis the exciting causes seem to become very active, and many teeth may be lost from caries or by reason of extraction for pulp and pericemental diseases. Extraction itself brings many evils in its train. Even advanced caries may be checked by proper filling or crown- ing, and if then prophylaxis receive due attention the prognosis for the teeth is generally good; indeed, it seems as though but few conditions exist dependent upon caries alone which are not subject to correction by some of the means within the resources of the profession. Hypersensitivity of Dentin The exposure of dentin to external agencies is so commonly followed by an increase in sensitivity that the condition requires description in itself. It is a general condition attendant upon abrasion, erosion, and caries, and has a therapeutics of its own. The term sensitive dentin applied to this condition is a misnomer; all vital dentin is sensitive, and its degree of sensitivity diflFers markedly in individuals; it is only when hypersensitivity is observed that the condition becomes pathological. Hypersensitivity of dentin may be defined as such a degree of 376 DENTAL CARIES sensitiveness of the dentinal fibrils as interferes with the comfortable excavation and shaping of a cavity of decay; or which, in the absence of dental ministrations, causes painful symptoms, as a rule, reflected about neighboring parts. Causes and Pathology. — Normally the dentin is protected from external agencies by the enamel, and in the early stages of gum recession by the cementum, though it has been shown that in some cases the dentin is not covered by either. (See p. 165.) With the removal of these coverings by caries, erosion, abrasion, or fracture, the terminal filaments of the dentinal fibrils become sub- jected to sudden variations of temperature ranging from a little above 32° F., the temperature of ice-water, to 130° F., that of very hot foods or liquids. These thermal stimuli at times give evidence of their effect by producing painful sensations. The pulp is stimulated through the odontoblasts and their relations with the terminals of sensory nerves in the pulp, and a degree of vascular overfulness occurs which may be denominated mild hyperemia. The effect of these reactions is to cause the sensory functions of the pulp to become somewhat exalted, and it therefore becomes more responsive to the stimuli. Apart from the effect of thermal changes, other substances act as irritants. The lactic acid and other bacterial products in the cavity of decay without doubt play a part in exalting the irritability of the fibrils. A slightly loosened filling holds the acid in contact, as such cases are often very sensitive. Salt, sweet, or acid substances intro- duced into the mouth are also evidently irritant, as active symptoms follow their application to hypersensitive dentin. Mechanical abrasion or erosion may irritate the fibrils, or at least expose them to the action of other irritants. As a rule, however, the abraded or eroded surfaces are protected from hypersensitivity by the process of eburnation. (See Transparent Zone.) The scraping of necks of teeth with scalers sometimes induces exposure of dentin. Within cavities of decay the hypersensitivity is greatest, as a rule, at the dentinal periphery. That at this point the dichotomous endings of the tubules present a greater number of fibrils to the action of the irritant is quite evident. (See p. 167.) In cervical hypersensitivity the cementum or enamel is removed by abrasion, erosion, or caries, and the fibrils are exposed. The presence of the granular layer of Tomes in this situation, and the possibility of this layer containing the expansions of the fibrils, are to be considered. In certain cases the irritation excited by the touch of an instrument to dentin adjacent to enamel is carried to the pulp by anastomosing HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS 377 dentinal fibrils. This was proved by a few cases, of which the follow- ing is an extreme one: In a central incisor secondary dentin had filled a portion of the pulp cavity (Fig. 358, SD). Caries had subsequently removed the incisal portion of this secondary growth and also the dentin con- taining fibrils leading from the pulp cavity to the middle of the incisal edge. The application of an excavator to dentin in the incisal portion of the cavity (at A), the fibrils of which could have no direct relation with the pulp, produced flashes of pain. This was unmistakably of the character of hypersensitive dentin. A professional friend claimed to feel sensi- tivity in a cervicolingual cavity of a molar in which the filaments had been destroyed by suppuration for one-third of the length of the canals. If his contention was true, indirect transmission of the sensation must have been conducted by ZZtZ Zntin'7^ d!111'- way of the granular layer of Tomes to the ondary dentin; a, point of level of the pulp and thence by the fibrils to tTtLT"'"'*''' ^°''"'''"' its substance. Spots of cervical hypersensitivity have been occasionally recorded as occurring in teeth the canals of which have been filled. Head^ records a case in which the dentin bounding the pulp canal remained hypersensitive for a year after the pulp was removed. In this connection the possibility of the presence of a vital pulp filament in the pulp canal, or of irritable apical tissue receiving the impact of liquid forced down upon it by a canal probe, or of a pericementum irritable to touch of any sort, must all have due differentiation. I have never seen a case of hypersensitivity of dentin in which some filament of pulp was not present in at least a part of the tooth. Dentin cannot become infiamed in the ordinary sense, as leukocytes cannot enter the tubules; nevertheless, the irritability of the fibrils, like that of other protoplasm, may be exalted (or lessened). It has been noted that during excavation of a cavity the irritability is, as a rule, greatest at the surface of the dentin — i. e., at the point at which irritants are present in greatest amount and the fibrils most numerous. With hypersensitivity other functions are increased, and in con- ditions producing a constant stimulation a constructive change may » Dental Cosmos, 1899. 378 DENTAL CARIES occur and the fibrils form tubular substances at their own expense. (See Transparent Zone and Tubular Calcification.) That the hypersensitivity is primarily, as a rule, a disease of the fibrils involved or of the fibrils and their odontoblasts is shown by the fact that occasionally of two cavities in the same tooth one will present a hypersensitivity and another none; again, one part of a cavity may be hypersensitive and the rest not so. In other cases perfectly normal dentin is hypersensitive, as noted when the attempt is made to reduce a sound tooth for bridge-work or a sound fissure is opened for prevention of decay. There are two theories accounting for the transmission of the impulse which is translated by the patient as pain: (1) That a con- traction of the whole cell, fibril and odontoblast, occurs, the sen- sory nerve endings being pressed upon in the act — i. e., contraction causes a lateral increase in size. (2) That a wave-like motion along the protoplasm is set up, causing excitation of the sensory nerves and due to the incompressibility of the water. (Gysi.) The first is analogous to the contraction of a voluntary muscle cell under nerve impulse. The whole muscle cell contracts, though the nerve ending is supplied to only a portion of it.^ If the con- tention of Robertson that the odontoblast is connected with the axis cylinders of the nerves be true, then the contraction pulls the nerve fibril. (See p. 172.) This hypothesis fits the symptoms as excited by both mechanical and chemical irritants, while the second theory does not. Symptoms. — A certain degree of uneasiness of undefined character may at times he noted in teeth containing cavities, but, as a rule, pain other than pulp pain is only felt upon the application of special stimuli. Of course, the presence of ferments, acids, etc., in a cavity are real stimuli. The infiltration of acid, salt, or sweet substances into contact with a hypersensitive surface is followed by a wave of gnawing pain reflected usually along the course of contiguous nerve filaments. While not definitely localized, owing to the fact that the pulp does not pos':ess a tactile or localizing sense, the pain may usually be referred to a certain part of the mouth. The pressure of an instru- ment upon the dentin is attended by a fiash of sharp pain, which continues for a time, but lessens if the contact be maintained. In this test the pain is localized in the affected tooth, the touch of the instrument being followed by a recognition of position by the tactile organ of the tooth, the pericementum. • Black; American System of Dentistry. HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS 379 Occasionally food forced by mastication against a hypersensitive surface, such as due to abrasion or caries in a crevice, will produce a sharp pain subsiding promptly, and which may not be repeated for some time. The mere rubbing together of opposing abraded surfaces may cause the symptom. Cavities dried for filling usually produce a steady pain, caused by dryness and relieved by an analgesic or by filling. It is beyond doubt that individuals differ as to the degrees of normal dentinal sensitivity; the dentin of one person may be cut freely without evidence of marked pain; in another the touch of an instrument to the newly exposed dentin is productive of unbearable pain. The difference in degree of irritability is manifested in another manner: If a mild sedative — for example, oil of cloves or an obtun- dent — be applied to the hypersensitive dentin of one person, it may remove the distressing symptoms, but with others it may be necessary to employ the most extreme measures to reduce in any degree the hypersensitivity. In some cases the exposure of dentin about the necks of teeth may induce such an unbearable local pain or neuralgic condition as to positively demand relief. In a few cases enamel has exhibited sensitivity. In one case the effort to open sound fissures about a cavity for prevention excited sharp pain, ceasing upon removal of the instrument. The patient was, hoM^ever, a sufferer from insomnia, and from the effects of morphine taken for it, and her dentin was exquisitely sensitive. In another patient the side of the enamel exposed by a cavity in a molar analogous to that in Fig. 358 gave flashes of pain when touched with an excavator point, though no evident direct path of trans- mission to the pulp could be seen. Caush's tubes and indirect trans- mission seem the only basis of explanation. (See p. 165.) There is a pseudohypersensitivity of enamel in some cases due to apprehension. The patients can be ridiculed out of the idea by demonstrating its absurdity, as, for example, by touching a cusp and then showing them the part touched. Pericemental irritability at times must also be excluded. There can be no question that systemic, nervous irritability from any cause aggravates the phenomenon of hypersensitivity, though whether it can make dentin more sensitive, or w^hether the patient is less able to endure pain, is not clear. The general perceptivity of the individual seems to play a part, and even apparently normal dentin may be exquisitely hypersen- sitive. Again, pain produced in excavating may be due to the character of the manipulation, heavy continued burring producing heat; lighter touches may excavate equally well, but produce much less pain. The dulness of the excavator or bur has a similar effect. 380 DENTAL CARIES Fig. 359 Diagnosis. — In the diagnosis the above characteristic symptoms are to be considered. The decisive test is made by pressing an instrument upon the suspected surface, when the characteristic pain is produced, subsiding upon or shortly after removal of the contact. Upon the pulpal wall of deep cavities doubt may exist as to whether the pain is due to pulp irritation. A suspected exposure may be differentiated by the localization of the pain upon touch to a point corresponding to the pulp horn or pulp body, or by the point catching in the exposure. Hypersensitive dentin will be more generally distributed or occur at points at which exposure is impossible. Pulp abnor- mality or approach may be detected by means of a drop of cool water or a blast of cool air from a syringe. (See Hyperemia of the Pulp.) Treatment.^ — The methods of treat- ment which have been followed for the relief of hypersensitivity of dentin, and the induction of such a degree of analgesia as will permit the necessary cutting of dentin, may be divided into general and local. General Remedies. — The general remedies employed are those which abolish or lessen the perceptive func- tion in the centres of the fifth pair of nerves, or which reduce hyperirrita- bility of the nervous system. Either general anesthesia or general ano- dynes are employed to lessen per- ception. The inhalation of a few whiffs of chloroform or ethylic ether lessens the perception of pain, or a mixture of chloroform, ether, and alcohol may be used. Chloroform is usuallv avoided in this connection on account of its dangers when used in the sitting position. Slight etherization, the inhalation being carried only to the benumbing point, affords marked relief from the pain incidental to the cutting of hypersensitive dentin. Nitrous oxid and oxygen have been employed with some satisfaction, administered by means of a nasal apparatus, which permits the mouth to be unobstructed. The Teter apparatus furnishes definite quantities of nitrous oxid and oxygen, which may be warmed to increase the anesthetic effect. The administration for excavation of cavities is 1 The Teter apparatus without warmer on apparatus stand. HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS 381 by the nose, and can be continued at pleasure. Fear contraindicates its use for children. ^ Gregg has devised a special nasal inhaler.^ The administration of general anodynes, particularly the com- bination of morphin and atropin, has been found useful in this field. IJ — Morphinae sulph gr. ^ Atropina sulph gr. yi^j M. et ft. pil. No. 1. Sig. — To be taken one-half hour before operation. Flagg noted that blondes bear morphin sulphate better than brunettes; particularly are nervobilious and bilionervous patients idiosyncratically opposed to its use, the physiological action of the drug being reversed or the after-effects being pronounced. Patients having dark hair and blue eyes may be expected to be thus idio- syncratic. For them he recommended morphin bimeconate solution in doses equivalent to \ grain of the salt, to be taken one the evening before and the other before the operation. Chloral in 5- or 10-grain doses, administered in water before the operation, has a quieting effect upon the nervous system. Ambler' has suggested the use of from 10 to 20 drops of fluidextract of piscidia erythrina, to be administered about ten minutes before operating. Drowsiness may be expected. Phenobromate, 10 grains, before operation, or 15 grains for any great pain, may be administered in a copious draught of water. For the reduction of excitement and nervousness in anticipation of dental operation, bromural, 5 grs., ordinarily to be administered while waiting, or 10 grs. in unusual cases, is highly recommended for this purpose by Hecker.^ It is also useful in insomnia, and its associated hyperesthesia. Hyoscyamin hydrobromate, -^^ grain, will be useful in those cases which are associated with muscular spasm or hysteria. The coal-tar derivatives, phenacetin, acetanilid, and others, are occasionally efficient. The preparations known as antikamnia (said to be a combination of acetanilid, caffein citrate, and sodium bicar- bonate) and ammonol (acetanilid and ammonium carbonate, equal parts) are to be preferred in this connection. The dose of the latter two is 10 grains, administered one-half hour before operation. The induction of the hypnotic state belongs in the category of means acting upon the nerve centres. The use of the ordinary suggestion that the work will not be unduly painful, considerate treatment, patience, and the employment of remedies all have a 1 Gregg. 2 Dental Cosmos, 1912, p. 355. 3 Ibid., 1901. * Ibid., 1909, p. 844. 382 ' DENTAL CARIES calming influence, permitting relaxation upon the part of the patient, who, if "keyed up" to expect great pain, will expect and feel unduly. The use of blue-light anesthesia consists in causing the patient to gaze intently for a few minutes at a blue-globed electric light having a reflector behind it. A blue veil is thrown about the head and lamp to exclude daylight. Short operations have been performed under its sedative, or, possibly, hypnotic effects, though it seems to fail in some cases. Local Treatment. — The local treatment of hypersensitive dentin may be considered from two standpoints, according to whether a concavity containing it requires excavation, or whether the hyper- sensitive spots are not to be excavated after treatment. Treatment in Cavities of Decay. — The remedies employed in the endeavor to reduce or abolish hypersensitivity in a cavity of decay at the time of operation are quite numerous; few are, however, always effective. They may be classed under two headings: 1. Those which temporarily benumb or anesthetize the fibrillse and prevent the transmission of sensation. 2. Those which chemically destroy the fibrillse for a distance, thus preventing transmission of sensation. Remedies which Benumb the Fibrillse. — Chief among these for its universality of application is dryness. Dentin, which protests against even the touch of an instrument while wet, has its sensitivity so lessened after the application of a rubber dam and drying, that it may be cut freely, in many cases without the aid of medicinal agents. So well is this recognized that isolation and drying of teeth are regarded as a necessary preliminary to cavity preparation. The degree of insensitivity induced. is in proportion to the dryness. The drying temporarily deprives the dentinal protoplasm of a portion of its water, and inhibits the transmission of sensation by reducing functional activity. A continuous but gentle blast of air passed from a compressed-air apparatus or double bulb through a heated metal bulb and nozzle, or through an electrically heated coil, should be employed until the dentin is desiccated. This is evidenced by its extreme whiteness. Other forms of hot-air syringes may be substituted with less satis- faction and greater fatigue to the operator. The double bulb may be operated by the patient. The application of absolute alcohol assists the drying because of its affinity for water. The addition of a little menthol to the alcohol assists by anesthetic action. The pain from the warm air may at first be quite severe, but even in greatly hypersensitive cases the nozzle of the syringe may soon be approximated to the cavity, though HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS 383 in some cases it may be necessary to make an application of a mixture of equal parts of carbolic acid and oil of cloves, or of gum camphor and carbolic acid (phenol camphor), both of which have some anesthetic effect. Menthol may be added to either. When desirable, their effect may be hastened by pressure with unvulcanized rubber. An instrument known as the "dehydrator" causes absolute alcohol placed in a special chamber between the bulb of the hot-air syringe and the nozzle to be vaporized upon the hypersensitive dentin. The drying effect is thereby augmented and the dentin satisfactorily obtunded. Some degree of dryness is, as a rule, a necessary preliminary to success with other applications. Following dryness, the excavation should be done with sharp instruments and burs. The latter should only be lightly touched to the dentin and be revolved at high speed. Letting the bur occasion- ally run free cools it. The heat of friction is considerable and highly irritating. The combination of potassium carbonate with glycerin makes a water-extracting combination having but little coagulating power. For this reason it may be used in the deeper cavities, but not in cases of almost exposed pulp, as in such cases its application is painful. I^ — Potassium carbonate gr. xv Glycerin f3j Mix in a mortar. To be applied on a pellet of cotton. (P'lagg.) It may be used with effect even upon slightly moist dentin. Not being escharotic to the gum, this remedy is exceedingly useful about the sensitive but undecayed necks of teeth, and may be freely applied after moderate drying of the parts. If necessary, the patient may be given the prescription and directed to apply by means of a clean tooth-pick, which should not be used a second time, as the mixture may be infected and spoiled. Its pain simulates that of zinc chlorid, but is less severe in its character. A mixture of tannin and glycerin has a similar effect. IJ — Tannin - 5Jori5 Glycerin f5j- Mix in a warm mortar. Refrigeration by a spray of ether or ethyl or methyl chlorid reduces the temperature of the fibrils and pulp, benumbing them. The rubber dam should be applied to isolate the teeth operated upon. 384 DENTAL CARIES Ether is applied by means of a double-bulbed atomizer, or one operated by compressed air; the chlorids are contained in glass tubes conveniently capped. The cap being raised, the heat of the hand causes vaporization of the agent within the tube, which forces the liquid out of the orifice of the tube in a fine but forcible stream. A spraying nozzle is also obtainable. The cavity should at first contain a pellet of cotton in order that the dentin may be gradually obtunded and painful response on the part of the pulp avoided. The method may be painful in application, but often satisfactory. Ether odorizes the operating room, and a flame must be avoided. Fig. 360 Ethyl chlorid spray tube. "Vapocain" and "potassocain," proprietary agents which consist of a 15 per cent, solution of cocain in ether, are applied to hyper- sensitive dentin upon the theory that the ether enters the tubules, carrying the cocain into contact with the fibrils; the ether evaporates, leaving the cocain in aqueous solution to benumb them. This requires several minutes. They are useful in the deeper cavities. Jack recommends that the cavity acidity be neutralized before their application.^ A 10 to 25 per cent, solution of cocain hydrochlorate in water may be forced into the tubules by applying it on a pellet of amadou, placing over this soft vulcanite rubber, and producing pressure with a burnisher for from three to six minutes. The pressure should be gradually applied. A gratifying degree of dentinal anesthesia may often be obtained. Adrenalin chlorid solution, 1 to 1000, plus chloreton^ or cocain, has been used in this manner with some effect. A few crystals of the cocain may be picked up on a pellet of cotton moistened with warm water and pressed upon the cavity surface. Miller^ has shown that by taking a modelling composition impres- 1 American Text-book of Operative Dentistry. - Parke, Davis & Co. ' Dental Review, 1906. HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS 385 sion of the cavity, then applying a few threads of cotton saturated with cocain to the floor of the cavity, then placing a thickness of rubber dam o\ er the entire cavity surface, replacing the modelling composition, and producing pressure, anesthesia can be produced when there is not a greasy condition of the cavity, nor thick layers of decalcified dentin nor much secondary dentin present. Cataphoresis (Greek kata, down, and phoreo, I bear or bring) is, in technical parlance, the transference of substances from the anodal or positive pole of a batter}' toward the cathodal or negative pole. They are thus carried into the tissues. Cataphoresis is to be distinguished from electrolysis, by which substances are decomposed and their elements carried from positive to negative or from negative to positive poles, according to their polarity. In cataphoresis a substance is carried unchanged from the positive toward the negative pole, after the manner of granules in protoplasm acted upon by the same force. (See p. 20.) As applied to dentistry, a primary current from a battery arranged with the cells in series has the positive pole or conductor connected with a resistance or current controller capable of being so manipulated as to gradually reduce the resistance to the current a fraction of a volt at a time. This is called a "fractional volt selector." This is usually a broken ring of graphite, to one end of which the incoming current is admitted by means of the conducting cord and travelling indicator; at the other end the current passes out by a similar cord, which in turn is attached to a milliamperemeter or instrument record- ing the quantity of current passing through the circuit. From this a cord leads to the positive electrode applied to the tooth cavity. To the face, neck, or wrist of the patient a moist electrode (negative) is applied, which by its conducting cord leads the current back to the negative pole of the battery. The current passes through the patient. The milliamperemeter is a convenient but not an essential feature of the apparatus, and a rod of graphite or a glass tube with w^ater resistance may be used. Fig. 361 shows the more elegant apparatus arranged almost as described. In the use of the cataphoric apparatus the tooth is securely in- sulated by well-ligatured rubber dam and cotton saturated with a solution of cocain hydrochlorate or citrate of a strength of from 10 per cent, to a saturated solution is placed in the cavity. The platinum anode is wrapped with cotton, dipped in the solution, and inserted into contact with the cotton in the cavity. The controller is now^ so manipulated as to gradually cut out its resistance to the current, and the high resistance of the dentin is gradually overcome. 25 386 DENTAL CARIES The cocain solution should be renewed as dryness occurs, as dryness increases the resistance. The cocain is carried along the fibrils to Fig. 361 the pulp by the electric current, and dentinal followed by pulpal anesthesia results. HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS 387 From eight to fifteen minutes, or sometimes longer, are required for dentinal anesthesia, which loss of time is largely regained in the facility of operation.^ Price^ has shown that pulp anesthesia is gained more readily by concentrating the action of the cocain upon the pulpal wall by means of a small electrode. If general dentinal anesthesia is required he prefers this method, as the pain receptivity of the pulp is abolished. A broader application anesthetizes the dentin. Woodward^ has shown that in the latter case the dentin in a cavity upon the opposite side of a tooth being operated upon ma}' remain sensitive. The pulp may be anesthetized by this method for removal. In difficult conditions this is a very valuable means of therapeutics. The pulp is not injuriously affected in ordinary applications, unless saturated by long application. A reaction resulting in hyperemia may take place. To obviate this, the pulp should not be oversaturated, the fibrils should be treated with carbolic acid, and in deep cavities a non-conductor should be used before filling. In case absolute insensitivity is produced the anatomy of the pulp must carefully be considered, so that it be not exposed during the excavation of the cavity. Insulation of the pulp from thermal shock subsequent to filling is also to have consideration. The pulp may have cocain forced into it by means of a powerful compound-pressure syringe. The Meyers syringe is one of the best. Fig. 362 The Meyers compound syringe for forcing cocain solutions through the dentinal tubules. It is filled with a 2 to 4 per cent, solution of cocain in water; a con- venient drill pit is made with a No. ^ bur; the nozzle of the filled syringe freed of air is forced into the opening and continuous or intermittent pressure produced without releasing the point for several minutes. It is well to allow the air to escape from the pit by holding loosely for a moment. No general cavity anesthesia will result until the cocain solution has infiltrated the area of pulp under- 1 Jack: American Text-book of Operative Dentistry. ' International Dental Journal, November, 1902. 2 Dental Summary, April, 1903. 388 DENTAL CARIES lying the fibrillar connections with the pulp. The forcing of cocain into so delicate a tissue should stop at that point, as more may pro- duce expansive pressure, and may cause a later pulp reaction, as cocain is, to a degree, a protoplasmic poison. The method is useful in pulp extirpation rather than in hypersensitivity, but has occasional use, especially in cervical cavities. Secondary dentin is difficult of penetration, and gradual approaches must be made. It should be so injected into only sound dentin. If the cervix of a cavity is used as the point of injection the pit should be made deeper than the syringe nozzle penetrates, as in this way the lateral tubules can carry the cocain, otherwise they may be occluded by the syringe point. The syringe nozzle may be made flat ended and the pit in the dentin be made with a cone-shaped bur. In another use of cocain a 1 per cent, solution may be injected with a hypodermic syringe into the gum over the apex of the root of a tooth, the object being to paralyze the sensory nerve leading from the pulp. It is not without danger to the heart, though it may be resorted to under proper precautions, such as using adrenalin with the cocain, administering food before the operation, as an empty stomach is an element of danger, the administration of aromatic spirits of ammonia, coffee, or brandy before operating. Other anesthetics are also used. The addition of adrenalin to the cocain inhibits the absorption of cocain from the point of injection; it also acts as a cardiac stimulant. Five drops of a 1 per cent, solution of cocain should be a maximum dose, and should be injected for posterior teeth into the alveolar gum to anesthetize the nerve trunk; in anterior teeth a subgingival injection is sufficient. (Honigmann after Braun.^) After such an injection into the gum a cut may be made to the bone, and a small sterile drill or bur be driven into the diploic structure. A blunt needle is then used to inject deeper. The introduction of a 5 or 10 per cent, solution of cocain upon cotton into the nostril, upon the side of operation, is endorsed by Peck, of Chicago, as a means of anesthetizing the nerve trunk leading from the upper incisors. Escat,^ of Toulouse, France, has observed that a 0.1 per cent, solution on cotton about the size of an almond placed in the nostril in close proximity to the anterior edge of the inferior turbinate, will, in twenty minutes anesthetize the anterior superior dental branch of the fifth nerve, which lies in close proximity to the nasal mucous membrane at this point. The entire tissue about the incisors and cuspids of the side is anesthetized, as is sometimes that of the opposite side in part. 1 Dental Cosmos, 1905, p. 1385. . 2 Ibid., 1908, p. 181. HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS 389 Soderberg' has shown tliat painless excavation of cavities other- wise uncontrolUihle may be effected by the use of nervocidin, an alkah)id obtained by Dr. D. Dalma from the East Indian plant gasu-hasn. Twenty-four hours are required for complete dentinal anesthesia without pulp anesthesia unless a second application be made. The primary effect of nervocidin being irritating, Soderberg recom- mends the additional use of cocain, both being mixed with zinc sulphate cement. R — Gum arable 5j Zinc sulphate §ss Water f5j— M. Dissolve the zinc sulphate in the water, add the gum arable, stir: let stand for twenty-four hours and strain. H — Of above solution f oij Nervocidin gr. x Cocain hydrochlorate gr. x — M. To a portion of the latter solution add uncalcined zinc oxid to make a cement, which is placed in the dried cavity. Uncalcined zinc oxid added to the first formula makes zinc sulphate cement. After excavation the acidity of the nervocidin should be neutralized. Buckley- has recommended : I^ — Menthol gr. xx Chloroformi . . fSss Etheris f5j — M. Sig. — Place a little in the cavity after the rubber dam is adjusted Hot water supplied by a tube leading from a coil heated by electricity and attached to the water supply pipe of the fountain cuspidor has been recommended by A. F. Merriman, Jr., for the obtunding of hypersensitive dentin in cases in which dryness is not readily obtainable, nor immediately or subsequently desirable. It is claimed that satisfactory analgesia is obtained, and that the mucous membrane of the mouth is not unduly uncomfortable, even when the heat is objectionable to the finger of the operator. The advantages of the method for excavation and grinding are obvious and most useful, particularly for trimming live teeth. Remedies "which Chemically Destroy the Fibrils for a Distance, Preventing Transmission of Sensation. — Agents which chemically destroy the dentinal protoplasm form the most extensive group of dentinal obtundents. They include salts of metals, such as zinc chlorid and silver nitrate; carbolic acid and its derivatives, and like bodies; the cresols, etc.; mineral acids, notably sulphuric, chromic, and nitric; organic acids — trichloracetic and lactic ' Dental Cosmos, August, 1903. = Ibid., 1907, p. 328. 390 DENTAL CARIES acids — (full strength) ; alkalies — sodium and potassium hydrates and carbonates. Zinc chlorid, silver nitrate, and carbolic acid all cause coagulation of the fibrils of the dentin. The mineral and organic acids chemic- ally decompose both protoplasm and the calcified tissues. The concentrated alkalies chemically destroy protoplasm and bring about its quick dissolution. Like all active chemical substances, the extent of their action depends upon the freedom with which they are applied. The application of any of these agents, as a rule, causes pain, the degree of suffering being usually in proportion to the depth of the cavity. For this reason the more powerful agents, like zinc chlorid and nitric acid, are to be confined to cavities of moderate depth, while carbolic acid, especially in combination with the oil of cloves, may be used in the deeper ones. Fused zinc chlorid is used in its deliquesced form, and is most active when some of the salt is still undissolved in the bottle. Its pain in suitable cavities is a full, bearable one, gradually increasing, sometimes in waves, until a crisis is reached, when the pain gradually ceases. It has a double action, not only coagulating protoplasm, but combining with its water, owing to its afiinity for the latter. On account of this property its action may be limited by warm water. An undue action of the zinc chlorid is indicated by a throbbing pain; this indicates that the pulp has been irritated. When, as occa- sionally occurs, no pain is produced, no obtundent effect is obtained. If this occur regularly the drug is oversaturated with water. Bogue has suggested that cocain crystals be incorporated with the chlorid of zinc as a means of alleviating the pain incident to the application. Miller, following Hoffheinz, advocated the use of equal parts of zinc chlorid and chloroform. Certain moderately deep cavities may be filled with oxychlorid of zinc cement, the free zinc chlorid acting as an obtundent. This requires a prolonged action, and is only resorted to in cases which do not admit of immediate work, or in which procrastination is desirable. A formula of wide renown is known as Robinson's remedy; this may be made in one or two ways: I^ — Potassium hydrate, (or Sodium hydrate), Carbolic acid p. seq. — -M. Reduce the gelatinous mass formed with alcohol. Or, ^ — Sodium hydrate (deliquesced), Calvert's crystal carbolic acid p. seq. — M. (Huey.) The liquid formed is spoiled when it effloresces upon the sides of the bottle neck. HYPERSENSITIVE DENTIN AND ITS THERAPEUTICS 391 The painfully caustic action of the sodium or potassium hydrate is modified by the carboHc acid. The appHcation of Robinson's remedy is useful in the simpler cavities and about the undecayed but hypersensitive necks of teeth. It is escharotic to the gum. If this remedy or zinc chlorid be required about the periphery of deep cavities the plan suggested by Jack, of varnishing the cavity floor with chloro-percha as an impenetrable protective is valuable. A method similar to the use of Robinson's remedy consists in apply- ing carbolic acid to a cavity and then without removing it, placing a few granules of sodium dioxid.^ Sodium dioxid alone in a slightly moist cavity liberates nascent sodium hydrate (also H2O2), which will destroy the gum protoplasm, and is somewhat effective in hyper- sensitive dentin. Carbolic acid in concentrated form may be applied to any cavity. Jenkins, of Dresden, has recommended that it be used hot; it is par- ticularly useful for cavities containing masses of softened dentin. A variation consists in the application to the cavity, upon a pellet of cotton, and heating it with a hot burnisher. Sodium bicarbonate is at times an efficacious remedy, and may be freely applied to the moist cavity. A 20 per cent, solution of ammonium carbonate, applied for five minutes or longer, is useful.- The nitrate of silver powerfully coagulates fibrillar protoplasm, forming the albuminate of silver, which turns black upon exposure to the light. It is useful in posterior teeth well out of view, and to which the rubber dam cannot well be applied. It is also useful about undecayed hypersensitive necks of molar teeth. It penetrates the dentin for a short distance. For this reason its use is ordinarily confined to posterior teeth, though in some obstinate cases of hyper- sensitive necks of lower incisors and cuspids it may be used. To prevent the production of hypersensitivity in teeth ground for bridge-work, it should be applied over the entire crown. It may be used in saturated aqueous solution upon the dried dentin, or the crystal rubbed upon the slightly moistened dentin. The crystal or fused silver nitrate rubbed upon abraded and sensitive occlusal surfaces often affords much comfort. Craven's method consists of taking up a few crystals upon a hot platinum wire, and then fusing them into a button upon its roughened end. This is then rubbed upon the dentin. Miller has shown that the silver deposit lessens the penetration of acid decalcification (Fig. 363). 1 H. J. Moore: Dental Review, 1906. 2 Thieaing: Dental Cosmos, November, 1903. S92 DENTAL CAttlES The subsequent use of sodium chlorid assists in partially removing the stains, argentic chlorid being formed. Register has suggested the use of iodin followed by ammonia for this purpose. Coming into contact with an amalgam filling, or a bit of amalgam, an intensely black deposit is instantly produced, which, while acid at first, is useful in slowly obtunding dentin in cavities out of view. Curiously enough, not all amalgams do this. For severe cases not yielding to local treatment at the time desired, the following has been recommended:^ Or, I^ — Trioxymethylen, Orthoform p. Make into a paste with carbolic acid. I^ — Menthol crystals 5 parts Phenol crystals 4 parts. Reduce to a syrupy liquid to be used in place of the carbolic acid in the above formula. These pastes are applied to the cavity walls over even decayed dentin, covered with a pellet of cotton, and sealed in with temporary stopping or cement for twenty-four hours only. Formaldehyd gas is liberated in the nascent state and desensitizes the fibrils by harden- FiG. 363 ) Diagram of a lateral perforation treated with gutta- percha; successful for seven years, when breakage of the crown occurred including the perforation: GP, gutta-percha; OZ, oxychlorid of zinc; A, amalgam. perforation. A slight movement of the pegs will permit their with- drawal, leaving openings in the amalgam through which the treat- ment may be subsequently conducted. The amalgam is then allowed to harden (Fig. 365). To carry on the treatment while 1 Artificial Crown and Bridge-work. THERAPEUTICS OF LOSS OF CROWN BY CARIES 409 hardening, form ocresolon cotton pellets may be inserted over the openings in the amalgam and sealed over with soft cement. After canal filling the canals may be fnrther reamed for screws or pins, which are inserted and the operation completed with amalgam or zinc phosphate if the condition of the crown admit of it; or, if crowning be required, this is arranged for in the building up with amalgam. A long perforation at a bifurcation may practically divide molar roots. This is to be made a complete division after treatment of the canals. Each section may be fitted with a pin and amalgam stump, to which a gold barrel is fitted. The barrels are each given an occlu- sal face, or the two a common occlusal face, and soldered together (Fig. 366). If one root be unsuitable it may be extracted and the other used as a foundation for a cantilever crown, a spur from which rests slightly upon the occlusal face of the adjoining tooth (Fig. 367), or the crown may carry a spur which rests in an inlay or filling in the adjoining tooth. A smooth plaque of low-heat, white gutta-percha (not temporary stopping) makes an excellent covering for a perforation. It is made larger than the opening to be covered, pressed to place, and the edges sealed with a hot burnisher. The covering filling will retain it in position. The approach to the perforation should be widely funnelled to permit a ready adaptation. If sepsis occur, the resulting abscess will occur opposite the perforation, or in some cases create a small pocket similar to a pyorrhea pocket. In all cases judgment must be exercised, and the attempt to conserve unsuitable cases avoided (Fig. 368). THERAPEUTICS OF LOSS OF CROWN BY CARIES If the portion of crown left after excavation be self-sustaining, but incapable of retaining a filling in the cavity, pins or screws may be placed in the root canal or the pulp cavity may be enlarged and made retentive. A filling is then built about or into the anchor- age so made. At times the remainder of a tooth crown will support a hollow metal crown. When the carious crown has broken away or filling has become practically impossible or undesirable, the original beauty or useful form of the tooth may be approximately restored by means of one of the many forms of dowelled porcelain crowns, specially constructed gold and porcelain crowns, or all-gold, hollow-metal crowns, or a 410 DENTAL CARIES Fig. 369 broad band may be adjusted and filled in with amalgam after setting with cement. If an anterior root be so hollowed out by caries as to be incapable of supporting a dowelled crown, with or without a cast base, it may be extracted, and the operation of transplantation performed, or, later, an implantation may be made. In the former operation the existing alveolus is enlarged if necessary to accommodate a tooth; in the latter operation a new alveolus is created by means of appropriate trephines and reamers. The tooth is to be prepared as for replantation (which see).^ If teeth have been lost by extraction, the spaces created may be filled by means of bridge-work or plates of various sorts. By common consent crown and bridge-work are considered a special department of dentistry. Therapeutics of Loss of Root by Caries. — This occurs in several ways : 1. After loss of the crown and the extension of the carious process into the interior of the root. In the later stages this root is rendered valueless for crowning purposes, and should be extracted. In some cases a transplan- tation operation would be warrantable, as in case of a single incisor, the other teeth being relatively sound. 2. If an artificial crown has been so placed as to expose the joint to caries, the process may proceed to a considerable ex- tent, but does not necessarily involve the root interior, owing to the presence of the pin. Filling with amalgam or other plastic, or the recrowning is demanded if feasible. The gum having grown in, much packing out may be required; abla- tion may be required as well. 3. In some cases penetrating cervical caries will cause a partial or complete amputation of a lingual or buccal root of an upper molar, or, possibly, a bicuspid. The pulp, of course, will have died, at least at the carious area. The cavity of decay should be cleansed and undercut, and an occlusal tap made for free entrance to the canals. The canals are to be reamed with Downie broaches. The canal of the decayed root is to be enlarged with Kerr root reamers, after which everything is to be dried; a canal probe, or the largest reamer used, which may have Method of restoring lost canal continuity. The cavity should have more retention form than shown, a ' For methods of implantation, see American Text-book of Operative Dentistry. CARIES OF THE TEMPORARY TEETH 411 wax in the spaces between the blades, is passed through the tap across the cavity into the farther portion of the root canal. Good amalgam is to be thoroughly })acked into the cervical cavity and hardened by wafering. When nearly set, the filling is supported against dislodge- ment and the canal probe is carefully withdrawn. After appropriate sterilization of canals with formalin solutions, and the filling of canal apices, an iridioplatinum pin is to be cemented into the involved canal and crown tap, thus strengthening the root against a threatened fracture. If actually separated by decay, excavation will make an open joint, which should be filled with amalgam after the pin has been run through the tap into the root. If this operation does not seem feasible, it is better to extract the separate root portion and trim the stump, as in ordinary root amputation. While the retention of an amputated root is seldom demanded, the editor has several in satisfactory use. The prevention of a threatened fracture is more often demanded. (See also Heteroplasty.) CARIES OF THE TEMPORARY TEETH Caries of the temporary teeth dift'ers but little from that of the permanent teeth. The pulp cavities are, how^ever, relatively larger, and the intensity of the carious process often causes rapid exposure ■ of the pulp. Owing to the flat character of the approximations of the teeth, there is often more approximal than occlusal caries, and the cavities often have weak peripheries. Children have a fear of dental offices, excited by unpleasant experi- ences or the talk of their elders, and they do not mention slight pain such as that excited by hypersensitive dentin. There is, however, abundant evidence that the dentin of the temporary teeth may be hypersensitive. In cavities of simple nature the fillings indicated for adults serve if the operations are well borne. The shapes of the teeth, the restlessness and fear of the little patients, and the free flow of saliva indicate, for the most part, the use of plastic fillings, though the rubber dam may often be readil}' used. In deep cavities not exposing the pulps, the methods employed for adults, of varnishing or insulating with gutta-percha and the subsequent use of zinc phosphate as a lining under metal fillings, are indicated. (See p. 401.) Certain occlusal cavities having small orifices and large interiors are well, and often permanently, filled with pink gutta-percha. Zinc oxid and eugenol made into a stiff paste often fills cavities acceptably, and lasts as well as oxj'phos- phate unless it is too freely masticated upon. 412 DENTAL CARIES If cavities are observed before pain has been complained of, and prompt and quickly subsiding response to applications of cold water is obtained, indicating a normal pulp, the cavity should be excavated, with more regard to removing the marginal caries than to thorough excavation, dried, and an application of a 20 per cent, solution of silver nitrate made for a few minutes, the cavity being subsequently filled. In cases of adjoining approximal cavities there is a disposition for the affected teeth to press together and lessen the size of the dental arch. Bonwill advised as a practice, followed by uniformly good results in such cases, to cleanse the cavities (Fig. 370) and insert masses of pink gutta-percha base-plate. The constant biting upon the gutta-percha causes a separation of the teeth, which increases the size of the arch and affords ^additional space for permanent successors. Hollingsworth introduced the idea of placing a small piece or cap of metal at the cervix, bridging the interdental space. A bit of gutta-percha is to be placed on the Fig 370 Under side of the cap to make a gutta-percha adaptation; then more is built over it. Bon- will advised that before the gutta-percha masses are inserted small pieces of blotting paper saturated with carbolic acid be laid against the dentinal walls and the gutta-percha be packed over them. The more efficient and Mode of preparing appro X- . . . ., . , imai cavities. pcrsistcut autiscptic silvcr nitrate may be ap- plied instead of the carbolic acid. Kirk advises that asbestos felt be heated to destroy any organic matter present in it which might combine with the silver, and then be soaked in a saturated solution of silver nitrate, dried;^ and kept in dark bottles away from the light. Small pieces of the prepared felt may be used as described. With cavities as good as shown in the illustration, wedging and contouring each tooth with amalgam, after the use of silver nitrate and varnish, is quite admissible after making suitable retention. There is no reason why occlusal extension for retention should not be made. The conditions will determine the choice of materials. The silver-nitrate method is particularly applicable to shallow cavities in which excavation for filling is impracticable. The dentin surface is cleansed and dried, and the fused silver nitrate is rubbed upon the surface. This may be done after the method of Craven: a platinum wire is dipped into the powdered salt and held over a flame until the powder fuses into a button. By this means applica- tion can be directly and accurately made. The arch is apt to become CARIES OF THE TEMPORARY TEETH 413 somewhat contracted, and food is liable to wedge between the teeth. Combination fillings of zinc phosphate or oxyphosphate of copper and amalgam are of advantage in case of frail walls. For the anterior teeth silicate, zinc phosphate, and gutta-percha fillings are useful, and for the posterior ones Ames' oxyphosphate of copper serves a good purpose. Caries is very liable to occur upon the approximal surfaces of the second temporary and first permanent molar. If the former be found largely decayed distally, the latter will usually be found decayed on the mesial surface. Amalgam in cavities well extended buccally and lingually, or gutta-percha, serves well until the second temporary molar is lost, when a good gold filling may often be introduced before the second bicuspid erupts. Fig. 371 Right upper temporary molar disked lingually and filled. Well-contoured fillings must be inserted in such a case. As a preventive measure during eruption of the first molar, the second temporary molar may be disked to the form shown in Fig. 371. If incipient or simple decay have occurred on the two teeth, or even the second molar alone, it is then best to wedge the teeth apart and to make a disk separation (on the temporary tooth only) from the lingual or buccal side, or both, and to contour the filling even in exaggeration, so that a minimum of contact shall exist. Any sur- 414 bENTAL CARIES face of dentin exposed by the disking should be included in the cavity, or, if this be not possible, then it should be rubbed with silver nitrate. Such surfaces should be carefully observed at regular intervals; indeed, if prophylaxis can be regularly instituted early and before caries of the first permanent molar, much good will be done. The pulp diseases resulting from caries of the temporary teeth will be considered with those of the permanent teeth. If the temporary teeth be so badly decayed as to be hopeless, so far as filling is con- cerned, they should be extracted. Occasionally the encircling of the teeth with pure gold bands cemented to place or filled in with amal- gam is good practice. In the main the temporary teeth, especially the molars, should be filled with some view to the longevity of the fillings, as they often have to do service for years, and the general health of the mouth is improved. The child should always be treated with kindness and truthfulness to establish faith, yet with sufficient firmness to command control. Under no circumstances should the child be given an excessive dread of dental operations, or be broken by nervous shock, as this attitude defeats the object sought. RECURRENCE OF CARIES Passing over, as disproved by Miller, the theory of Palmer, that caries recurs about fillings as the result of electric action, it may be stated, as proved by scientific and clinical experience, that it recurs because after teeth have been filled conditions exist which may favor the collection of microbic plaques and stagnant food material even more strongly than the original conditions, and that when recurrence has been prevented the work has been done in such a manner as to prevent such collections. The specific defects which favor the formation of bacterial plaques may be epitomized as follows: 1. Lack of approximal contact (food wedging between teeth). 2. Roughness of the filling at an otherwise good approximal con- tact point which menaces the approximating tooth or the margin of the cavity by causing food retention and the spreading of microbic plaques. 3. Unremoved excess of filling material at margins producing a ledge which collects food, etc. The edge of a crown may act in a similar manner. An excess well beneath the gum is more apt to produce gingivitis than caries. PROPHYLAXIS OF CARIES 415 4. Exposure of the cavity margin due to lack of covering hy the fining material, whether not properly placed, flaked away, or flue to fracture of margin during the filling process or subsequently thereto. 5. Exposure of the cavity margin due to shrinkage or shifting of the filling material. The use of material not enduring mastication in places subject to it; the washing out of cement from the joint of an inlay or combination filling or dowelled bandless crown has much the same effect, though often much delayed. 6. Solubility of the filling material, permitting the cavity wall to become exposed. 7. Roughness of tooth surface, produced by polishing fillings with rough approximal trimmers, coarse grit strips, disks, or wheels. Exposure of dentin by overpolishing may be classed with the above. 8. Lack of hygiene of surfaces which tend to decay, partly due to lack of extension of cavity margins. Even poor margins, if well extended, may not decay, whereas existing at or near contacts they are menaces. Lack of extension of approximal cavities often causes failure through failure to include all carious enamel. Lack of exten- sion of a filling into a fissure adjoining it, which fissure may be decayed or invite subsequent decay. Treatment. — The treatment of recurrent caries does not differ materially from that of primary caries. Repairs to obliterate crevices, breaks, or new decays may at times be made; but so often is it the case that apparently slight recurrences are found after removal of the filling to involve the entire cavity wall, that the only sound recommendation applicable to all cases is that the filling be removed and the cavity reprepared and refilled. The exception exists when, after the new cavity of decay is all excavated, the adaptation of the filling is seen to be perfect. Decay at two or more points of recurrence not subject to accurate repair or general inferiority of the filling should condemn the entire piece of work. PROPHYLAXIS OF CARIES If the factors of caries be removed from the mouth, caries cannot occur. That a clean tooth will not decay is a dictum many years established. The microbic plaques and fermentable food substances acting as the causes of caries should, therefore, be kept from collecting upon the teeth. The longer they remain the further they may spread laterally over the tooth surface. In the absence of absolutely exact knowledge of the relation of general systemic conditions to the production of microbic plaques, it may be said that the general health should, if possible, be maintained 416 DENTAL CARIES by the correction of any morbid body state, as, without doubt, perfect good health is a corrective of morbid oral secretions. (See p. 336, etc.) Apart from this, oral cleanliness is of great importance, not only for the health of the teeth, but of the gums, and, indirectly, of the stomach and intestines, which can but be affected by unhealthy oral conditions. Thus while the general health may influence the mouth, the mouth may influence the general health. It has been noted that caries is markedly lessened in well-kept dentures. The first step in the prevention of caries is the removal of all possible causes of bacterial plaque formation. Cavities should be obliterated by means of exactly adapted, perfectly contoured, highly polished, insoluble (in so far as utilizable) fillings, the margins of which are extended into areas subjected to friction by ordinary forces, such as food excursions, brushing, etc. Departures from this principle are to be made for well-judged reasons only. Black kept a record of caries of the enamel over-riding the angle frqm the approximal surface to the buccal or lingual, and found that it occurred only in about one case in a thousand persons. He had previously concluded that these angles were areas of relative immu- nity, kept so by food and brush excursions, and that if possible the cavity should be extended to and not beyond the angle. Hoffheinz claims that it is not so much a question of extension, but of contouring to prevent the contact of margins. By these means centres of infection are "removed, and the problem is reduced to the care of the superficies of the teeth. Calculus should be thoroughly removed, the teeth highly polished and kept polished. This operation mechanically removes the plaques. To prevent their return, daily cleansing of the teeth by the patient has always been practised, and a thorough cleansing once a month or of toner by the operator has been shown by D. D. Smith to be highly efficacious. The patient should be instructed regarding the location of the plaques producing dental disease. A good method is to apply tincture of iodin to the teeth, then douche them with water, which removes the iodin from the clean part. The teeth will gener- ally then look like Fig. 305, which, while a figure of decay, will take the place of a special illustration. While thus stained the effectiveness of floss, etc., can be readily demonstrated. DAILY CLEANSING OF THE TEETH A well-made, stiff brush, having a lengthened tuft of bristles at its tip and its brushing surface serrated, is to be moistened and DAILY CLEANSING OF THE TEETH 417 well charged with a good antiseptic tooth-powder or paste without coarse grit. It is to be grasped in the palm of the hand with the ball of the thumb placed upon the back of the handle, or exactly the reverse, according to the movement desired. The bristles are to be passed over the buccal and lingual surfaces of the teeth, from the gum toward the occlusal surfaces, by means of a dexterous, wiping motion imparted by a turn of the wrist. This cleanses the inter- proximal spaces so far as accessible to the brush. By a light to-and- fro motion, spreading the bristles over the cervices, the lingual and buccal cervices are freed of soft deposits which occur after each meal. Unless the gums be actually torn, this light friction is not injurious. Special attention is to be paid to the buccal surfaces of third molars, which are often ignored even by conscientious patients. This is due to a habit of giving a downward sweep of the brush-tip, which escapes the rather upwardly placed third molar. The lingual surfaces of incisors are cleansed by means of the stiff tip of the brush. In cases of advanced recession of the gum about incisors, a brush with all the bristles except those of the tip cut away (and the stubble ground down) is advantageous. This is also useful for the lingual surfaces of bridge-work. Occlusal surfaces are to be freely brushed. A light brushing after each meal imparts to the mouth a pleasing sense of cleanliness, which has a good moral effect upon the patient, and removes from about the teeth much fermentable material. The teeth should be thoroughly brushed upon retiring with a tooth- powder containing castile soap and free from coarse grit, as pumice or coarse chalk, to remove any debris about the teeth, and the anti- septic and antacid treatment to be mentioned employed. Salol should be omitted, because of its tendency to produce labial eczema; while aromatically agreeable, it has little antiseptic value. A small rubber band should be stretched between the teeth, the inner end released, and then drawn through the interdental space, wiping the approximal surfaces and embrasures. This places the mouth in a fairly aseptic state for the night, during which the oral fluids are at rest and less interfere with fermentation or neutralize its products. Before breakfast the mouth should again be treated with the brush and antiseptic to remove the bacteria developed during the night. Once a week the patient should rub the powder over the inter- proximal spaces, and carry floss silk between the teeth and rub the approximal surfaces, with the object of removing any bacterial collection upon these surfaces. The floss silk should not be forced into the gum, as this will injure the gum margins and force infected material into it, but should be 27 418 DENTAL CARIES first carried gently beneath the gum, wrapped half around the tooth, and then sawed up over the contacts and be brought out from between the teeth. It should be reintroduced at the same interspace and the adjoining tooth polished. After cleansing the teeth at night an antiseptic should be held in the mouth for the space of two minutes, for the purpose of devitalizing bacteria present. For this purpose phenol sodique in 12.5 per cent, solution in water (1 to 7) is as valuable as any agent, though many harmless and effective preparations are sold for this purpose. In a mouth specially prone to caries of the teeth, it is well to use, once or twice a week, a disguised mercuric chlorid wash, 1 to 2000, for the space of two minutes. The object is to thoroughly devitalize oral organisms and promote the action of the milder and more agree- able antiseptics. The following is a useful formula i^ • 3 — Mercuric chlorid gr. vj Thymol . . gr. ij Menthol gr. v Oil eucalyptus gtt. x Glycerin fgij Alcohol • fSiJ Aquse gaultherise ad Oij — M. S. — Use as directed as mouth wash. Finally, after the above treatment, Phillips' milk of magnesia (magnesium hydrate in suspension) should be taken in concentrated form into the mouth, rinsed about, and drawn by suction between the teeth. The excess is to be expectorated and the residue left in the mouth. It is alkaline, slightly astringent, and is credited with some antiseptic property. These processes do not consume much time if the patient be systematic. The brush itself should be sterilized after using. A good glass brush holder is sold which has a small portion of paraform placed in the lower part, and is capped with a metal screw cap. In this the brush may remain until again needed. Dr. Percy R. Howe calls attention to the valuable attributes of a 1 per cent, solution of sodium sulphate, followed by a 1 per cent, solution of sodium bicarbonate, in the dissipation of coagula and mucinous collections in the mouth, rendering the saliva clear and limpid.^ Lime-water also removes this viscidity, and dissolves mucinous plaques. Lime-water has also been shown to possess the property of dissolving bacteria plaques. The periodical cleansing or prophylaxis suggested by D, D. Smith involves the monthly rubbing down of all surfaces accessible to a 1 C. R. Jackson: Dental Summary, 1904. 2 Dental Cosmos, 1905. DAILY CLEANSING OF THE TEETH 419 wedge-.shaped wooden i)olishing point directed by a hand carrier. Powdered pumice is the abrasive suggested. The point is to be gently insiiniated beneath the free gum margin for the purpose of effecting a cleanliness there, which shall prevent collections liable to produce pyorrhea alveolaris. This method may be supplemented by a careful rubbing down of contact points and embrasures by means of floss silk charged with powdered pumice as an additional precaution against approximal caries. The slight cleansing apparently required after a few ^•isits is a strong argument in favor of these prophylactic cleansings. In case of fairly cleanly mouths free of other disease than caries the patient ma\' be instructed in the use of a wood point held in a simple porte- polisher, such as a tube of thin nickelled brass bent at one end to an angle of 45 degrees, and the prophylaxis by the operator executed three or four times a year only. This wood point is useful in cleansing the lingual surfaces of bridge-work, and if floss silk can be passed through a space in a bridge, as for example by using shoemaker's wax on the end of the floss to give it stiffness, the floss will cleanse many parts of the bridge, if it be a fixed piece. Periodical examinations should be made at short intervals, pref- erably at the time of cleansing, for cavities of decay, roughness of filling margins, or accidents to the same. By these means the soil, may be rendered unsuitable to the growth of caries fungi, and their localization at the contacts and other favoring spots is largely pre- vented. Silver nitrate, 40 per cent, to saturated solution, may be applied to surfaces likely to decay, as sulci, contact points, etc., as a means of prevention in mouths subject to same.^ As a systemic prophylactic the diet may be modified and potassium sulphocyanate may be used. (See p. UO.) Some dentists pursue the policy of filling only the larger cavities existing in a mouth, the others being neglected until a subsequent period. Such a method is to be condemned as being a neglect of a plain duty and as tending to the propagation of caries in the mouth. The presence of cavities, calculus, and pyorrhea alveolaris in the mouth all tend to cause infection of the digestive tract, with produc- tion of inflammatory (catarrhal) disturbance, and to cause infection of parts in close association with the teeth as well. Undoubted cases of septic intoxication and infection from decayed teeth and other oral conditions have been reported, the connection ' L. C. Bryan and others. 420 DENTAL CARIES having been shown by their cure after removal of the local cause alone; in other cases the parts (as the stomach) having the second- ary infection well implanted, have required special treatment in addition to the removal of the primary exciting cause. ^ (See Systemic Effects of Pyorrhea Alveolaris.) The evils attendant upon sepsis are to be pointed out to patients who have often a seeming indifference to conditions ranging from simple uncleanliness to loathsome filth within the mouth, which would alarm them if existing in any other part of the body. Aside from all considerations of health or tooth integrity, it is poor economy, and especially for poor people, to neglect these measures which are largely applicable. The prophylaxis of the teeth apart from periodical cleansings is a matter for careful instruction and exhortation of patients who are apt to be persistent backsliders. PROPHYLAXIS IN SYSTEMIC DISEASE During a prolonged illness, seasickness, pregnancy, etc., the pro- phylaxis of the teeth should be as rigidly enforced as possible as a means of preventing decay of the teeth and sepsis of the mouth. It has been shown that during pregnancy osteomalacia may occur, and that it represents a demineralization by decalcification of the bones of the mother. Whether or not this may influence caries of enamel is not certain, though acid secretions occur from the gum margins, but there is no reason why the resistance of the fibrils of the dentin should not be lessened, or even that the dentin may not be to an extent demineralized, as positively claimed by some accurate observers (Black to the contrary). An excessive osteomalacia may be held to represent a deficiency of osteogenetic nutritive material for the child. This would lead to an inferior development of the child's temporary teeth. Any abnormal condition of the mother should be corrected, if possible, in order that her general nutrition and that of the child may not suffer. Probably upon the congenital constitution of the child depends much of its future susceptibility or immunity to caries. Accepting the decalcification theory of osteomalacia, the use by the nursing or gravid mother of mild alkalies internally, such as a tablespoonful of lime water repeated, and the use of lime-containing 1 Hunter; International Dental Journal, 1S99, abstract from Transactions of Odontological Society of Great Britain. PROPHYLAXIS IN SYSTEMIC DISEASE 421 foods, as the cereals, and mineral waters as beverages, cannot hut he of values as antacids furnishing a neutralizing agent for the acid, while the lime probably enters into the development of bone (Hare), and, therefore, would be useful in supplying, via the placenta, mother's milk, and later the child's food, the element needed for the development of teeth. The use of glycerophosphate of lime and soda has been suggested. The teeth should receive all needful care during pregnancy, that the mother should not suffer pain, but work should be of a temporary nature, if necessary, to avoid shock, especially at about the third month of gestation. Attention has been called to the fact that during menstruation a systemic hyperacidity exists, which can be combated by the use of lime internally and milk of magnesia or lime water locally. SECTION IV DISEASES OF THE DENTAL PULP CHAPTER XV CONSTRUCTIVE DISEASES Diseases of the dental pulp are both acute and chronic. Accord- ing to the anatomical features, they may also be divided into con- structive and destructive. The acute diseases are usually destruc- tive; in the chronic, structural and constructive changes are com- monly noted. Constructive diseases of the dental pulp are those attended by the formation of deposits of new masses of calcific substance. Destructive diseases are those which cause retrogressive and necrotic changes in the tissues of the pulp. The essential differ- ence between the two classes of disease is in the mode and character of the degeneration — the one is acute, the other chronic. Pathologically there is no abrupt line of demarcation between diseases of the dentin and those of the pulp, as the dentinal tubules contain the fibrillar prolongations of the odontoblasts of the pulp. Effects produced upon the fibrils cause, therefore, a pulp reaction which may lead either to a construction or destructive activity according to the grade of hyperemia or inflammation set up. As infection may travel via the tubules even septic inflammation may result before the pulp is exposed. Moreover, after constructive changes which are accompanied by more or less atrophy and degeneration, the pulp may undergo the more acute destructive changes. While the exact relations between symp- toms and pathology are not all worked out and the symptoms are aften obscure, due to the fact that the pulp is without the sense of touch or exact location, and, therefore, the pains induced are reflected, as a rule, yet clinical observation and the a:-rays have done much to relate the symptoms and pathology, and one must depend upon these and applied tests for at least a tentative diagnosis, of which confirmation may be sought. 424 CONSTRUCTIVE DISEASES OF THE DENTAL PULP The pathological conditions of the pulp are judged by the phenom- ena induced by applications of air or water of varying temperatures, and by the presence of certain appearances of the tooth, which, taken with the symptoms and tests, lead to a fair inference of the disease present. It was pointed out by Black^ that if a healthy tooth be isolated by a double layer of rubber dam, and a jet of water at a temperature of 40° F. be directed against the tooth, a paroxysm of pain is produced. A jet of hot water will also induce a similar pain, and if the patient's eyes be shielded no difference in the sensations is noted; that is, the pulp responds to thermal stimuli, hot or cold, indifferently. The organ is accustomed to variations of temperature between 60° and 105° to 110° F., and within this range, in a condition of health, takes no apparent cognizance of this degree of change. With a decrease in the amount of dentin covering the pulp — e. g., with the advance of caries — the reaction to thermal stimuli increases in promptness until, when the pulp is nearly exposed, the response is immediate. As the pulp irritation increases there is prompt response to lesser degrees of temperature change, until the pulp comes to respond immediately to water at a temperature of 85° F. or there- about, and slightly over the bodily temperature, 102° F. Later, another feature makes its appearance; instead of a sharp contrac- tion pain, applications of moderate thermal stimuli are followed by a heavy, throbbing pain. Later, similar pains occur in the absence of tangible external sources of irritation. In conditions of abscess intense pain is later caused by hot applications, and cold applications afford relief. In pulp degeneration the response to thermal stimuli may pursue the opposite course. The normally prompt response is followed by delays in reaction, until it is only after the continued application of cold to the exterior of a tooth that a paroxysm of pain is induced. In these cases there follows after a relatively long time an increasing response to heat, as in the former instance, the reaction occurring only upon decided or prolonged heat stimuli. Following upon the period of increased response to heat, in both cases there comes a period of quiescence, in which there is no response whatever to applications of intense cold, even that produced by the evaporation of a spray or ethyl or methyl chlorid — i. e., the sensory function of the pulp is paralyzed. These are the available subjective evidences of the pathological condition of the pulp; while they indicate with a degree of accuracy, 1 American System of Dentistry, vol. i. TUBULAR CALCIFICATION 425 useful in clinical work, the alterations in the pulj), the exact relations between the reactions and the morbid anatomy of the organ are not entirely clear. It is assumed that, in consequence of the loss of the normal protective covering of the pulp, its sensory and perhaps vasomotor nerve fibers become stimulated, overstimulated, irritated, and then paralyzed by thermal stimuli in the progress of caries. The bloodvessels, which retained their tonus up to a certain point, suffer vasomotor irritation ; next, paralysis leading to their dilatation and to the throbbing pain. Later, even change of posture is sufficient to cause distention of the paralyzed vessels, hence pain in resuming the reclining position. Stimulation by cold, until the later stages, causes a sharp, continuous pain, ascribed to the paroxysmal con- traction of the vessels. In the stages of paralysis heat causes further distention of the vessels, and, if gases be present, causes their expansion with pressure upon nerve filaments. The decreasing and delayed response to thermal stimuli must be referred to three sources: (1) An increase in the non-conducting covering of the pulp — i. e., a lessening of the amount of the fluid contents of the dentinal tubuli and a thickening of the dentinal walls, which necessarily implies a recession of the pulp from its normal position; (2) to degeneration of the sensory nerve fibers themselves; and (3) changes in the walls of or about the bloodvessels, which check vasomotor response and changes in the caliber of the vessels. These' three classes of reactions still further emphasize the division of the pulp diseases into two types, the acute and chronic; the first class of reaction is associated with the acute destructive diseases ; the second, with the chronic constructive but degenerative conditions. CONSTRUCTIVE DISEASES OF THE DENTAL PULP The constructive diseases of the dental pulp include all the second- ary dentin formations, tubular calcification, the formation of pulp nodules, and calcareous degeneration of the pulp. Tubular Calcification. — Definition. — By tubular calcification, or, to express the condition more accurately, tubular dentinification, is meant the change that occurs in the dentin which leads to an obliter- ation of the dentinal tubuli by deposition of dentinal material along the inside of the walls of the tubules, with a corresponding atrophy of the fibrils. It is a sclerosis of dentin analogous to osteosclerosis. Causes and Occurrence. — The apparent cause is a mild degree of irritation, not passing the stage inducing constructive metamorphosis, and apparently caused by direct irritation of the fibrils, more par- 426 CONSTRUCTIVE DISEASES OF THE DENTAL PULP ticularly through the action of thermal shock, brushing, mastication, or action of acids. It occurs in the course of mechanical abrasion and erosion of the teeth, under metallic fillings, and probably a modification of the process precedes the slow invasion of dental caries. It begins at once the enamel is removed from the dentin at any point, and the dentin subjected to irritation, showing it to be due to a stimulation of the whole odontoblastic cell (including its. fibrillar prolongation). It occurs in some degree as a normal vital change due to age, and is common in persons who are victims of the gouty or rheumatic diathesis. Pathology.— ^The fibril is lessened in diameter as the lumen of the tubule becomes smaller. There is sometimes an increased, but more often a lessened, sensitivity of the dentin. Other phases of the condition are discussed under transparency of the dentin, to which the disease corresponds. (See p. 360.) The altered dentin becomes translucent, acquiring a horn-like appearance, and, usually, secondary dentin formation begins coinci- dently with it. Andrews claims that granules of calcific matter are pushed into the fibrillse by the odontoblasts and deposited along the inner wall of the tubule, even to obliteration of them. These gran- ules give the color to abraded dentin in the region of the pulp cavity. Tubular calcification is, for the most part, to be regarded in the light of an effect due to a physiological process. It may be regarded as a physiological barrier erected against the progress of caries, erosion, or abrasion, threatening the invasion of the pulp. While it delays the disintegration of the tissue, it does not prevent it. In the cases due to age or the irritants produced by goutiness, it is probably a local expression of a general sclerotic change, the intercellular substance (tubule wall) being formed at the expense of the cellular (fibrilla). In senility the change in the dentin may cause the teeth to be almost transparent. It requires no treatment. Secondary Dentin. — Definition. — By secondary dentin is meant a deposit of dentin upon the wall of the pulp chamber, as the result of pulp stimulation after the pulp has enjoyed a physiological period of rest from dentin formation. It is always attached to the dentin. Causes. — The cause of formation of secondary dentin is a stimu- lation of the pulp to increased functional activity. This stimulus may be provided by any constant irritation of the dentinal fibrils, as, for example, when exposed at necks of teeth, upon abraded or eroded surfaces, or within cavities of decay. The presence of metallic fillings, conductive of thermal changes, may provide the necessary stimulus. Gold crowns upon ground-down crowns of vital teeth have ,a similar effect. The slightly irritative effects of oxychlorid of zinc SECONDARY DENTIN 427 often produce much secondary dentin. It is associated with tubular calcification. A pulp capping may provide the stimulus and new Fig. 372 Secondary dentin formed after exposure of pulp by fracture during extraction. (Tomes.) Bicuspid in which a formation of secondary dentin has failed to ob- viate perforation of the pulp cavity by resorp- tion. (Tomes.) Harding's case of united fracture. The uniting material is of coarse osseous structure with numerous lacunal spaces. (Tomes.) dentin fill the orifice of exposure. Absolute fig. 375 exposure wdthout treatment has been recorded as productive of secondary dentin. In two cases described by Charles Tomes, pulps widely exposed by fracture of crowns during extraction covered themselves completely in. The histological record, as seen in the photo- micrograph, demonstrated that a plastic exu- date was first exuded, which later calcified as an amorphous mass. Next an irregular lamina was formed, and lastly, dentin containing tubules. It is to be inferred that both the pulp and its odonto- blasts may take part in the process (Fig. 372) . I have seen one case in which a wide exposure had been covered in sufficiently to enable me to gently indent the covering, which was Elastic layer of calcific material formed over an exposed pulp. (From a case.) 428 CONSTRUCTIVE DISEASES OF THE DENTAL PULP convex, with a ball burnisher. Upon removal of the instrument it resumed its original shape, owing to its elasticity. The periphery of the original exposure was clearly defined (Fig. 375). In another case of known exposure with bleeding the patient kept eugenol on cotton in the cavity. After several weeks the exposure could not be again discovered. Age seems to be a cause of general secondary dentin formation, but no doubt certain forms of irritation are introduced Fig. 376 Fig. 377 Fig. 376. — Secondary dentin filling the pulp chamber in a case of abrasion of a cuspid tooth: a, portion lost by abrasion; c, abraded surface; d, secondary dentin, filUng a portion of the pulp chamber, and acting as a protection to the pulp; e, slender point of the pulp — irregular deposits are seen on the walls of the pulp chamber, as at /; g, cylindrical calcifications in the root portion of the pulp chamber. Fig. 377. — Secondary dentin from the same specimen as Fig. 376, magnified sufficiently to show the difference in primary and secondary tissue: a, abraded surface crown; 6, secondary den- tin; c, primary dentin; d, junction of primary with secondary dentin; e, remains of pulp tissue; /, small ova^ masses of calcific material. (Black.) competent to produce the changes; for example, slight looseness of teeth, causing a constant pulp stimulation. At times reflex irrita- tion seems to be a competent cause, as in cases of partial abrasion the unworn teeth may be affected in equal degree with the worn ones. Pathology and Morbid Anatomy. — The formation is usually noted opposite to some area of injury, and may be distinguished from normal dentin by its translucency, or sometimes by its color, which SECONDARY DENTIN 429 may be a light brown. The deposit may be of fairly regular or irregular distribution, and even tumors attached to the dentin have been described (Figs. 374 and 378). Black has shown that in the deposits against normal dentin the first-formed portion contains an almost normal number of tubules, but their direction is sharply changed. As the deposits become thicker the tubules become fewer, and finally the dentin becomes amorphous in character (Fig. 381). Fig. 378 Dentinal tumor within pulp chamber: A, diagram of the tooth, with dotted line showing the position of the section B. In B the pulp chamber is shown in section, nearly natural size, show- ing the tumor within. C is an illustration of the tissue of fhe tumor; a, a, the primary dentin; 6, irregular tubules connecting the newgrowth with the primary dentin — most of these are very dark and irregular; c, c, a calcospherite included in the mass; d, apparently a bloodvessel calcified; e, calcified tissue; /, a finely granular mass; g, a spur of very transparent dentin. Dentinal tubules appear at h, h. (Black.) Black relates these appearances with the gradual atrophy and dis- appearance of the odontoblasts. As the pulp becomes smaller it also necessarily undergoes atrophy. Hopewell-Smith, treating of secondary dentin under the title of "Adventitious Dentin," mentions several varieties: (1) Fibrillar, or that containing tube-like markings finer and less regular than in normal dentin. This would correspond to that in Fig. 378, h. (2) Areolar, that containing interglobular spaces formed by the non- 430 CONSTRUCTIVE DISEASES OF THE DENTAL PULP union of calcospherites. (3) Cellular, or that in which the connective- tissue cells of the pulp remain encapsulated in the calcifying matrix. (4) Laminar, in which laminated spherites appear (Fig. 378, c). (5) Hyalin, having a granular or ground-glass-like appearance (the amorphous substance of Black) (Fig. 378,/). He regards the adven- titious dentin as formed by pulp cells rather than by the odonto- blasts. In these cases the pulp deposits calcoglobulin against the dentin. Apparently in some of Black's cases the calcoglobulin was deposited about preexisting fibrillse which continued to persist in the new formation, the remaining odontoblasts receding, while in Tomes' cases the pulps were compelled to calcify a plastic exudate as a sort Fig. 380 Fig. 379. — Illustration of the narrowing of the pulp chamber in a molar (superior) by the deposit of secondary dentin resulting from abrasion, showing the portions of the chamber in which the deposit usually occurs. The light-shaded portion (&) shows the original dimensions of the chamber, which, in this instance, seems to have been pretty large; a, a point of deep abrasion; c, c, remaining pulp chamber, which is mostly filled with irregular masses; d, one of the root canals. It will be observed that the narrowing of the root canal is within the original pulp chamber. (Black.) Fig. 380. — P.D., primary dentin; S.D., secondary dentin; P, pulp chamber; D,D, nodules, of basis for the beginning of tubule formation. This is probably the case in formation of secondary dentin as a repair of exposure under a cap. Black has shown that in abrasion the deposit is more regular than in caries, without doubt due to the fact that the thermal irrita- tion in caries is more irregular than the irritation of the fibrillse by abrasion. A deposit projecting from any point about the pulp cavity side into the pulp is called a "dentinal tumor" (Fig. 378). The entire crown may be removed by abrasion and yet the pulp be protected. It some cases the protective action ceases and the pulp becomes closely approached or exposed (Fig. 265), probably due to a cessation of secondary dentin formation, the result of degeneration and loss of odontoblasts, or it may be due to very rapid wear (a later stage of Fig. 376). SECONDARY DENTIN 431 The mode of deposition upon the sides of the canal in abrasion, shown by Fig. 376, is quite characteristic, and sometimes annoying in that it permits an unlooked-for exposure, which, upon cocain anesthesia, causes one to follow a fine opening for an eighth of an inch or more before finding a proper canal. Deposits in canals may occur, lessening their lumen and increasing the difficulty of canal exploration (Fig. 374). "Secondary growths in cases of abrasion are not confined alone to the abraded teeth, but other teeth which have escaped wear may be affected in equal degree. In all of these cases there is direct evidence that the odontoblastic layer has been stimulated to increased activity and produced the regular secondary deposition."^ (See Reflex Hyperemia of the Pulp.) Secondary dentin is often accompanied by other constructive changes in the pulp — i. e., pulp nodules and calcareous degeneration (Figs. 380 and 386). jMiller has shown that dentin resorption by the pulp may be repaired by a new deposit of secondary dentin, which Hopewell- Smith has shown to be of the nature of cementum. Tomes* describes and illustrates a peculiar case of united fracture occurring in the practice of Mr. Harding. In an incisor an oblique fracture occurred which entirely separated the fractured segment, yet a plastic exudate from the pulp occurred which, when calcified, attached it to the fixed portion of the tooth. The new formation did not resemble dentin (Fig. 373). Fig. 294 illustrates a case of repair of an incisor fractured at a point well up beneath the gum, a condition reasonably insuring asepsis. A firm reattachment occurred. I have seen such a fracture which resulted in pulp death and the coronal portion remained in situ for two years (according to the patient). This would give time for such a plastic exudate to form. In another case I was compelled to remove a pulp for hyperemia two months after a fall fractured a tooth in this location. Kirk^ records a case of immediate replantation in early life, followed in old age by root resorption. The tooth, when extracted, contained secondary dentin, which could only have formed as the result of a reattachment of the pulp. W. H. Trueman'* reported that hypersensitive dentin was noted some years after a replantation imder similar conditions. Osteodentin. — Tomes states that secondary dentinal deposits may assume the character of osteodentin, a form of dentin found in the 1 Black: American System of Dentistry, vol. i. 2 Dental Surgery. ' Proceedings of the Academy of Stomatology, 1902. * Ibid. 432 CONSTRUCTIVE DISEASES OF THE DENTAL PULP teeth of some animals, in which the tissue presents combined char- acteristics of both bone and dentin. He cites the example also that elephants' tusks are frequently repaired with osteodentin after injury. The specimen illustrated (Fig. 382) was taken from a case in which the coronal portion of the pulp chamber was almost obliterated by a deposit of secondary dentin. Probably some of the pulp cells have taken on the characteristics of osteoblasts. Tissue resembling cementum seems to be frequently found as a tissue of repair (Fig. 382) . Fig. 381 Calcification or deposit of secondary dentin, resulting from caries of an incisor: A, diagram of section of incisor, showing caries at a, and secondary dentin at b. B, illustration magnified 200 diameters, to show the tissue of the secondary dentin: a, pulp chamber; b, b, secondary dentin; c, primary dentin. It will be noticed that the dentinal tubes in the secondary dentin gradually disappear, giving place to a clear calcification. (Black.) Results of Secondary Dentin. — The formation of large masses of secondary dentin unquestionably brings about a degenerative con- dition of the pulp which may become a cause of neuralgia. The pulp may die, and, becoming infected, may produce pericemental irrita- tion. In one case seen the secondary deposit in the pulp chamber had separated the canal filaments of the pulp of a multirooted tooth into independent pulps, one of which was dead and the others alive and undergoing degeneration. The specific symptoms were those of pericementitis — i. e., elongation and tenderness to percussion. In another case of a first upper bicuspid the lingual filament was SECONDARY DENTIN 433 perfectly covered in and vital. The buccal filament, likewise enclosed and isolated, contained an abscess within the pulp. The symptoms complained of, however, were those of acute peri- cemental irritation, simulating incipient septic apical pericementitis (Fig. 414). It has been shown by Hopewell-Smith that microorganisms may enter the pulp by way of the spaces or tubes in adventitious dentin. In Burchard's case a molar containing a deep cavity filled with zinc phosphate gave vague pain, finally referred to the tooth, which respo ded only faintly to hot applications and not at all to cold ones. Secondary dentin was found complicated by calcareous degeneration — i. e., a degenerated pulp was present. Fig. 382 Osteodentin: A, outline of incisor, showing a narrowing of the root canal at 6 by a deposit of osteodentin. B, illustration of the tissue: a, primary dentin; b, line of the beginning of a growth of secondary dentin; c, secondary dentin; d, layer of granular matter; e, osteodentin; this has the lacunae at g and dentinal tubes at k; /seems to be the surface of the osseous deposit; i, irregular crystalline deposits; h, the pulp chamber. X 350. (Black.) (Tomes.) In certain cases a deposit extends well into a canal, totally obliter- ating it for much of its length. Unless symptoms be present it may ordinarily be left. In such cases thermal tests for pulp vitality seem often inconclusive. The electric current should be a more satisfactory means of diagnosis, provided the dentin be moist. Secondary dentin is sometimes quite hypersensitive, as shown by attempts at entering the^pulp; in most cases it is quite insensitive until the pulp is reached. It is also difficult, as a rule, to force cocain through secondary dentin, even with a compound syringe, and arsenic acts 28 434 CONSTRUCTIVE DISEASES OF THE DENTAL PULP slowly, though it devitalizes if the dentin be sensitive. (See Dry Gangrene.) Treatment. — Secondary dentin which has been regularly deposited, and particularly in the canals of anterior teeth, calls for no treatment. Should, however, great hypersensitivity of the dentin and pulp, or pulp disease, be evident or inferred from symptoms, the pulp should be removed by forcing in cocain, or arsenic is used. Canal open- ing ma}^ involve a search of some difficulty and necessitate the removal of much dentin. The canals may be much constricted, especially at that portion nearest the pulp chamber. The condition may be more or less complicated by the presence of pulp nodules or calcific degenerations in addition to the secondary dentin. Pulp Nodules. — Definition. — Pulp nodules (pulp stones, nodular calcifications) are masses of more or less translucent, calcific material, apparently the result of secretion, having a fairly definite histological structure differing from that of dentin, and occupying a position within the pulp substance. They are rarely fused with the dentinal walls of the pulp chamber, and then are included by formation of secondary dentin about them. Occurrence. — While these growths may occupy the pulp chambers of teeth in which the pulp has been the seat of direct irritation, their occurrence is by no means confined to such teeth. They are found not only in teeth which have suffered abrasion, erosion, and slowly pro- gressing caries, but, as pointed out by Black, they may, and frequently do, form in other teeth of the same denture which are not directly involved in the irritation. This investigator notes that irritation of the pulp of one tooth of a denture very frequently causes a general hyperesthesia (due to mild reflex hyperemia) of the pulps of all of the teeth. This is particularly^ notable in the type of persons classed as neuralgic. It is also common in persons of the hyperacid diathesis. Nodules are found much more frequently in the teeth of middle-aged persons than in those of youth, although they may be present as early as the ninth year, as shown by skiagraphy. They occur more frequently multiple than single. Some of the larger nodules are evidently formed by the coalescence of smaller ones. Pathology and Morbid Anatomy. — The structure of pulp nodules does not resemble that of dentin; they possess about the same degree of translucency and hardness as secondary dentin. Outwardly they may assume almost any form; they range in size from minute bodies to a size sufficient to almost obliterate the pulp (Figs. 380 and 386). A section of a nodule exhibits the presence of a number of concen- trically laminated bodies, recognizable as hardened calcospherites. Black found them to rarely make up any considerable portion of the PULP NODULES 435 bulk of the nodule. The remainder of the nodule is made up of structureless material which may contain a few fine tubes. He also found deposits in the i)ulp which throw light upon the possible origin of nodules in some cases, and to some extent upon the conditions under which they may be formed. In the pulp of Fiu. 3S3 PA A pulp nodule fused to the parietes of a pulp cavity. Prepared by grinding: PN, pulp nodule; D, dentin of the tooth. X 15. From section by J. F. Colyer. (Hopewell-Smith.) a second molar of a girl, aged fifteen years, in which there had been decided subjective evidences of pulpitis recurring at intervals for a period of two months, he found a mass representing a pulp nodule in its soft state. " About one-half of the coronal portion of the pulp was involved in the inflammation; lying a little inside of the layer of odontoblasts were several masses similar to Fig. 385, having globular 436 CONSTRUCTIVE DISEASES OF THE DENTAL PULP forms in their mass or attached to their margins. The globular bodies present the laminated appearance of calcospherites." These masses may in all probability be interpreted as intermediate products in the formation of nodules; they have not yet become calcified. Fig. 384 Section of a pulp nodule, showing many calcospherites, as pointed out by a, a. (Black.) A small nodule may be made up of laminated, structureless material, the laminae being arranged about a central nucleus, the nature of which is not clear, but may possibly be calcified dead cells (Fig. 387). Fig. 385 The conditions of calcification of nodules are not definitely known. Hopewell-Smith considers that they are deposited by the pulp cells as a secretion about themselves,**and that the cells are later obliterated or may persist in situ (Fig. 388). He also describes and illustrates PULP NODULES 437 a case of a nodule which had within it a pulp cavity containing pulp tissue. Pulp nodules occur, as a rule, in the better grades of teeth which show constructive tendencies upon the part of the pulp. It is possible that in these pulps the pulp cells under conditions of irritation secrete calcoglobulin, which in part is developed into spher- ites and in part remains without definite histological characteristics. The masses are probably calcified after their deposition. Whatever Calcification of the dental pulp: At A is shown the outline of a lower molar with a ca\-itj- at 6. The pulp chamber is much reduced in size and filled with calcific material, as shown in B. a, a, large granular mass of calcific material, which is verj- transparent, but finely granular. A very few irregular lines are seen in the centre, which slightly resemble dentinal tubes; b, an erratic growth of irregularly formed and unusually transparent dentin; c, line of the growth of dentin from the floor of the pulp chamber — the growth from other directions is so perfectly regular as to leave no markings; d, margin of the ca^-ity of decay; e, a bundle of cylindrical forms of calcific material extending down into the root canal. These extended to the apex of the root. (Black.) the origin of the masses — ^by cell secretion or otherwise — the histo- logical record indicates a gradual increase in the size of the deposit. Pressure upon the nerves results in irritation. Pulp nodules are usually found in the coronal portion of the pulp, but sometimes exist in the root portions, either free or embedded in secondary dentin. If they obstruct the lumen of the canal they cause interference with the circulation and nerve tissue and may produce great pain. As in the case of secondary dentin, nodules may be produced by reflex 438 CONSTRUCTIVE DISEASES OF TEE DENTAL PULP hyperemia, as the}^ are quite frequently found in teeth near to an impacted tooth. Symptoms. — Multiple nodules may exist in a dental pulp and give rise to no evident symptoms whatever, as is shown by their presence in extracted teeth, many of them free from caries, and in which there was no history of pain. On the contrary, the pulp of a tooth may be the seat of intractable pain without a depth of carious invasion which would lead to the inference of acute pulp disease; and relief only be secured through devitalization of the pulp, which upon examination may reveal a small pulp nodule. Fig. 387 A pulp nodule isolated from the pulp. Shows its central nuclear formation and its con- centric lamination. Prepared by grinding. X 50. From collection of G. W. Watson. (Hopewell- Smith.) The symptoms attendant upon the presence of nodules, so far as they can be made out, appear to be of two types — those associated with small and those with extensive deposits. Reflex pain is the common associate of both. Small Deposits. — While it is true that pulp nodules may some- times exist in apparently sound teeth without inducing pain, yet the pulps of teeth containing them become excessively hyperesthetic under what are ordinarily mild sources of irritation. This is mani- fested, first, through the contents of the dentinal tubuli; the dentin becomes exquisitely sensitive and cool water directed into a shallow PULP NODULES 439 cavity produces a paroxysmal and excruciatingly painful response from the pulp. In the absence of direct, extraneous irritatidn of the pulp, the dental symptoms may be absent, but a persistent neuralgia may be located at some distant point. Pain in the ear is a frequent symptom. Occasionally an obstinate scalp neuralgia, with the exist- ence of a hyperesthetic spot, appears. Pain in the eye, with tender- ness over the supra-orbital foramen, is also common. Guilford^ has reported a case of tic douloureux of two years' standing, the result of pulp nodules. The pain may be recurrent or persistent. If, in the absence of a more probable explanation of the pain, a pulp nodule be FiQ. 388 p.v M N M N 'J'lie formation of the pulp nodule. Prepared by Mr. Hopcwell-Smilh's process. I'N, pulij nodules; MN, meduUated nerve bundles; P, pulp tissue; C, capillary. X 230. (Uopewcll- Smith.) suspected, and arsenical applications be made to devitalize the pulp, it is found that not only is intense pain caused, but examination after even a week or more shows the pulp to be still vital and hypersensi- tive; and, in order to effect its destruction, repeated applications and large doses of arsenic must be used. Cocain introduced by cata- phoresis is also apt to be slow in action. Large Deposits. — In extensive deposits of pulp nodules the dentin may be almost devoid of sensation, and applications of heat or cold, even in large cavities, may be followed by delayed and faint ' Private communication. 440 CONSTRUCTIVE DISEASES OF THE DENTAL PULP pulp response. Such cases, however, commonly give a history of reflex neuralgia and vague dental pains extending over a period, it may be, of years. With some large deposit the pain may be exquisite. Diagnosis. — Their diagnosis by means of the x-rays is positive (Figs. 389, 390, and 391), but their diagnosis by symptoms may only be inferential and confirmation be lacking until after devitalization of the pulp and the finding of the pulp nodules in its substance. The tardy action of arsenic is also observed in the cases of large deposits, it being frequently necessary to devitalize the pulp piece- meal, and sometimes the arsenic will hardly be tolerated at all. Fig. Fig. 390 Fig. 391 Pulp nodules in the radicular and coronal portions of the canal. (Skiagraphs by Price.i) First and second bicuspid roots filled. Pulp nodule in first molar. (Skiagraph by Lodge.) Treatment. — Pulps inferred or shown by a:-rays to contain nodules should be removed. The cataphoric apparatus or compound syringe or even ordinary cocain pressure may be used to benumb the pulp by cocain; at least, sufficiently for the removal of the nodule. If desired, the remainder of the pulp may generally but not always be anesthetized by the same means and removed. The bloodletting attendant upon removal of the bulb of the pulp usually permits an arsenical application for devitalization of the remainder of the pulp to be painlessly made, but this is not always the case. The same result may be attained by drilling open the'pulp cavity while the patient is under the influence of nitrous oxid gas or somno- form, or, possibly, intra-alveolar injection of cocain. At times arsenic may be applied to the pulpal wall of the cavity, if one exist, or in a specially prepared pocket, without production of painful reaction. After forty-eight hours a portion of dentin is to be removed and a stronger application made. When the pulp is closely approached, the arsenic is to be left a week or longer in position, when, as a rule, ' Items of Interest, 1901. CALCIFIC DEGENERATION OF THE PULP 441 the nodule may be removed. Another application may then be left in position for a week or longer to insure devitalization. If, after devitalization, the nodule or calcific degeneration be found as a spicular deposit in the mouth of the canal, it may usually be removed by teasing it from side to side, first soaking the part with a sodium dioxid solution, or 50 per cent, sulphuric acid, which quickly destroys the organic matter of the pulp. Pericemental reactions are quite apt to follow the removal of such pulps. This result is best obviated by awaiting the thorough death of the pulp filaments before attempting their removal. If such reaction arise, strong sedatives, such as menthol solutions, are to be applied on cotton as root-canal dressings, and counter- irritants are to be applied to the gum. (vSee Non-septic Apical Peri- cementitits.) Calcific Degeneration of the Pulp. — By a calcific degeneration is meant the infiltration of inorganic matter derived from the lymph into tissue which is dead or undergoing degeneration. It occurs in any part of the body in which the necessary conditions are present. (See p. 82.) Causes and Pathology. — The conditions apparently necessary for the production of calcific degeneration are those which occur in a semistagnant blood current. An acid reaction occurs owing to the presence of an excess of carbon dioxid, which favors deposition of inorganic matter. The albuminous matter of the tissue undergoes degenerative changes owing to the faulty nutritive supply and waste removal. Probably some cells die. They or their constituents have some affinity for inorganic salts which are taken up from the lymph. Thus gradually the tissue becomes infiltrated. Those causes which produce a sufficient degeneration of pulp tissue to induce the above process are: (1) The pulp exhaustion due to the formation of secondary dentin or pulp nodules; (2) continued hyperemia or chronic inflammation in which venous hyperemia plays a part. Pathology and Morbid Anatomy. — The calcic material, unlike the cases of nodular calcification, encloses the anatomical elements of a pulp in process of degeneration in a mass produced by deposition, not secretion. In the root portions of pulps in which fibrous ele- ments have become pronounced the calcification may be tubular or cylindrical in character, the nature of the calcareous masses being apparently a deposition about and along the fibers (Fig. 392). The pulps are, of course, living. There is a comparative absence of cellular elements in the pulp — i. e., they have atrophied, degen- 442 CONSTRUCTIVE DISEASES OF THE DENTAL PULP erated, and been absorbed. Upon optical examination the masses are seen to be opaque, are brittle, and decidedly unlike pulp nodules in form. Another evidence of the cellular degeneration is seen in the great ease with which such pulps are removed after devitalization, even the most minute apical portions freely coming away after slightly catching a hook in the pulp — i. e., the usual odontoblastic attach- ment to the dentin is not present. When extracted these pulps have a granular feel to the fingers, and when dry may be quite stiff (Fig. 393). Fig. 392 A, outline of a lower molar, with a large carious cavity at a; h, pulp chamber; the shaded portion, c, was occupied by cylindrical calcifications. B, cylindrical calcifications. X 100. (Black.) Symptoms. — Degenerations of the pulp, as a rule, present symptoms of reflex pain, vaguely referred to other parts. The response to hot applications is usually greater than that to cold ones, and both are delayed — i. e., five seconds or more may elapse before pain follows Fig. 393 Lingual filament of pulp of an upper molar, broken in extraction. The rigidity of the filament was due to the presence of calcific granules. a severe test like the intensely cold spray of ethyl chlorid or a hot burnisher or blast of hot air. At times with an open pulp chamber the symptoms of chronic pulp inflammation are obtained. There may be a painful reaction to arsenic applied to the pulp. CALCIFIC DEGENERATION OF THE PULP 443 Diagnosis and Treatment. — The x-rays should afford a positiv'e diagnosis, but in their absence the diagnosis, apart from the infer- ence from the symptoms, is a postmortem one. In cases warrant- ing the interference, in which there is a delayed response to intense thermal tests applied to a filling or a clean pulpal wall, the dentin over the pulp should be removed and the pulj) devitalized. Upon removal of the pulp it may be found to contain one or more large or many granular masses. Fig. 393 illustrates a case discovered upon fracture of a molar during the operation of extraction. In another case the pulp was slightly bendable when extracted, but after drying for a half-hour became at its apical end of needle-like sharpness and stiffness. It was filled with calcific granules. The constructive diseases of the pulp are an evidence of an attempt upon the part of the pulp to protect itself; but with the exception, perhaps, of a very regularly deposited secondary dentin the effects react upon the pulp itself, causing its destruction. To what extent, therefore, secondary dentin is beneficial is an open question. Evidences of constructive action upon the part of the pulp may occasionally be noted in the temporary teeth — e. g., secondary dentin following deep abrasion. There do not seem to be any observations as to the formation of nodules or calcific degenerations in the pulps of temporary teeth, but there is no good reason why they should not occur, particularly after abrasion. The pulp diseases of the temporary teeth are usually of an acutely destructive nature, which may account in some degree for the absence of reports touching this subject. CHAPTER XVI DESTRUCTIVE DISEASES OF THE DENTAL PULP This class of pulp diseases consists of those of an acute character, although chronic diseases may arise as sequels of the original con- ditions. They are essentially destructive in character and attended by prompt degeneration of pulp tissues. The most important, clinically, are those having an evident association with disorders of the bloodvessels of the pulp. HYPEREMIA OF THE PULP Hyperemia of the pulp is an excess of blood in the more or less dilated vessels of that organ. It is of two forms: active or arterial hyperemia, and venous or passive hyperemia or congestion. These two classes differ in their probable direct causations and in effects. Active Hyperemia of the Pulp. — Definition. — Active or arterial hyperemia of the pulp is an excess of blood in the dilated arteries and capillaries of the pulp, the pulp functions being increased in mild continued cases or disturbed by a gradual passage of the condition into a venous hyperemia in more severe cases. Direct Causes. — The most common cause of active hyperemia of the pulp is a lessening of the non-conducting covering of the organ, enamel, and dentin, leading to an increased response and continued irritation of the pulp through thermal stimuli. A similar condition consists in the presence of large metallic fillings in close proximity to the pulp, through which abnormal thermal stimuli are received (Fig. 394) . Fillings through which prompt pulp response to thermal changes are felt are a direct menace to the continued health of the pulp. It is surprising, however, to what an extent the pulp may protect itself against such stimuli by the formation of secondary dentin and tubular calcification. Thus cervical cavities filled with gold often produce a pulp hyperemia, of which the patient com- plains as painful reaction to cold, but which passes away in a few weeks. The vigorous use of sandpaper disks in finishing large fillings may precipitate an attack of pulp hyperemia, but only if the pulp is in a critical condition. The loss of tooth substance mentioned HYPEREMIA OF THE PULP 445 may occur either through abrasion, erosion, fracture, or caries. The condition frequently occurs without direct exposure of the dental pulp, and at times when cavities are relatively shallow. Even the simple cervical exposure of dentinal fibrillae may cause it, but does not often do so. Septic dentin beneath fillings acts as a cause by con- stantly irritating the dentinal fibrillae. The leaving of septic dentin in a cavity and a firmly placed yet leaking filling may so act. Inclu- sion of saliva beneath a metal or gutta-percha filling, and the imper- ceptible shifting of a filling during placement, are causes of septic dentin. Amalgam may so shift if slight yet excessive force be used in finishing at the first sitting. The sign is the appearance and Fig. 394 Fig. 395 Fig. 396 Fig. 397 Fig. 394. — A, Cavity or metal filling approaching pulp; B, hyperemic (sometimes inflamed) pulp; C, area of hyperemia of apical tissue, due to extension from the pulp or possibly to back pressure of blood. Fig. 395. — A, Area of non-septic inflammation of apical tissue due to injury as from a blow or malocclusion; B, hyperemia or mild non-septic inflammation of the pulp due to overflow from the apical tissue. Fig. 396. — A, pyorrhea pocket; septic inflammation at C; B, area of lesser inflammation; D, hjTDeremia of pulp; E, normal tissue. Fig. 397. — A, ulcerated or necrotic alveolar wall due to injury and infection; B, inflammation more or less non-septic (lesser inflammation) ; C, hyperemia of pulp due to overflow of blood at B. An abscess on an adjoining root has the same pathology. If extending to the molar it infects its pulp from the apex. disappearance of moisture at a visible margin as the filling is moved. This is often unobserved unless one be very thoughtful of its possi- bility. The cement beneath an ill-fitted crown also appears to become saturated with saliva or serum, and its odor indicates septic irritation. This is less likely to occur under gutta-percha, but odor can be noted in some such cases. Hyperemia may occur from the presence of a pulp nodule. All pulp hyperemias, if intense, may extend into the apical tissue and cause pericemental hyperemia with symptoms of tenderness to touch (Fig. 394). Indirect Causes.^ — Pulp hyperemia may also be caused by injury or disease of the apical tissue of a tooth containing a vital pulp. Mal- occlusion from any cause, overfull fillings or crowns, a blow, or 446 DESTRUCTIVE DISEASES OF THE DENTAL PULP . overmalleting, or the extrusion occurring in pyorrhea alveolaris/is competent to produce it. A pericemental hyperemia is first produced, which extends into the pulp (Fig. 395). An abscess upon an adjacent tooth may have its area of hyperemia extend into the apical tissue of the tooth adjoining, thus producing hyperemia of the pulp (p. 129). A fairly deep pyorrhea pocket may frequently act in a similar manner upon the pulp of the tooth (Fig. 396). An intense hyper- emia or inflammation in the pulp of one tooth may, by reflex action, produce hyperemia, with its characteristic response to hot and cold applications, in another tooth, or be due to the causes exciting hyper- cementosis. An aphthous ulcer upon the gum over a tooth has pro- duced arterial hyperemia of the pulp by reflex or by indirect action. Also an ulcerated alveolar process resulting from infected alveolus, or the use of alveolar forceps, or even the regular healing of an alveolus after extraction, may cause it in a healthy adjoining or even distant tooth. Also any irritation along any branch of the fifth nerve or any of its terminals may reflexly induce a hyperemia of the pulp (Fig.' 397). Unquestionably, systemic conditions, as malaria, or syphilis, or irritation in another part of the body than that supplied by the fifth nerve, as the uterus or bladder, may excite pain in the teeth, which, if repeated, sooner or later excites a hyperemia, as in the case of scalp tenderness from dental disease, and which will probably be tempo- rary. Infarction has been induced by malaria, etc. The mode of hyperemia production is probably a dilatation of bloodvessels due to vasomotor disturbance produced by reflex action. Apart from the hyperemia occurring in inflammation and that due to septic dentin, or a septic extradental inflammation, it may be said that arterial and venous hyperemia are mainly due to non-septic causes, and even in septic cases to be mainly in itself aseptic, in so far as the pulp is concerned. Symptoms. — The symptoms of arterial hyperemia vary according to the degree of vascular disturbance. So long as a qtiick, sharp pain is produced by contact with cold or hot substances, ceasing immediately, and only reappearing in response to direct stimuli, no serious vascular disturbance is inferred; but when paroxysms of sharp pain, lasting from many minutes to hours, follow upon an application of cold to a carious cavity, an unbroken enamel surface, a filling, or an area of erosion or abrasion, a profound disturbance of the vessels of the pulp is indicated. The pains, in the absence of direct irritation, are, as a rule, but vaguely located. During paroxysms it is of a lancinating character, and usually reflected to another part than the tooth affected — e. g., HYPEREMIA OF THE PULP 447 a sound tooth at a distance, the gum between or above the teeth, the ear, the eye, the supra-orbital region, the infra-orbital region, the scalp, the chin, the arm, etc. As a rule, when an upper tooth is affected, the pain is located in the superior maxillary division of the fifth nerve; if a lower, in the inferior maxillary division. The pain varies in intensity from a vague uneasiness to an acute neuralgic attack, with tender spots over the point of emergence of the nerve tracts, as at the supra-orbital and infra-orbital and mental foramina. The neuralgic pains are not always constant; they may disappear from the second or third division of the fifth nerve and appear in the first. The proof of the direct connection between the pulp pain and the neuralgia may, in some cases, be clearly made out by the thermal test. When a jet of cool water is directed against the tooth whose pulp is affected, it may produce, in addition to a local pain, an aggra- vation of the neuralgic pains, but one must carefully exclude the extradental causes before diagnosticating a necessity for interference with the tooth tested. Pathology and Morbid Anatomy. — The one distinctive and charac- teristic anatomical condition associated with active hyperemia is an irregular dilatation of the vessels of the pulp.^ Fig. 398 represents a section of the pulp of a tooth extracted during a paroxysm of acute pain — "acute paroxysms of pain lasting for an hour or more were occasionally occurring in consequence of very trivial changes of temperature; the condition had existed for several weeks." In some cases of a similar character — i. e., presenting the same symptoms, but extracted during an interval of quiet — nothing remarkable is presented. The gradual enlargement of the veins indicates the lessening outlet at the apical foramen; or, in other words, the begin- ning and establishment of a venous hyperemia. The most rational explanation of the dilatation of the vessels is that it is an irregular paralysis of vessel walls — i. e., of vasomotor nerves. Whether the more usual painful responses of the pulp to thermal stimuli are due to the stimulation of vasodilator fibers, which causes hyperemia, is a matter of doubt; but the pathological conditions noted in pronounced hyperemia signify a paralysis of vasoconstrictor fibers. Subjected to repeated overstimulation, they become inactive and the vessel walls yield to the pressure of the blood column. Black's researches indicate that the vessel walls may recover their tone and the vasoconstrictor nerves their functional activity after paralysis. Certainly, clinical experience shows that ' Black: American System of Dentistry. 448 DESTRUCTIVE DISEASES OF THE DENTAL PULP _ in all purely arterial hyperemias, or even those associated with mild venous hyperemia — for the two may be inseparable — in cases with symptoms, the cases can be cured if the causes can be removed. Diagnosis and Prognosis. — Diagnosis of hyperemia of the pulp is made through observance of a combination of signs and symptoms. The symptoms leading to its detection are paroxysms of pain induced by thermal stimuli and a history of pain in the region in which this response is elicited. The signs of the condition available for diag- nosis in the order of their importance and frequency are carious Fig. 398 Hyperemia of the dental pulp, showing the injection of the vessels: a, a, membrana eboris, or layer of odontoblasts; 6, b, b, b, vessels distended with blood; c, c, c, c, points from which the blood has fallen in handling the section. (Black.) cavities, not exposing the pulp, the presence of large, well-made metallic fillings, or recently made fillings of any sort, deep erosions or abrasions, the presence of leaking fillings (septic dentin), fractures exposing the dentin, metallic crowns on teeth containing vital pulps, sound or filled teeth affected by pyorrhea, by infected socket, or aphthous ulcer or abscess near by; by blows, or reflexly from other teeth. Sound or filled teeth with pulp nodules, or hypercementosis, may be diagnosticated by the a:-rays only. HYPEREMIA OF THE PULP 449 It is to be remembered that arterial hyperemia may be of several grades of severity, according to the vascular disturbance. The diagnosis is made purely by differentiation, and sometimes only by trying the therapeutic test. The causes acting and other possible pulp diseases must be fairly considered and excluded before a certain diagnosis can be made. As a rule, the absence of pulp exposure and the character of the response to thermal tests are the decisive phenomena. The pulp cannot be examined in daily prac- tice, hence these signs warrant a diagnosis of hyperemia. Exposure of the pulp or the close proximity of the infective mass should lead to a diagnosis of inflammation. Dilated bloodvessels from the dental pulp in hyperemia, from tooth extracted during a paroxysm of intense pain. (Black.) The temperature of the water used in testing should not be lower than 60° F., and should be applied drop by drop. A normal pulp will rarely respond painfully to afew drops of water at the temperature named, flowed into a cavity; but a hyperemic pulp will almost invari- ably respond vigorously. As a rule, a current of air from a chip blower is a test of sufficient severity. In the absence of a carious cavity the source of the pain is to be sought in large fillings, testing each tooth by dropping cool water on the filling; in cases of erosion or abrasion the test is made upon the exposed dentin. The tooth which responds with a quick paroxysm of intense pain, passing away slowly, is diagnosticated as the seat of pulp hyperemia. In making this test doubt may arise as to which of two adjoining teeth is at fault. A small square of rubber dam, with a single hole punched in its centre, may be passed over the tooth to be tested, thus isolating it, yet the water will remain in the mouth. As before 29 450 DESTRUCTIVE DISEASES OF THE DENTAL PULP stated, however, the location of a hyperemia pulp does not always mean the location of the cause, which may be exterior to the tooth, and should be looked for elsewhere before interfering with the pulp hyperemia. The prognosis of arterial hyperemia is favorable for pulp conser- vation in extradental cases and in cases of cavities of decay which admit of cleansing without pulp exposure, or in cases of filled teeth if the fillings are removed, and in which the paroxysms have not been too severe or too often repeated. Properly protected from thermal shocks the vessels may recover their tone. It is also favor- able in cases of light blows or malocclusion if rest of the apical tissues be secured. It w^ould be favorable in cases of deep erosions which can be filled with non-conductors; but this condition is rarely seen in erosion. It is favorable in fractures without exposure if caps can be secured in place, but is unfavorable in ordinary abrasions unless deeper than the general occlusal level, or in sound teeth the pulps of which are irritated without evident cause. In cases of actual exposure of the pulp it contra-indicates attempts at conservation, except in the mildest varieties and most favorable circumstances, and then only when conservation is important. Practically no one can diag- nosticate a pure hyperemia in such a case. Treatment. — The therapeutic principles involved in the treatment of this condition are the removal of the source of irritation and the securing of physiological rest. The treatment is directed toward immediate relief of the existing condition and the prevention of its recurrence. If a carious cavity exist, it is to be freed from debris, and the grosser portions of the carious dentin are removed; the pulp, if unexposed, is to have the layer of softened dentin covering it left unremoved, if leathery and not disintegrated. Sedative agents are imperatively called for; of those used the most effective being the oil of cloves or eugenol, equal parts of oil of cloves and phenol, equal parts of phenol and camphor (phenol cam- phor), equal parts of phenol and thymol (thymophen), a saturated solution of thymol in alcohol or of menthol in chloroform or menthol, 3 parts, phenol, 1 part, or solutions of cocain. Thymol or menthol crystals may be added to any of these. Dentalone and Phenandyne are valuable semi-proprietary preparations. These agents are all germicides as well as sedatives, and, therefore, sterilize the dentin of cavities in which they are sealed. They are to be applied upon a pledget of cotton and carefully secured in place by means of temporary stopping, oxysulphate of zinc, soft zinc phosphate, or facing amalgam; sometimes by the use HYPEREMIA OF THE PULP 451 ot cotton and thickened tincture of benzoin or similar varnish. In from twenty-four to forty-eight hours the tooth is placed under the rubber dam and excavated, if not a case of filling removal; its walls are varnished, and o\'er the wall nearest the pulp a disk of softened gutta-percha is laid. Over this zinc phosphate paste is flowed. "Formagen" or " Jodoformagen" may be used in place of the gutta-percha. A stiff mixture of eugenol and Hubbuck's zinc oxid is a very valuable sedative cement which hardens in saliva and may remain a time as a test and then be in part left as a permanent floor covering. It is usual to complete such fillings with zinc phosphate or gutta-percha, to remain for six months or a year. The conduc- tivity of zinc phosphate is too high to be used as the sole material over pulps which have been the seat of pronounced hyperemia. In mild cases the filling may be completed at once. If the pulp be exposed, it is probably the part of wisdom to remove it immediately by cocain anesthesia or by arsenic after sedation or depletion, though if for any special reason capping be demanded, it may be done. When the hyperemia is active both cocain and arsenic may be resisted. If desired, the protective pocket-like coverings made for arsenical applications may be utilized for the reception of the sedative appli- cation. (See Coverings for Arsenic.) The following history of a case offers a good example of hyperemia (so diagnosticated). A central was drilled lingually with a round bur, by a dentist who mistook a vital tooth for the one threatening an abscess. Finding it vital when the pulp was exposed at a minute orifice, he filled with gold, evidently laying a cylinder of gold across the exposure. For two years the pulp reacted to cold, the response finally becoming so severe that each effort at cleansing the teeth caused pain from thermal shock. As the adjoining tooth was without a lingual pit, and the electric light showed a deep filling, it was removed, and the condition related found. The attempts to remove the pulp by cocain pressure failed four times, once after sedation, and repeated applications of arsenic were necessary. It not infrequently happens that it becomes necessary to assist the pulp arteries to recover their tone by means of counterirritants applied to the gum over the apex of the root. This is especially true in cases of pulp capping. Dental tincture of iodin (iodin, Siij; alcohol, 5j; dissolve by succussion;^ or potassium iodid, sat. sol., and zinc sulphate, sat. sol., p. sq., with iodin crystals to complete saturation"^) is to be applied in spots to the gums, or a mixture 1 Flagg. - Northrop. 452 DESTRUCTIVE DISEASES OF THE DENTAL PULP of equal parts of tincture of iodin and tincture of aconite may be painted upon the gum. A mixture made of two parts of tincture of aconite and one part of chloroform is recommended by Jack/ to be applied to the cleansed and dried mucous membrane by means of a pad of cottonoid, one-half inch wide by three-quarters of an inch long. It should be held in place by the finger for fifteen seconds. Tincture of aconite upon cotton, placed in the rubber cup-applicator of a cataphoric apparatus and held against the gum for a half minute while the current of a few cells is active, will produce a circum- scribed area of irritation which may later lose its epidermis. This amount of irritation is valuable. A capsicum plaster may be used. For any case of obdurate pain systemic sedation or derivation may be employed. (See Pulpitis.) - In cases of abrasion or erosion an obtundent is applied; an exca- vation having a retentive form is made, which is varnished and filled; or in abrasion the pulp may require removal. A tooth containing a large metallic filling must have the filling removed, and after reducing the hyperemia a non-conducting layer must be placed between the pulp and the filling. The precaution should always be taken, when the pulps of teeth in which cavities have been prepared respond unduly to the temperature test, to cover the dentinal walls with a layer of non-conducting material. In the absence of this precaution the constant overstimulation of the pulp by thermal impulses con- ducted through the metallic filling may at any time result in hyper- emia. If mild hyperemia occur after filling with metal, it ordinarily passes away after a few weeks. The fibrilloe at first rebel, then become tolerant, owing to tubular calcification, etc. In the cases due to hypersensitive dentin the powerful coagulant silver nitrate, formaldehyd, etc., are to be tried. (See Hypersensitive Dentin.) In the cases due to apical irritation not only must counterirritants be applied to the gum, but it may be necessary to cap an adjacent tooth with a rubber dam guard in order to guard against the irri- tation of the apical tissue by overocclusion. (See Acute Apical Abscess.) If the hyperemia is of a gradual onset and clue to an overoccluding filling or crown, this is, of course, to be reduced to normal occlusion. If due to the overocclusion induced by chronic pyorrhea, the over- occluding tooth is to be shortened. If of acute onset, a guard may also be necessary. As illustrating its effectiveness in combination with removal of the cause, may be cited a case of an upper third molar 1 American Text-book of Operative Dentistry. HYPEREMIA OF THE PULP 453 with a small pyorrhea pocket on the mesiolingiial aspect of the root. It overoccluded one thirty-second of an inch, each bite producing excruciating local j)ain, with also reflex to the ear. In twenty-four hours' use of the guard, the pocket having l)een treated, the occlusion was almost normal, the reflex pain gone, and the guard was removed and the tooth brought to normal occlusion. In all cases of cause external to the tooth the cause alone is to l)e treated. Trichloracetic acid, or silver nitrate in saturated aqueous solution, may be applied to inflamed bone or aphthje; while "dry socket" or exposed and ulcerated alveolus surface must be treated as indicated. (See Index.) The patient is to be directed to avoid the use of very cold or hot substances. Idiopathic hyperemia occasionally aflFects teeth in which there is no loss of enamel or dentin, and when this condition occurs leads to suspicion that the pulp is the seat of nodular deposits; though cases have occurred, particularly of lower incisors, in which none were found after devitalization. Some form of apical traumatism may also be looked for, or reflexes. If not found, the pulp usually requires devitalization, though counterirritants may be tried. The test of success of remedial measures is the gradual reduction of response to slight variations in temperature — /. e., the pulp gradually bears higher and lower temperatures until, approximately, a normal tolerance is established. As shown by Jack, this varies for hot applications from 152° F. to 118° F., and for cold ones from 74° F. to 32° F. In order to determine the rate of tolerance normal to the individual, he suggests that sound lower incisors be isolated by the rubber dam and tested by throwing upon them first water at a temperature of 80° F. The temperature of the water is then gradually lowered or raised until slight pain is produced by the test. The point registered by the thermometer will be the normal limit of thermal tolerance for the particular test. The data gained are useful in determining the progress of a case of hyperemia. A lack of success in the reduction of the arterial hyperemia is evidence that the more severe condition of venous hyperemia has supervened, or perhaps an infection has caused a true inflammation. When, after fair trial of conservative treatment, the pulp is per- sistently irritable, it should be removed. In the devitalization of hyperemic pulps there is often painful reaction to any of the means employed. Some of these pulps resist cocain pressure in any form even after sedation ; some yield after sedation. Sedation or depletion should precede arsenical applica- 454 DESTRUCTIVE DISEASES OF THE DENTAL PULP tions, and if at any time arsenic produce a painful hyperemia or aggravate one previously existing, it must be removed and sedatives used before its renewal, or it may be applied at another portion of the tooth while sedatives are kept against the pulp. It is evident that such a grade of vascular excitement as exists in cases of exposed dentin is quite capable of producing the constructive diseases of the pulp described as secondary dentin and pulp nodules. On the other hand, inflammation of the pulp has produced resorption of the walls of the pulp chamber. Pulp Irritation from Electric Action. — It is of quite common occurrence that galvanic electricity causes pulp irritation. The cataphoric current too long continued may induce a hyperirritability of the pulp amounting in some cases to evidence of hyperemia, which may subside under proper treatment or eventuate in pulp death from venous hyperemia. The occasional connection of a newly placed or bright amalgam filling with a gold filling, bridge, plate, or clasp, through the medium of saliva or food (which amounts practically to the same thing), will, at times, produce painful galvanic shocks in a vital tooth. Dr. Franz Trauner^ has reported that such pain has been felt in devitalized teeth. This is outside of the editor's experi- ence, and should not occur in totally devitalized teeth, as the electric current is a test for pulp vitality. The mouth mirror, or a fork or pin, touched to a new amalgam filling, may also produce the pain, but a nickelled steel instrument usually does not. Treatment. — With cataphoresis, the mischief being accomplished, the case must be treated as other arterial hyperemias. In the case of shocks from the presence of the two metals it may be ignored if slight and the filling new, as it will probably soon pass away. A well-set and brightly polished amalgam filling may be tarnished if necessary by touching it with a 1 per cent, solution of silver nitrate; or, if good color be a necessity, the pulp of the tooth may be well insulated by means of a gutta-percha substratum, or the pulp may be devitalized. If the fillings be in adjoining teeth, they should be contoured so as to touch persistently if possible. If in the same tooth, the fillings should be connected by either amalgam or gold. Painful shock is sometimes produced by the animal electricity discharged from the operator during dry, cold weather. It usually occurs when the finger is placed upon a metal filling, or the plugger point is returned to a metal filling. Touching the metal part of the chair before approaching the patient will obviate this disagreeable contact. > See Dental Cosmos, 1903. HYPEREMIA OF THE PULP 455 Venous Hyperemia of the Pulp. — Definition. — By venous hyper- emia of the pulp is meant a condition of the pulp in which the return of the blood in the pulp to the heart is mechanically prevented. Causes, Pathology, and Morbid Anatomy. — But two causes seem competent to produce such a venous hyperemia. These are: (1) A preexistent arterial hyperemia; (2) thrombosis of vessels at the apex of the pulp canal. In arterial hyperemia the excess of blood is contained in enlarged capillaries and arterial trunks. The enlarged main trunks or trunk at the apex of the pulp must compress the veins, as the apex of the canal is unyielding. In proportion to the severity of the arterial hyperemia, therefore, are the emergent veins unable to remove the blood collected in the capillaries and venules, which gradually enlarge into varicosities in consequence. It has been shown by Hopewell-Smith^ that thrombosis of the small veins and capillaries throughout the pulp may result in rupture of the arteries, and hemorrhagic extravasations occur — either single or multiple. These he terms hemorrhagic infarcts, although the description given more accurately denotes a minute venous hyper- emia. (See Fibroid Degeneration of the Pulp.) Black has shown that the diapedesis of red corpuscles, which is a characteristic result of engorgement of the veins in venous hyper- emia (see p. 119), occurs in the pulp. Edema, which usually accom- panies venous hyperemia in other situations, cannot well occur in the pulp because of its unyielding surroundings (Fig. 400). It is possible, however, that fluid may exude into the perivascular spaces, compressing the cellular elements. Black has shown that deposits of lymph may thus occur in pulpitis. The intense congestion and distention of the vessel walls permit a free diapedesis of red corpuscles into the pulp tissue. Disintegration of the red cor- puscles may occur and the coloring matter of the corpuscles may be diffused through the dentin, giving it a pink discoloration tech- nically known as "suffusion." The infiltrated dentin may then become progressively discolored through the characteristic changes of color noted in connection with gradually decomposing hemoglobin - — becoming brown or blue, and finally blue black. Cases have occurred of coronal suffusion in which the pulp vitality has persisted for months. In some cases the bulbar portion alone may be dead. Partial gangrene and the general darkening of the tooth may be present even in a single-rooted tooth with the pulp partly alive. This is proof that collateral circulation exists in the pulp. In cases 1 Dental Cosmos, 1907. 456 DESTRUCTIVE DISEASES OF THE DENTAL PULP of suffusion even all the root of a molar ma}' be suffused, and peri- cementitis, associated with such a hyperemia, seems particQlarly intractable. The vasomotor paralysis is extreme. If a tooth receive a blow of sufficient severity, its pulp may die without much evidence of pulp pain. On the other hand, if the blow be less severe, it may give evidence of an arterial hyperemia, gradually increasing in severity. Fig. 400 Section of hyperemic pulp, showing aneurysmal dilatation of the vessels, extravasatioDS of blood, and red blood disks escaped apparently by diapedesis: a, a, dilated vessels; b, b, fc, extrava- sated blood. Besides this, red blood disks are plentifully distributed everywhere in the neighbor- hood of the veins. The tooth was extracted during a paroxysm of pain. (Black.) In the former case; it is probable that the bruising of the apical tissue produces a condition of thrombosis at the apex which involves the pulp by shutting off both its afferent and efferent vessels. A stagnation results, and death from lack of nutrition occurs. This is also termed "jugulation." In the latter case the thrombosis has not occurred, but an arterial hyperemia is set up by the irritation of the pulp nerves, and may go on to venous hyperemia, or, possibly, it might produce the extrava- sations leading to fibroid degeneration of the pulp (which see). HYPEREMIA OF THE PULP 457 It is quite probable that rapid death of the i)ulp in pulpitis is due to the associated venous hyperemia. Kirk^ mentioned an interesting case of venous hyperemia with intense suffusion of all the teeth as the result of hanging. In such a case there was arterial blood supplied to the teeth, but the venous flow was checked. Symptoms. — The symptoms of this condition, in the absence of definite data, can only be inferential. When the paroxysms of pain are continuous, instead of temporary — that is, when the pain, instead of temporarily subsiding, maintains a constant intensity for hours and does not respond promptly to sedative therapeusis, and is accom- panied by a sense of fulness rather than sharp agony — a condition of serious venous congestion is inferred. The case from which Fig. 400 was taken had been the seat of intense paroxysmal pain for some hours. Upon close approach to such a pulp, blueness of the horn instead of pinkness may sometimes be seen. Prognosis. — Perfect recovery from this condition is extremely doubtful, so that if the pulp be not intentionally devitalized and removed, it will undergo degenerative changes. The fact that pulps have remained alive for years, after having been the seat of marked congestion, scarcely warrants the attempt to save so seriously crippled an organ. Treatment. — The prognosis being doubtful, the pulp should be obtunded and devitalized. x\s the pulp pain does not ordinarily yield to sedatives, it should be gently exposed if the excavation does not accomplish its exposure. An antiseptic is to be applied, and by means of a very sharp puncture probe the pulp is to be delicately punctured. A free flow of blood follows, which relieves the vascular engorgement. When this is accomplished the cavity is to be syringed out with warm water, and a pellet of cotton containing a saturated solution of menthol in chloroform may be sealed in the cavity, or simply retained by means of a second pellet of cotton saturated with inspissated tincture of benzoin or chloro-percha. After twenty-four hours an arsenical application may be made for the purpose of pulp devitalization, or the pulp may be removed by other means if tolerated. If desired, the bulb of the pulp may be taken out under general anesthesia, or, possibly, under cocain pressure anesthesia, though intense hyperemia counteracts, as a rule. The extreme paralysis of the vessel walls is occasionally shown by persistent hemorrhage after depletion, and which resists ordinary effort at limitation. In some cases the intense pain may continue ' Private communication. 458 DESTRUCTIVE DISEASES OF THE DEXTAL PULP as well. The application to the pulp of a mixture of powdered thymol and dried alum, equal parts, taken up on a pellet of cotton moistened with a saturated solution of thymol in alcohol, has proved useful in some cases. A general anodyne may be required for relief of the pain. INFLAMMATION OF THE PULP (PULPITIS) Definition. — Pulpitis is the occurrence of the phenomena of inflam- mation within the pulp tissue. The characteristic emigration of leukocytes from the bloodvessel into the perivascular tissues must have occurred. Causes. — This morbid anatomy is usually found associated with dis- eases of the tooth crown or pericemental tissue which admit bacteria to the pulp. At the same time it is quite possible that a non-septic irritant, such, for example, as a partially absorbed extravasation of red corpuscles or undue pressure of a filling upon a thin lamina of healthy dentin overlying the pulp, or as has occurred of a metal filling upon or even extending into a pulp, or an escharotic applied to the pulp may induce the characteristic pathology of inflammation. (See Inflammation, p. 121.) According to the character of the cause, therefore, inflammation of the pulp may be divided into simple and infective. It may be that a simple inflammation may become an infective one owing to the association of bacteria — e. g., the pressure of a foreign body may initiate the process and the inflamed pulp become a soil for the propagation of the bacteria present. The causes of pulpitis may be grouped under three headings: 1. Mechanical or physical causes, which irritate by acting as foreign bodies, or by pressure. 2. Chemical causes, which act as irritants by either producing a chemical destruction of pulp tissue, or by irritation without direct destruction. In the former case the dead tissue acts as a foreign body against which the pulp reacts in an effort to cause its exfoliation or absorption. 3. Parasitic or infective, which cause the phenomena of infective inflammation. Pulpitis is classified, according to its extent, into partial and com- plete; according to its duration, into acute and chronic; according to its infective character, into purulent and non-purulent; and, again, according to the character of the degeneration which follows upon the inflammatory process. While pathologically these conditions may INFLAMMATION OF THE PULP 459* be clearly dift'erentiated from one another, they may be reduced to more compact groii])in^s accordino- to their clinical si<)nificance. For exami)le, acute ])ul])itis is frequently infective, partial, and purulent; chronic pulpitis is frequently' non-infective, extensive, non-purulent, and followed by secondary degenerations. It is, however, often purulent, and. of course, infective. P'or the sake of convenience, pulpitis will receive a clinical division into acute and chronic. Acute Pulpitis. — By acute pulpitis is meant that form of inflam- mation of the pulp which runs an acti^'e and more or less violent course toward pulp death, and has associated with it acute par- oxysms of pain. Causes. — The causes of acute pulpitis are direct and indirect, intrinsic and extrinsic; the vast majority of cases being due to extrinsic causes. The direct intrinsic causes are hemorrhagic extrava- sations accompanying venous congestion, or thrombosis, pulp nodules, and injury of the vessels at the apex of the root. The direct extrinsic causes are, perhaps, invariably associated with bacterial invasion, a possible exception being the pressure of filling material upon a thin elastic lamina of softened dentin, covering the pulp. The dental pulp is intolerant of the slightest pressure, and rebels vigorously when subjected to compression. Irritating drugs may also act as irritants — e. g., zinc chlorid. It is not necessary that the pulp should be exposed to permit bacterial infection, and extensive bacterial invasion is probably not necessary for the production of pulpitis. The waste products, ptomains, etc., of bacteria may find their way to the surface of the pulp via the dentinal tubuli, through a layer of softened dentin, and excite inflammation. It is extremely probable that infection of the pulp is an invariable consequence of its exposure; but as a pulp may be exposed without subjective evidences of hyperemia or inflammation, it follows that infection does not necessarily imply inflammation, though the absence of acute symptoms may be accounted for by the escape of the effusions into the cavity of decay. The presence of a gross irritant, such as a mass of food debris, vegetable seeds, bread crumbs, etc., in contact with the pulp will precipitate an acute inflammation in which bac- terial relations must be taken into consideration. "The severity of the inflammation does not appear to be propor- tionate to the number of bacteria present, and in a highly inflamed pulp we may be able to find but few bacteria. . . . The conclusion seems to be justified that the inflammation is due to the combined action of the bacteria and their products (acids, ptomains, etc.) with which the carious dentin becomes 460 DESTRUCTIVE DISEASES OF THE DENTAL PULP impregnated."^ Goadby has shown that the Streptococcus brevis and Bacillus necrodentalis may pass through the tubules of even secondary dentin. Pulpitis from injur}- of the vessels at the apex of the pulp must be mentioned. It may occur in consequence of blows, biting upon hard substances, too rapid wedging, the rapid movement of teeth in orthodontia,^ and the progressive loosening of teeth in pyorrhea alveolaris. In these cases the pericementum is primarily affected by a non-septic pericementitis which extends into the pulp, producing a venous hyperemia as an accompaniment, and the teeth are tender upon percussion. Pain in the teeth upon assuming the recumbent position, dull, heavy uneasiness about the jaws, and inordinate response to thermal stimuli, particularly to heat, point to pulpitis. Fig. 401 Inflammation of dental pulp: a, a, normal cells; 6, b, b, b, inflammatory elements; c, cells in process of division (^^ inch). (Black.) Bacteria from an abscess on an adjoining tooth or from a pyorrhea pocket may infect a pulp from the apex. This will cause the death of a single pulp, but only inflammation in a multirooted pulp. Infection by way of the blood stream is a possibility. The pressure of an impacted tooth may also act as a cause. Morbid Anatomy and Pathology. — In determining the existence of pulpitis, no matter what the symptoms which have presented or the condition as to exposure, etc., the microscopic examination of sections of the affected organ constitutes the only decisive test ; if the changes 1 Miller: Dental Cosmos, 1894. 2 Buckley, through a circular letter to orthodontists, obtained opinions that the upper centrals and laterals are most liable owing to the frequency of displacement, character of movement prominence of location, and the curve of lateral roots. Items of Interest, December, 1910. INFLAMMATION OF THE PULP 401 characteristic of inflammation he ahsent, no mutter what the symp- toms, pulpitis did not exist. The essential feature of the process is emigration of the white blood corpuscles from the small veins into the Fig. 402 Interstitial pulpitis with pulp notlulc in sUu. (V. A. Latham.) Minute inflammatory focu.s within the tissues of the pulp: a, a, arterial twngs; 6, a nerve bundle; c, collection of leukocytes. (Black.) intercellular matrix of the pul]). At first the inflammatory elements (leukocytes) are scattered through the spaces between the pulp cells (Fig. 401); at a later stage the territory is occupied by round indif- 462 DESTRUCTIVE DISEASES OF THE DENTAL PULP ferent cells alone. The inflammation may be widespread, as shown in Fig. 402, or may be localized to some portion of the pulp, as one horn of a pulp; Black noted also inflammatory action occurring in small islands (Fig. 403). Swelling of the pulp (from exudation) cannot occur unless there be a break in the wall of the pulp chamber through which additional space can be gained. Black has recorded that "he found beneath the layer of odontoblasts in the region of an exposure an unmistakable deposit of inflammatory lymph. The case had a history of severe toothache for two days, two weeks previously. The pulp exhibited evidences of previous extravasations of blood from hyperemia." There is evidence that the pulp may recover from attacks of inflammation, and that resolution occurs. In some cases, as shown under the head of calcareous degeneration, the tissues may become infiltrated with calcic material. In others, chronic degenerative changes — inflammatory degeneration — may supervene. Suppuration of the pulp is a common accompaniment of pulp inflammation; this, being necessarily infective, will be described separately. Gaskell^ has reported a case where a central incisor entirely free from caries exhibited on its palatal aspect a pinkish tinge, which increased in depth until the enamel overlying crushed in, revealing the pulp of the tooth lying inimediately beneath; there had been a resorption of a large mass of the dentin lying between the pulp and the enamel. The pulp was removed and the tooth filled. No history is given as to the condition of the root, whether resorption had occurred there or not. Shortly after, the adjoining central incisor exhibited a like pink coloration, which increased, leading to the inference that resorption was in progress in this tooth also. At the suggestion of E. C. Kirk the patient received continued doses of arsenic iodid and the compound syrup of the hypophosphites, in the hope of inducing a general and local constructive metamorphosis. This treatment was followed by a gradual disappearance of the pink coloration, an evidence of a redeposition of dentin. In the absence of histological data it is impossible to state just what was the nature of the repair tissue in this particular case, but Miller^ has shown that the pulp may take up a resorptive function and remove dentin which may later be redeposited as anomalous tissue. The new dentin does not contain tubules, but has the characteristics 'of cemental tissue^ (osteodentin), or even bone with Haversian systems'* ' Proceedings of the Academy of Stomatologj', Philadelphia, 1S95. 2 Dental Cosmos, August, 1901. 3 Hopewell-Smith: Histology and Pathohistology of the Teeth. * Salter. INFLAMMATION OF THE PULP 463 (Fig. 404). Tliis jirocess has its analofi;iie in the tusks of elej)hants and also in the pnxhiction of IIowshii)'s hvciniit in the resorption of the pericementum, these hicuntie hiter being filled up with cementum. There have been cases of inflamed pulp in teeth decayed while yet impacted. In these cases there is usually some form of sinus connecting the tooth with the mouth. Symptoms. — The early stage of inflammation is an arterial hyper- emia, and as the leukocytes collect in the venules a venous hyperemia is established. No matter how far the area of stasis extends, beyond it will exist an area of arterial hyperemia. Owing to the enclosing canal walls and constricted apex a general venous hyperemia may be established which causes the death of the pulp. Fui. 404 Resorption of the walls of the pulp chamber and redeposition of new calcific matter: a, pulp chamber; b, c, d, portions of resorption areas not refilled and walled ofT by the new deposit-forming cavities occupied originally by the pulp tissue. (Miller.) In view of these facts it is not surprising that the symptoms of pulp inflammation take on somewhat the characteristics of both arterial and venous hyperemia. The diapedesis of leukocytes and exudation of fluid cause the phenomena of heavy, boring pain and a feeling of internal pressure. The pulp ifriay be exposed and no symptoms be present. A sudden pressure of food or toothpick, suction upon the pulp or the contact of cold or hot, salt, sweet, or acid substances, may excite an attack of throbbing or lancinating pain. This may be localized in the tooth 464 DESTRUCTIVE DISEASES OF THE DENTAL PULP or may be reflected to other teeth or the parts mentioned under hyperemia. The assumption of the ■ recumbent position permits an increased flow of blood into the paretic vessels of the pulp and increased suffer- ing results in correspondence with the law that inflamed parts are always more painful in the dependent position. (See Pathological First Dentition.) Indeed, recumbency is sufficient at times to induce a paroxysm in a comparatively quiet but inflamed pulp. Under a capping or filling pressing on the pulp or thin dentin the pain may begin as a slight pain and gradually increase in intensity, or it may respond as a sudden agony, beginning even some time after the operation. In the later stage of pulp inflammation the pain is of a heavy, boring, continuous character, the pericementum becomes somewhat hyperemic, and the tooth responds to tapping. In case of a highly irritable pulp, however, the concussion of the pulp produced by tapping may readily cause pain. In pulpitis the pulp responds both to heat and cold, but, as a rule, more to the former than to the latter. There have been many cases of reflex neuroses developed by inflamed pulps, reflex pains in the face, eye, ear, neck, scalp, chest, arm, heart, etc., as well as functional disorders of the eye, ear, and brain. One case of dementia prsecox was cured by removal of a tooth with inflamed exposed pulp.-^ Diagnosis. — The diagnosis is largely inferential and made by observation of the symptoms and conditions existing. The pulp may be exposed or closely approached by caries, or the pulp may be approximated by a large filling. If there be a leak about the filling, a septic fluid or actual decay beneath the flUing may be the exciting cause. In the absence of evident causes such sepsis is always to have consideration, and, if necessary, the filling must be removed and tests applied. The more obscure causes, such as abscesses upon adjoining teeth, infection from the pericemental tract in the course of pyorrhea, looseness of teeth or traumatisms, are to be carefully considered. If the tooth involved be uncertain, each tooth should "be placed under rubber dam and tested thoroughly. Prognosis. — The prognosis is always bad for the comfortable conservation of the pulp, and it should be removed and the canal filled. Treatment. — The treatment of pulpitis involves the reduction of the amount of blood in the vessels of the pulp, the sterilization of the infected area, the relief from the pain, and the removal of the pulp. It is usual to excavate the cavity of decay thoroughly enough to 1 Upson: Dental Cosmos, 1910, p. 529. INFLAMMATION OF THE PULP 465 remove from over the pulp decayed dentin which would prevent the action of remedies or act as an irritant. The cavity is then washed and a sedative applied. (See p. 450.) A creamy paste of bicarbonate of soda in carbolic acid has been recommended.^ The addition of a trifle of powdered alum to any of the sedatives acts as an astringent to the vessels. During the half hour succeeding the application the pulp should give some indication of relief. If it be somewhat decided, a portion of the remedy used should, if possible, be sealed in the cavity for twenty-four hours. The covering may be prepared first as for arsenic. (See Coverings for Arsenic.) If not possible to seal it in, it may be covered with cotton saturated with a varnish made by evaporating tincture of benzoin. This varnish hardens like sandarac varnish, but, unlike it, is not irritant. Claims are made for alcohol used as for pressure anesthesia. If after the first half hour no indication of relief has been obtained, it is well to expose the pulp and to relieve the engorged vessels by delicately puncturing it. (See Extirpation of Pulp.) After exposing the pulp it will perhaps exude a bead of pus, which makes the diag- nosis one of pulp suppuration. After free bleeding, which may be encouraged by means of warm water, the sedatives will usually act. It may be necessary at times to employ short general anesthesia (nitrous oxid gas, etc.) as a means to obtain free bloodletting. Every- thing being prepared, the patient is anesthetized and the bulb of the pulp cut out, or in a single-rooted tooth the entire pulp may be taken out. At times cocain pressure anesthesia is effective at least for the removal of the bulb of the inflamed pulp, and sometimes of the entire pulp; often, however, it causes too much pain. In case of partial extirpation, not only is free bleeding induced, but the diseased pulp tissue is largely removed. When hemorrhage ceases arsenic may be applied, or pressure anesthesia attempted. If the hemorrhage be obstinate the application of powdered thymol and dried alum may be used. (See Venous Hyperemia.) When sedatives are used upon the pulp, counterirritants applied to the gum are aids of great value, and are to be used as described under Arterial Hyperemia. Instead of these the principle of depletion may be employed. Deep cuts may be made with a sharp bistoury in the gum overlying the root apex. The anastomosis with the vessels of the apical tissue is expected to cause the cuts to act as openings made in veins leading from the inflamed pulp. According to Nancrede, depletion on the venous side of an inflamed area markedly reduces engorgement. In 1 Gerdtzen. 30 466 DESTRUCTIVE DISEASES OF THE DENTAL PULP addition to these measures catharsis is a valuable means of derivation ; a tablespoonful of sulphate of magnesia is to be dissolved in a goblet of water and taken internally at least a half hour before a meal. If the pain be obdurate and its return feared, two |-grain sulphate of morphin tablets may be dispensed, preferably by the operator, to be taken only in case of severe pain and an hour apart. Acetanilid and phenacetin are also useful. The following is a useful anodyne and antineuralgic prescription: I^ — Acetphenetidini (phenacetin) , Acetanilidi : . . . . aa gr. xxx Quininse sulphatis gr. xv — M. Pone in capsulas no. vi. S. — One morning and evening. (See also Treatment of Facial Neuralgia.) HalP has suggested: Bf — Aspirin 5s3 Codein gr. iss M. et. ft. chart No. vi. Sig. — One every half hour until relieved. Quiet of the pulp must be secured before an arsenical application is made, or the latter merely increases the irritation instead of promptly devitalizing. Should such an irritation occur or be feared, arsenic may be sealed in an opening made in another part of the tooth (a "pocket"^), with a view to devitalizing the pulp through an avenue of healthy pulp tissue. At the same time the pulp may be quieted by sedative applications made in the cavity of decay. Instead of drilling a special pit, the arsenic may be applied at a portion of healthy dentin in the cavity, which is at some distance from the orifice of exposure; over the latter the analgesic may be placed. SUPPURATION OF THE PULP DefiniUon. — By suppuration of the dental pulp is meant a forma- tion of pus on its surface (ulceration) or in its substance (abscess). It occurs both as an acute and as a chronic affection. Causes. — The immediate cause of suppuration of the pulp is the ingress of pyogenic organisms to the pulp. As in inflammation of the pulp, while usually associated with direct exposure of the pulp, suppuration may occur in pulps covered by softened or even unsoft- ened dentin. ' Dental Cosmos, 1910, p. 1085. * ^ Flagg. SUPPURATION OF THE PULP 467 Fia. 405 Arkovy^ first observed infection of the pulp while still co^•e^e(l by a layer of iinsoftened dentin (Fig. 405). Goadby has shown that microorgan- isms may penetrate even secondary den- tin, a condition not infrequently seen (Fig. 414). Miller states that sections of the over- lying dentin in a case of suppuration of the pulp showed the same forms of bacteria as were found in the pulp itself. Bacteria which have entered the body through wounds, etc., may be deposited in the pulp as well as in any other part of the body, wherever there may be a - . , . __., ., Invasion of pulp by micrococci. lessened resistance at the time. While (Arkovy.) Fig. 406 A, diagram of lower molar with caries at a which exposes the pulp; the darkened portion at 6 shows the extent of the inflammation; the rest of the organ was free from inflammatory change. B, illustration of the inflamed tissue, showing a part destroyed by suppuration at a; the odonto- blasts are undermined at b; the bloodvessels which were filled with blood clot in the section are left blank here, that they may be more apparent. (Black.) bacteria may thus enter from the circulation, there is usually abun- dant opportunity for their entrance from the mouth. Suppuration 1 Diagnostik der Zahnkrankheiten. 468 DESTRUCTIVE DISEASES OF THE DENTAL PULP of the pulp is a not infrequent sequel of the capping of pulps which have given evidence of a previous hyperemia or inflammation. [Fig. 407 Acufe suppurative pulpitis in the coronal portion; /, intensely inflamed horn; A, abscess; V, bloodvessels engorged with blood; S, superficially inflamed horn; A'^, nest of inflammation. X 10. (Bodecker.) Morbid Anatomy and Pathology. — Anatomically pulp suppuration (purulent or pyogenic pulpitis) is of two general varieties: one begins upon or close to the surface of an exposed pulp, and gradually destroys the organ through a process of progressive ulceration SUPPURATION OF THE PULP 469 (Fig. 406); the second, that confined in the substance of the pulp, causes the gradual destruction of a i)art of the pulp through the formation of circumscribed abscesses (Fig. 407). Ulceration of the Pulp. — Of these two forms, ulceration is the more common. The capillaries (Fig. 406) are blocked with coagu- lated blood (they are left open in the illustration to clearly mark their position); the intercapillary meshwork is occupied by inflam- matory exudation ; the surface of the pulp is eroded and covered with pus corpuscles; the ulcerative process is undermining the layer of odontoblasts. The suppurative process penetrates the body of the pulp, following the direction of its veins and hollowing out the organ Fig. 408 FiQ. 409 Fig. 410 Fig. 411 Fig. 412 /\ ■ / --> Microorganisms found in cultures from gangrenous pulp. (Miller.) into a deep cavern. Black regards the persistence of the layer of odontoblasts as indicating an inferior vitality, as it shows they are less susceptible of change of form than the other cells of the organ. The process of ulceration may continue for weeks or months until the entire organ has been destroyed molecularly. The necrotic por- tions undergo putrefactive decomposition, probably passing through the same stages that any albuminous substance passes in its serial decomposition, into the end-products — ammonia, carbon dioxid, hydrogen sulphid, and water. "Very interesting and instructive results were obtained by exam- ining the material from different parts of the same tooth. In the case illustrated in Fig. 408 the pulp chamber at a was wide open and 470 DESTRUCTIVE DISEASES OF THE DENTAL PULP filled with food particles, which had a foul, half-putrid odor; at b the pulp was putrid and foul-smelling; at c there was a small abscess, filled with pure white pus, while the tissue between this point and the apex of the root was highly inflamed and bright red. Material from the pulp chamber (Fig. 408, a) contained the forms shown in Fig. 409; material from point b those shown in Fig. 410, and from the point c those shown in Fig. 411. We perceive a gradual dimin- ution of the large cocci, and the appearance of small, delicate cocci and diplococci." (Miller.^) The editor has observed cases of vital but finally ulcerated pulps under canal fillings. In one case twelve years had elapsed between the partial canal filling and the more recent observation. Symptoms. — If the cavity of decay be open the pus and serous exudate may freely escape, so that the symptoms may not exceed a dull, gnawing pain, which is usually reflex in character. As a rule, the response to cold will be much delayed or even absent. Intense pain may exist when the pus cannot find exit owing to food debris being massed in the pulp chamber, or owing to the presence of a filling or mass of secondary dentin. The case then resembles and practically becomes one of abscess of the pulp. The chief diagnostic feature of pulp ulceration is the presence of the subacute inflammatory symptoms described above and the presence of a pulp partially removed by decomposition of its upper portion. Thus if the pulp chamber be open at one horn, and a probe may be passed into it for a short distance until it comes into contact with an irritable portion of pulp, and when withdrawn have the odor of putrefaction, the diagnosis is clear — loss of pulp substance by putre- factive changes, presumably by suppuration. In some teeth it may be by partial gangrene. Many phases of this condition may be seen; thus in an extreme case one canal of a lower molar contained a highly irritable vital filament of pulp extending but one-quarter inch from the apical foramen; a second canal was entirely occupied by a per- fectly vital but ulcerating filament; the third canal contained an entirely dead pulp. The bulb of the pulp had disappeared, doubtless by suppuration. Treatment. — The treatment of pulp ulceration in its early stages involves the opening of the orifice of exposure, the sterilization of the superfices of the pulp, and pulp removal. Superficial sterilization may be accomplished by removing the pus or putrefactive material present by means of warm 3 per cent. 1 Dental Cosmos, 1894. SUPPURATION OF THE PULP 471 hydrogen dioxid. The saturated solutions of thymol in alcohol or menthol in chloroform, or 2 per cent, formaldehyd or diluted formo- cresol may be sealed in position against the pulp for twenty-four hours as an antiseptic. The application of arsenic may then be safely made. In favorable cases the bulb of the pulp, or even the entire pulp, may be removed at the first or second sitting by means of cautiously apphed cocain pressure anesthesia. In some cases, however, the patient will rebel. When a part of the canal filaments alone remain, after syringing to remove pus, the pressure anesthesia may be resorted to. A long thread of cotton is saturated with carbolic acid or carbolic acid and cocain, and gently packed into the canal against the pulp fila- ment. Pressure with vulcanizable rubber is now produced, and after a few minutes the pulp will be sterilized and anesthetized sufficiently for removal. It is better to treat each canal separately as a general pressure will probably fail. Puncturing is also useful at times (which see). Arsenic may be cautiously placed on cotton half-way up a canal against such a pulp filament. Another method consists of packing a thread of cotton dipped in carbolic acid tightly against the filament, in which thrombosis is thus induced. Abscess of the Pulp. — Abscess of the pulp is usually situated near the point of exposure of the organ. It may be confined to one horn of the pulp, or may involve nearly the entire substance of the pulp, the peripheral tissue of the pulp being unbroken. Abscess may exist at some distance beneath the surface of the pulp, and the latter be still covered with a layer of dentin. Burchard once uncovered the horn of a molar pulp which was covered by a lamina of hard dentin, and no fluid appeared; but upon passing a sharp probe into the white area of exposure for over one-eighth of an inch or more there was a free flow of pus which quickly filled the larger carious cavity. A pulp removed entire from a tooth, and which was yellowish white in color and unbroken, showed upon section its interior hollowed out into an enormous abscess cavity (Fig. 413). The bloodvessels were blocked; the peripheral tissues were unaltered; between the odontoblasts and the abscess cavity, the latter lined with pus corpuscles, evidences of inflammation were plenty. Black found that the odontoblasts retained their form after neighboring cells of the pulp had been destroyed. Miller's^ researches show a preponderance of cocci and micrococci in cases of enclosed abscess; cocci and diplococci were of constant occurrence. Many of the forms, both cocci and bacilli, were cultivable 1 Dental Cosmos, 1894. 472 DESTRUCTIVE DISEASES OF THE DENTAL PULP upon gelatin and agar-agar. Some of them, cocci and bacilli, brought about the liquefaction of gelatin; others did not. So that it must be inferred that infective inflammation and necrosis of the pulp may occur without suppuration. (See Gangrene of the Pulp.) In some instances streptococci were found. In the freely exposed pulps varieties of organisms were found which would render clear the possibility of a general infection by way of the dental pulp. Symptoms. — The usual symptoms are as follows: In a tooth con- taining an enormous filling, one in which the pulp has been exposed, or in a tooth having a large carious cavity, the patient gives a history of discomfort or decided pain, appearing at intervals, sometimes Fig. 413 Transverse section of inferior bicuspid pulp, one-half diagrammatic: a, abscess cavity; 6, embryonic cells at the periphery of the abscess cavity; c, occluded bloodvessels. (Burchard.) appearing and disappearing suddenly, the existing condition having been ushered in by dull, gnawing pain, which is usually not positively located, although it may be. The pain grows in intensity, and, in contradistinction to the pulp conditions previously described, pain is relieved instead of increased by applications of cold. It may be, however, that the prolonged contact of iced water may induce a response. The response to heat is marked, so that a mouthful of hot coffee or even the warmth of the tongue may precipitate an attack of severe and continued pain. Pain produced upon passing from a warm to a cold atmosphere, and vice versa, is also symptomatic. If the pulp be freely exposed and pricked with a sharp instrument, a flow of pus follows in many cases, and the relief is almost immediate. SUPPURATION OF THE PULP 473 Fig. 414 III the earlier stages a period of throbbing pain may follow evacuation of the pus. In other cases the response to heat may decrease until it is almost absent, and the case only be seen when evidences of the action of bacterial products upon the pericementum appear, which they usually do in the later stages of pulp suppuration, when the tooth becomes loose, extruded, and tender upon percussion. The symptoms of pericemental disturbance may simulate those of incipient, acute, apical abscess, even though a quarter of an inch or more of apical pulp tissue exist in a vital though highly inflamed condition. Upon clinical evidence it is assumed that the inflammation of the pulp produces inflammation of the apical tissue (Fig. 414), In one case the gum and contiguous parts about an upper molar were swollen, apical abscess diag- nosticated, and a free flow of pus followed by blood obtained upon opening the crown. An examina- tion made twenty-four hours later, after symptoms had subsided, de- monstrated all three pulp filaments to be alive when a j^ost hoc diagnosis of extensive abscess of the pulp was made. If untreated, symptoms of pulp and pericemental disturbance may disappear for weeks or months; but if the parts be not perfectly sterilized and reinfection prevented, it is only a question of time when septic pericementitis will arise. Diagnosis. — The most valuable diagnostic sign is the peculiar reaction to thermal stimuli — the decreasing, then absent response to cold, and the increasing reaction to applications of heat. This reaction, together with the continued gnawing and full sensation in the tooth, usually affords a diagnosis which is confirmed by evacuating pus from the pulp, which exudes usually as a minute bead followed by blood, although the reverse order may obtain. In cases where several teeth are involved in the diagnosis, differ- entiation is made by isolation of each tooth by means of a small square of rubber dam. The thermal test is then applied. The pres- ence of a quantity of secondary dentin will confuse by causing dulness of response. In such case the electric test should be resorted to. (See Dry Gangrene.) In some cases secondary dentin will have formed in the pulp cavity and the abscess may be found in one of Abscess of the pulp after formation of a large amount of secondary dentin, dividing the pulp into two portions: S D, secondary dentin; V P, abscess or confined pus; I, area of apical inflammation. (Diagrammatic.) (After case in the mouth.) 474 DESTRUCTIVE DISEASES OF THE DENTAL PULP the filaments, while the other will be apparently healthy. Fig. 414 is a diagram of a number of cases seen in practice. Fig. 415 Chronic suppurative pulpitis terminatng in calcification of the pus and atrophy of the pulp: A', larger abscess, filled with calcified pus; A^, abscess at the periphery of the pulp; A^, A^, small longitudinal abscesses, all calcified; N, calcified nerve bundle; C, C, calcareous depositions in the fibrous pulp tissue; P, P, pigment clusters from pre^'ious hemorrhage. X 10. (Bodecker). Prognosis. — General experience regards ulceration and abscess of the pulp as precursors of the death of the organ. Usually this is by progressive suppuration. It is undoubtedly true, however, that attempts at circumvallation of the dead tissue are made in some cases (Fig. 415). The pus cells undergo degeneration and the CHRONIC INFLAMMATION OF THE PULP 475 abscess site may be the seat of calcareous deposits. Even in these cases death is delayed, not averted. The remainder of the pulp undergoes atrophic changes, and commonly suppuration reappears. Treatment. — The treatment of the case consists in relieving the existing pain, completing the devitalization of the pulp, and removing it in such a manner that no organisms or dead matter are carried beyond the apex of the root. To secure relief, evacuation of the pus is imperatively necessary. The organ is freely exposed, exercising no pressure in gaining free access to it. If pus does not flow upon exposure of the surface of the pulp, a sharp, slender, sterilized probe is quickly passed into the substance of the pulp, when, if pus be present, it vnW usually escape freely through the opening thus made and be followed by blood. If the pus formation be limited and circumscribed, throbbing pain may follow, which promptly quiets under an application of cocain in glycerin or other sedative. The application is not made until the pus flow ceases. A pellet of cotton wet with a 1 per cent, solution of formalin, or a saturated solution of thymol in alcohol or other antiseptic sedative, is laid upon the pulp and the cavity is sealed for twenty-four hours (never longer), and then an arsenical application is made. Should the exposed portion of the pulp be insensitive it is cut away until access is had to the vital portion, where the arsenic is to be applied. The pulp may sometimes be anesthetized by cocain for removal. The rubber dam need not necessarily be applied for the treatment preliminary to devitalization, but the pulp should be kept under the influence of antiseptics. CHRONIC INFLAMMATION OF THE PULP In cases in which the resistive force of the pulp is great and the causes of less violent nature or less violent in action, the inflammation may be of low grade and continue for some time. Pulp ulceration may pursue a chronic course, as has already been described. Abscess of the pulp may also become chronic, and the pulp may even encap- sule the pus area, and, the bacteria dying, the abscess area may become the seat of calcareous deposits. Sclerosis of the Pulp. — Inflammation of a low grade may persist in the pulp for long periods, giving rise to an increase of its fibrous tissue with atrophy of the cellular elements, producing a condition found in chronic interstitial inflammation in some other tissues — a sclerosis. Instead of the usual distribution of myxomatous tissue, bands and bundles of fibrous tissue appear. The pulp appears 476 DESTRUCTIVE DISEASES OF THE DENTAL PULP shrunken and stiff, bloodvessels are contracted and sclerotic, and the nerve fibers have undergone partial or complete atrophy and degeneration (Figs. 416 and 417). Fig. 416 Chronic inflammation of the pulp, areolation, and degeneration. (Black.) Black found that in the late stages of sclerotic atroph}^ areolae developed in the bundles of connective tissue, the inflammatory Fig. 417 Pulpitis arteriosclerosi.s; nerve degeneration. (V. A. Latham.) elements having disappeared and the areolae being occupied by fluid. Arkovy describes the condition as reticular atroph}^ of the pulp (P'ig. 416). CHRONIC INFLAMMATION OF THE PULP 477 The condition would point, as suggested by Black, to venous hyperemia as the cause of the edema rather than inflammation; but the evidences of former chronic inflammation in the existence of the bundles of reticulated tissue show this to have been the essen- tial condition. The observations of the -same writer indicate that atrophy of the odontoblasts is a usual accompaniment of all of the chronic pulp aft'ections. Fig. 418 ■■^^fe- "■^?^:^' A, a first lower molar with a cavity at a completely filled by an hypertrophy of the pulp, which has grown out through the orifice, exposing the pulp at h. B, a field illustrating the tissue of the growth, which is composed almost entirely of granulation tissue of a very primitive type, a, a covering of epithehum presenting papillae; 6, epithelium apparently without papillse. (Black.) Sclerotic and other chronic degenerations of the pulp usually present the history of one or more attacks of pulpitis in the past, with more or less continuous uneasiness extending over a long period. The response of the pulp to all tests becomes diminished and dull. Treatment. — Such pulps are to be devitalized and removed. Chronic Hyperplastic (Hypertrophic) Pulpitis. — When the pulp is exposed over a wide area, long-continued chronic inflammation may lead to an enlargement of the organ w4th a protrusion of an altered pulp mass through the orifice of exposure, producing the condition known clinically as fungous pulp. When the growth 478 DESTRUCTIVE DISEASES OF THE DENTAL PULP extends bej'ond the boundaries of the orifice and then increases in bulk it forms a pedunculated mass to which the term polypus of the pulp has_been applied. Fig. 419 Hyperplastic myxomatous pulp, which filled a carious cavity: M, lobules made up of papillae of a myxomatous structure, rich in capillary and venous bloodvessels; G, calcareous globule; E, epithelial cover of papillae. X 10. (Bodecker.) Morbid Anatomy and Pathology. — The growth has its origin in a chronic inflammation of the body of the pulp; the organ swells, and contact with the sharp edges of the orifice of exposure excites a continued irritation, leading to further proliferation of the cells of the inflamed part, so that a large mass of embryonic tissue is formed (Fig. 418), termed by Black granulation tissue of a low type. As in the granulation tissue of repair, bloodvessels grow into this mass, so that it may bleed at a slight touch. Black noted in his case illustrated a covering of squamous epithelium upon the periphery CHRONIC INFLAMMATION OF THE PULP 479 of the growth, which might he interpreted as the transformation of mesoblastic into epiblastic tissue, l)ut the correct explanation beyond doubt is that advanced by the same author, that the epitheHum is transplanted from the gums, and grows after the manner of a skin graft. The growth does not contain nerves. The cavity in which it lies is often fairly free from decalcified dentin, the walls appearing as though subjected to an absorbent action. Fig. 420 Acute pulpitis: S, secondary dentin; B, bay-like excavations filled with medullarj' or inflam- matory corpuscles; V, transverse section of a bloodvessel; M, multinuclear body. X 300. (Bodecker.) These growths may undergo further changes; higher organization of the granulation tissue occurs and fibrous tissue is formed; the cells may undergo degenerations, first granular, then fatty, and suppu- ration and gangrene may occur. Tomes^ records a case where calcification of an hypertrophied section of a pulp occurred; but as the case was due to traumatism (fracture of a tooth), difterent vital conditions existed from those in the cases under discussion. Actual calcification of the mass is scarcely possible, although calcareous degeneration may occur within the fungous mass (Fig. 419). While the growth occupies a cavity of decay, it seems at times to have acted upon the carious dentin so as to remove it by absorption, leaving the cavity more or less clean. ' Dental Surgery, third edition. 480 DESTRUCTIVE DISEASES OF THE DENTAL PULP Resorption of the walls of the pulp chamber may occur as an accompaniment of chronic pulpitis. What appears to be an idio- pathic dentin resorption is described on p. 462, Black records a case where, after pulp capping in a lower molar and the insertion of a large gold filling, the tooth was examined at the end of ten years; for two or three years the pulp had given evidences of irritability, and when the pulp was removed the pulp chamber was found enor- mously enlarged and opening into the pericementum between the Fig. 421 Fig. 422 Fig. 423 Fig. 424 Hypertrophy of pulps. (Garretson.) roots of the teeth. Fig. 420 exhibits resorption of previously formed secondary dentin with the probable agency through which the resorption is brought about. The area of resorption is invaded by numerous multinucleated cells, which are evidently performing the function of odontoclasts. As shown by Miller, Hopewell-Smith, and others, a reconstructive change may occur and adventitious dentin be redeposited in the area of resorption (Fig. 404). Fig. 425 Fig. 426 Hypertrophy of the gum. (Garretson.) Hypertrophy of the pericementum. (Garretson.) Symptoms. — The symptoms of chronic pulp inflammations and degenerations are usually those of long-continued discomfort, with reflex pains, which rarely persist into the latest stages of degeneration. The response to heat and cold, present at first, declines until the pulp scarcely reacts, and then but slowly. No nerve fibers develop in the hypertrophic pulp tissue, so that the newgrowth has no sensitivity in itself, although pressure upon it may cause sharp pain through the still vital pulp nerves themselves. CHRONIC INFLAMMATION OF THE PULP 481 Four or five of these hypertrophies may exist in a mouth, filHng whole cavities of decay, the surrounding tooth structure being in various stages of disintegration. They seem to be comparatively insensitive to mastication (Fig. 422). Hypertrophy of the pulp also may be associated with pulp ulcera- tion, the growth arising from one canal of a tooth. Regeneration of an extirpated pulp has been claimed, but I have never seen any cases that were not referable to the above form of hypertrophy, or to a fungoid growth from the pericementum. Diagnosis. — The only condition with which hypertrophic pulp may be confounded is a pedunculated growth of gum tissue through a cavity at the neck of a tooth beneath the gum margin or through a perforation either accidental or by caries (Fig. 426). It is impor- tant to differentiate between these conditions, because, if an appli- cation of arsenical paste be made to a fungous gum, the destruction of tissue may extend into the sound pericementum. The physical appearances of the two are alike: they both bleed freely and have about the same degree of sensitivity. Histological examination of this class of hypertrophy of the gums, conducted by Dr. Luigi Ancone,^ of Italy, demonstrated that the growth is a simple exaggeration of the normal elements of the part. If the tumor be central to the tooth tissue and the latter not decayed out to very thin walls, it may be at times laid aside by means of a blunt instrument and be seen to have its origin from an orifice of exposure (Fig. 421). As a rule, a hyperplastic pericementum Avill be found to have its attachment much lower or more lateral than a hyperplastic pulp, and the pulp cavity be seen to have been en- larged by caries, even more than shown in Fig. 346. It is then fairly inferred to be a gum mass, especially if the tooth has never been operated upon. The diagnosis may be a doubtful one, in which case the rubber dam is to be applied, the polypus frozen by means of a spray of ethyl or methyl chlorid, and the mass removed with a sharp blade passed across its peduncle. The source of the tumor may then be usually clearly seen. As an alternative proceeding the tissue may be thoroughly saturated with a strong solution of trichloracetic acid and then ablated. If any fur- ther doubt exist, the pulp is to be sterilized with hydrogen dioxid, etc., and a pellet of cotton saturated with oil of cloves, carbolic acid, or dental tincture of iodin is laid upon it, and over this temporary stop- ping is firmly packed. By this means the growth may be pressed away until it is seen to arise from either a pulp chamber or a perfora- ' Abstract from I'Odontologia, by Dr. W, Dunn, in International Dental Journal, 1899. 31 482 DESTRUCTIVE DISEASES OF THE DENTAL PULP tion made by decay or accidental excavation into the pericemental tract. Pressure anesthesia may be resorted to partly as a diagnostic measure. In such case no danger exists beyond the possible forcing of cocain into the gum tissue. Nervocidin should be useful in cases Fig. 427 ■ H, henlorrhagic infarct; R, rupture of bloodvessel; D, dentin; O, vacuolated odontoblasts; F, early fibrosis of pulp. X 250. (Hopewell-Smith.) of doubt. Skiagraphy should afford a diagnosis. Hemorrhage may be checked with alum and thymol in powder or solution, or by the use of trichloracetic acid, silver nitrate, or zinc chlorid solution. Treatment. — If the case be one of pulp hypertrophy, arsenic may be applied or pressure anesthesia attempted for pulp removal. Crystals of iodin have been used with satisfaction in combination CHRONIC INFLAMMATION OF THE PULP 483 with pressure for pulp devitalization.' If a perforation exist, it is to be treated by sealing the orifice with gutta-i)ercha, copper amalgam, or oxyphusphate of copper cement. (See p. 4(37.) Fig. 428 DO DO Horizontal section of fibroid degeneration of the pulp in situ. Prepared by Mr. Hopewell-Smith's process: D, deeply stained dentin; .S, large areolar spaces; DO, degenerate odontoblasts; P, fibroid tissue of pulp. X 45. (Hopewell-Smith.) ' Truman. 484 DESTRUCTIVE DISEASES OF THE DENTAL PULP Infarction of the Pulp. — The production of infarction may result as described under Fibroid Degeneration, and as described consists of minute circumscribed hemorrhages from end arteries into the pulp tissue. This differs somewhat from a true infarction. (See p. 113, and Fig. 427.) Fibroid Degeneration of the Pulp. — Apart from the degenerations due to inflammatory conditions, a form of degeneration occurs "as a natural old-age termination of the life of a healthy pulp," and similar to senile changes occurring in the pericementum. (See Fibroid Fig. 429 Fibroid degeneration of the pulp: D, dentin with tubules; FO, fibroid odontoblasts; P, atrophied pulp tissue. Degeneration of Pericementum.) This change, as described by Hopewell-Smith,^ occurs in teeth of the aged in whose mouths simple alveolar resorption has occurred, though later he^ has shown that it may occur in the pulps of young persons, in sound teeth extracted for irregularity, and even in teeth in which the dentinal wall or pulp cavity is not completed to a typical calcification. He regards it ' Histology and Pathohistologj' of the Teeth, 2 Dental Cosmos, 1907. DECENERAriON OF THE PULP 4So as due to a i)rimary throml)()sis of the (•ai)illaries and veins, with permanent dihitation of the arteries, with or without tiny hemorrhages, the Lack of colhiteral circuhition and lymphatics contributing to the atrophy. As a cause he suggests chemical changes in the blood through systemic derangement, as anemia, chlorosis, or exhaustive diseases, the red corpuscles being fewer Fig. 430 Fatty degeneration of the pulp. (V. A. Latham.) and the leukocytes and blood platelets increased, thus favoring a thrombosis of small vessels; also, that here inflammatory changes in the pericemental tissue might interfere with the pulp circulation sufficiently to produce it. Clinical Significance. — While the form of thrombosis or fibrosis may not be diagnosticated because of lack of related symptoms. Hopewell-Smith argues that they should be suspected in weak and unhealthy patients, and that such suspicion should contraindicate 486 DESTRUCTIVE DISEASES OF THE DENTAL PULP Fig. 431 Cloudy swelling; parenchymatous degeneration; pulp nodules. (V. A, Latham.i) Fig. 432 Colloid degeneration of the pulp. Compare with Fig. 49. (V. A. Latham.) 1 Dr. Vida A. Latham's illustrations are from her paper on Some Pathological Features of the Pulp, Journal of the American Medical Association, September 22, 190G. DEGENERATION OF THE PULP 487 conservative operations, also that they may exphiin certain (Hfficulties of devitaHzation or anesthetization of the pulp or cause a related change in the pericementum or brittleness in the dentin. Morbid Anatomy. — "The odontoblasts become sheaved with or without fatty degeneration; the arteries, permanently distended, undergo hyaline degeneration; a reticular atrophy occurs, with dis- appearance of cells and nuclei of both pulp and \essels and nerves, and, at the same time, the connective-tissue fibers undergo hyper- plasia. The pulp goes more or less gradually through the stages shown in Fig. 427, finally producing the stage shown in Figs. 428 and 429, in which the pulps are shrunken and may have left the wall Fig. 433 Great thickening of nerve bundle. From a case of chronic neuralgia. Patient had many teeth extracted for neuritis. (V. A. Latham.) of the pulp chamber. Many areolar spaces appear which may be arranged in chains. The odontoblasts are degenerated. The pulp stroma is very dense, has a clear, fibrous structure, becomes very marked in staining, and is highly differentiated from the surrounding tissue. The bloodvessels, nerves, cells, and connective tissue have all disappeared, and their place is taken by a new, firm, fibrous structure devoid of cells, nuclei, or any regular arrangement of constituent parts. "There is no calcification of the pulp and no obliteration of the dentinal tubules. 488 DESTRUCTIVE DISEASES OF THE DENTAL PULP "The proximate cause and associate phenomena are not as yet clearly related." Fatty Degeneration of the Pulp. — During the course of degenera- tion of the elements of the pulp fatty changes may occur as in other parts. The fatty changes occur in the walls of the arteries and sheaths of the nerves, and in the odontoblasts.^ Cloudy swelHng also appears. (Latham.) (See p. 78.) Colloid Degeneration of the Pulp. — The demonstration of colloid material within the pulp has been made by Latham, as shown in Fig. 432. She states that it may become calcified. The condition is very rare. Other degenerations such as Wallerian, hyaline, and amyloid have been noted. ^ It would seem that the pulp may be subject to any form of degeneration seen elsewhere. Fig. 434 Neoplasm of the pulp. (V. A. Latham.) Nerve-end Degeneration of the Pulp. — The degeneration of nerves occurs in the pulp as it may in the pericementum and from the same causes that produce endarteritis. The bundles may be enlarged. Neuralgia may be associated with it. ' Hopewell-Smith. 2 Talbot: Dental Cosmos, 1909, p. 1150. DEGEXERATIOX OF THE PULP 489 Neoplasm of the Pulp. — Latham claims that a neoplasm may occur in the pulj), and offers the photomicrograph shown in Fig. 434 as proof of the fact. I do not know of any cases iii which such a pulp condition has been related with a malignant growth outside of the pulp cavity, though it may not be impossible. INIany of the destructive pulp diseases occur in the pulps of the temporary teeth, and are to be treated in like manner, except as to the use of arsenic, which, being accompanied by greater danger, should, for the most part, be replaced by nervocidin, pressure anes- thesia, or cantharides. This point is discussed at length in the chapter upon Removal of the Pulp. If the tooth roots be largely resorbed. the pulp may bear capping even when ulceration has occurred. The pulp may die under this capping, when the case is further treated as indicated. (See Chronic Apical Abscess.) CHAPTER XVII METHODS OF REMOVAL OF THE DENTAL PULP AND ROOT-CANAL FILLING There are four general methods by which a patient or pulp may be prepared for the operation of pulp extirpation. These are as follows : 1. Anesthetization of the patient and removal of the pulp during the period of anesthesia. 2. Anesthetization of the pulp by cocain, or in some cases by nervocidin, and the removal of the pulp. 3. Anesthetization of the apical tissue and removal of the pulp. 4. Devitalization of the pulp followed by its removal. 1. General Anesthesia. — The pulp of a single-rooted tooth may be readily extirpated while the patient is anesthetized by nitrous oxid, nitrous oxid and oxygen, or by somnoform. The instruments should be in readiness, the patient anesthetized, the pulp uncovered by an engine bur, and the pulp extirpated with a barbed broach or Donaldson cleanser. In cases of multirooted teeth the available anesthetics are ether, which is rarely used for the purpose, and nitrous oxid administered by nasal inhalation. The latter is accomplished by means of a special apparatus having a hood covering the nose, of which the Teter appliance is the most notable example. This is designed to prolong the anesthesia by administering nitrous oxid and oxygen. As it is equally applicable to the otherwise painful excavation of cavities of decay and extractions, it is a valuable means for accomplishing this purpose also. (See p. 380.) The otdinary outfit is, however, of value by enabling the operator to remove the diseased bulb of the pulp of a multirooted tooth, after which and while the patient is conscious other methods of removal of the radicular portions of the pulp may be employed. 2. Anesthesia of the Pulp. — For this purpose cocain is almost uni- versally employed. There are three practical methods by which it may be introduced into a pulp : (a) By pressure accomplished by means of raw vulcanite. A strong solution (50 per cent, to saturated solution) of cocain hydrochlorid is made in water, or preferably in some mild antiseptic solution ANESTHESIA OF THE PULP 491 which does not cloud on admixture. A small piece of amadou (spunk) is saturated with it and laid upon the orifice of exposure. The cavity is filled with the rubber, and upon this is placed a flat-ended plugger or burnisher broad enough to concentrate the force upon the amadou. A broad piece of amadou placed over the rubber is sometimes of assistance in preventing the slipping about of the rubber. Gentle pressure is now made and a slight pain is usually felt. The pressure should be maintained until this passes away, then it is increased little by little until some force is exerted. The rubber and amadou are then removed, the pulp cavity opened, the progress of the anes- thesia tested with a fine broach, and the pulp lifted away. Some prefer to place a prepared pellet or crystal of cocain upon the pulp. For multirooted teeth the pressure should be prolonged, and to prevent return of sensation and hemorrhage while extirpating it is well to instil carbohc acid into the pulp tissue by means of a fine, smooth broach. In some cases the operation fails because the direction of the pressure has been aw^ay from rather than toward the pulp or because the spunk has slipped from its place. Sometimes the orifice of exposure may be enlarged, but as sensation is discovered a fresh application must be made. In cases with large foramina the appli- cation may fail; with the incomplete foramen of moderate size it is more successful. Sometimes repeated applications fail of eflFect, though the appli- cation is not painful, and at times the pressure is not tolerated at all, owing to the irritability of the pulp, due to continued hyperemia or infiammation. Even six or eight applications have at times failed even when a fair and accessible exposure existed. Sedation for a day or two sometimes permits a successful application. The pressure is sometimes tolerated, yet failure results. This action of cocain corresponds to that in inflamed tissue. In cases of cavities without walls to confine the rubber, it is well to enclose the buccal and lingual embrasures with the thumb and forefinger. In very broad occlusal cavities the finger-tip confines the rubber nicely. When only canal filaments are present, any septic matter present should be removed by syringing repeatedly with an antiseptic solu- tion; then the canals should be thoroughly dried, and the cocain, dissolved in an antiseptic, is carried on a cotton thread into the canals and against the pulp remnant. A small piece of rubber is placed in one canal and the pressure confined to that canal by means of a plugger which will about fill the canal. The action is then repeated in the other canals. This produces better results than a general pressure over all the canals at once. 492 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING If used after arsenic has been applied the results are not usually so good, but sometimes the method is successful. To avoid the intro- duction of arsenic into apical tissue all sloughing portions should be removed. When the pulp is not exposed, the application to the dentin over the pulp permits advance, a pocket being created in the dentin with a bur, which aids the; further instillation of the cocain; finally, the pulp is exposed and the anesthesia is completed. Clyde Davis recommends for the purpose of producing the exposure the use of a drop of 1 to 1000 adrenalin chlorid followed by a drop of 37 per cent, formaldehyd, then pressure with raw vulcanite. Where calcific formations are present they present some difficulty, though with persistence one may be enabled to anesthetize the pulp. Cook recommends an application of 10 per cent, sulphuric acid for a few minutes, followed by sodium bicarbonate previous to a reappli- cation of the pressure anesthesia, as highly effective in aiding penetration of the cocain. There is a possibility of the introduction of cocain into the general circulation, and some systemic effect may be noted, though often this will be due to the agitation of the patient. Some patients have complained of tingling in the fingers. If syncope be threatened aromatic spirit of ammonia should be administered, the head lowered, the feet elevated, and smelling salts or amyl nitrite applied to the nostrils. It is always well to administer aromatic spirit of ammonia before using cocain for any purpose. Hemorrhage following the extirpation of the pulp is sometimes copious. To avoid this, carbolic acid should be instilled into the pulp tissue by means of a smooth broach. A fine Donaldson cleanser may be passed to the apex of the canal and slowly twisted, the oper- ation consuming several minutes. This torsion of the pulp largely limits the hemorrhage. If it occur it should be allowed to check itself, though if desired a trifle of a mixture of powdered alum and powdered thymol may be taken upon cotton wet with phenol- camphor gnd passed to the end of the canal. Deliquesced zinc chlorid checks hemorrhage promptly; a dilution is less painful. It is an open question whether canals from which living pulps have been removed should be filled immediately or not. There is liable to be a secondary hemorrhage, particularly when adrenalin is used with the cocain. Many prefer to fill at once, claiming that surgical pericementitis is the only result. The writer, as a rule, wraps a twist of cotton upon a Swiss broach, dips it into phenol-camphor, then into formocresol, and applies it to the canal. This, as a rule, permits the healing of the parts without much tenderness, and ANESTHESIA OF THE PULP 493 really consumes but little more time in the aggregate. Moreover, the formocresol tends to mummify the fibrils left in the dentinal tubules. As an alternate upon the immediate filling side a paste of Vf — ThyiiKjl 1 part Parafoini .1 part Zinc oxid 1 part Glycerin 1 part may be used with gutta-percha cones to accomplish the same result. All work should be done under aseptic precautions. Where applic- able and not liable to be too painful, the rubber dam should be applied. The writer often uses napkins instead, and relies upon the carbolic acid instilled into the pulp and the formocresol dressing to maintain asepsis. This is repeated if the cavity be douched out. (b) When considerable dentin overlies the pulp, or when a tooth is sound, the most expeditious method of cocain anesthesia is by means of the compound syringe (Fig. 435). This consists of a strong metal Fig. 435 The Myers compound syringe for forcing cocain solutions through the dentinal tubules. syringe, the piston of which is actuated by means of levers which multiply the power of the hand. The Myers syringe is one of the best, though several forms are obtainable. The syringe nozzle is embedded in a small hole drilled in the dentin by one of two methods: The hole may be made small with parallel sides, as when drilled with a .No. ^ bur; the syringe nozzle has then slightly conical sides at the point intended to jam a fit when introduced with force into the drill pit. In the other method the drill pit is made wdth a cone- pointed bur or bud bur, and the syringe point is made flat-ended, a form easy to maintain upon the point. A 4 to 10 per cent, cocain solution is sufficient, and all air must be expelled from the syringe. It is wise also to expel all air from the drill pit by a slight pressure while the syringe point is loosely held in the pit. Then a rotary motion under forward pressure embeds the point. If no leakage occurs the force of the piston drives the cocain through 494 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING the fibrils in the tubules and into the pulp. The pressure must be maintained for about three minutes. The anesthesia is then tested by drilling with a No. | bur in the direction of the pulp. If the dentin be sensitive the syringe is to be reapplied. Often the bur sinks into a sensitive pulp mthout warning by dentinal sensitivity. In such case the syringe is reapplied for a moment, when, as a rule, the anesthesia will be complete. In all cases when testing, the drill hole should not be enlarged, as this prevents reapplication. Too much cocain should not be introduced, as it has happened that the area about the apical tissue has been profoundly injected, with, of course, possibility of systemic complication. This warning applies to the second application rather than the first. When desirable, the enamel of a sound tooth which is to be crowned may be ground away until the dentin is reached, or if enamel must be removed in only limited degree, as for a tap upon the lingual side of an incisor or in the fissure of a bicuspid, a "spot" is first made with a dentate bur, then a spear drill is driven through the enamel only just reaching the dentin. The drill hole is then enlarged as widely as permissible, after which the pit is made in the dentin with a No. | bur. The lingual side of upper incisors will permit of suflBciently direct pressure to enable the operator to centre the syringe point, but in many cases in which crowns are indicated the labial side may be used with advantage, especially at the neck when the cementum is exposed. Later, the entrance tap is made in line with the pulp axis. The labial or mesiobuccal side must always be used in the lower teeth, unless a cavity be used, sometimes preferably at the neck, sometimes higher up. In cavities having sufficient dentin over the pulp the pit may be made in the pulpal wall, and if for any reason it is needed the drill pit may begin at the cervical portion of the cavity and extend into the root dentin and parallel with the pulp. The pit must be deeper than the syringe point will penetrate, so that the pressure may force the solution laterally through the tubules, which are at a right angle to the axis of the pulp and the pit. In some cases solu- tion of antiseptics have been as effective with this instrument as the cocaifi solution. According to BrouardeV of Paris, the effects of cocain are acute and chronic. The former develop usually in ten or fifteen minutes, or even up to three-quarters of an hour after the injection. They are: precordial anxiety, filiform and extra rapid pulse, lividity of the face, coldness in the extremities, and abundant perspiration; rise in tem- perature, irregular respiration, tinghng sensations in the hands, » Dental Cosmos, 1905, p. 1508. ANESTHESIA OF THE PULP 495 blunted tactile sensibility, excitement, loquacity, weeping, anger, or hysterical fits; bilious vomiting with or without diarrhea; anuria, symptomatic epilepsy, followed by motor and sensory paralysis. Death occurs in from two minutes to five hours after administration, though in the chronic cases fatality usually does not result. Placing the patient in the horizontal position, giving inhalations of amyl nitrite, and, if further cardiac stimulation be necessary, hypodermic injections of ether or strychnin. The chronic poisoning occurs mostly in those addicted to its use. Some develop a tolerance of the drug, withstanding from 30 to 120 grains. Tachycardia and intense psychic disturbances, leading to physical and mental collapse, are observed. (c) The third and least desirable form of cocain anesthesia of the pulp consists of its introduction by the cataphoric current. It has the disadvantage of consuming more time, but may serve when patients are timid. A 10 per cent, solution of cocain hydrochlorid is applied to the pulpal wall of the cavity, the tooth being previously placed under rubber dam. The anode of the cataphoric outfit is applied to the cotton and the cathode placed in the hand or at the cheek. The dentin may be anesthetized as well. If desired, this method may be used to obtain a pulp exposure and the pressure method employed to complete the operation. When beginning with an exposed pulp, about fifteen minutes will be required unless hyperemia of the pulp exists, when a longer time will be required. As with the pressure method, there may be occa- sional failures. It will be noted that there is advantage in time and convenience in the pressure methods. (d) The fourth method of producing pressure anesthesia consists in the use of carbolic acid in place of the cocain or in case of obstinate canal filaments of a solution of cocain in carbolic acid. When pulp nodules or calcific degenerations exist there may be some difficulty in introducing the cocain, but after a first or second application the nodule may be lifted away and further pressure made, though even at this point failure may occur. In all cases presenting difficulty in introduction, desiccation is a valuable preliminary. Cook^ recommends an application of 10 per cent, sulphuric acid for a few" minutes, followed by sodium bicar- bonate previous to a reapplication of the pressure anesthesia as highly effective in aiding penetration of the cocain. Claims are made for eucain, eucain and alcohol, and alcohol alone for producing pulp anesthesia by pressure. 1 Dental Review, 1905. 496 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING (e) The fifth method of producing pulpal anesthesia is by the application of nervocidin, an alkaloid obtained by D. Dalma from the East Indian plant gasu-basu. Arkovy recommended that a portion be applied to the exposed pulp for twenty-four hours, when it may be removed painlessly. Soderberg^ suggests the addition of a small amount of cocain hydrochlorid to overcome the primary irritating effect of the nervocidin. If dentin be over the pulp, an additional application of twenty-four hours' duration is required to obtain an exposure. (See p. 389.) Sprays of rapidly vaporizable substances, such as ethyl or methyl chlorid, directed against the exposed pulp, the tooth being isolated under rubber dam, will, in some cases, render the pulp entirely insensitive, although, as a rule, they fail to entirely anesthetize to the apical foramen. The method is painful and not applicable in many cases of highly irritable pulps. (See p. 383.) 3. Anesthesia of the Apical Tissue. — The third general principle upon which pulps may be extirpated consists in paralyzing the nerve filament leading from the pulp to the larger branches of the fifth nerve. If the nerve in the apical tissue can be prevented from transmitting sensation, the operator may remove the pulp surgically without pain. The apical tissue is to be located as nearly as possible, the gum sterilized, and an injection of about 5 drops of a 1 per cent, solution of cocain containing adrenalin injected as near the periosteum of the bone as possible. This is expected to infiltrate the apical tissue via the collateral vessels in the bone. To permit the accomplishment of this a little time should be allowed. On drilling the dentin to open the pulp cavity, one should note the presence or absence of sensation, and upon exposure a smooth broach should be used to test the state of the pulp. In the use of this method precau- tion should be taken to administer an antidote before using the cocain. What is called diploe anesthesia Has been employed to relieve the pain of dental operations, and consists of cutting to the bone after the above injection, perforating the bone, and injecting into the diploeic structure. A small hole is made in- the cortical layer of bone and a blunt hypodermic needle used to complete the anesthesia. A few drops of solution only are injected. A method employed by some bridge-workers consists in notching and excising sound crowns. It is often the case that for a short period after the excision the pulp is insensitive and can be lifted away with a broach. If for any reason this should fail, other immediate methods can be employed. Claims have been made for a slight sidewise blow struck upon the tooth to paralyze the pulp nerves by a stretching shock. 1 Dental Cosmos, 1901 and 1902. DEVITALIZATION OF THE PULP -197 4. Devitalization of the Pulp. — Devitalization of the pulp by the use of arsenic trioxid as a preliminary to its successful removal is the oldest of the methods employed at the present day/ and, as shown, it still has to be resorted to either from necessity or convenience. The method has its value in the very teeth in which its use is least objectionable, namely, the posterior teeth. There is no danger in the use of arsenic in teeth having completed roots or in unresorbed temporary teeth, provided the arsenic be accurately sealed in the cavity so that it does not escape upon the gum. If it does escape it may destroy the gum or pericementum and cause partial necrosis of bone or the complete loss of the tooth together with some bone. The pulp always dies through a process of venous hyperemia induced by the protoplasmic irritant and poison. Some of this is absorbed by the pulp. This hyperemia is progressive from the pulp bulb toward the apex of the root, and there it causes the death of the apical portion of pulp through interference with its nutrition. Sometimes this hyperemia of the pulp extends into the apical tissue, but if the pulp be left in situ, necrosis of apical tissue never results, but, on the contrary, the hyperemia becomes resolved after the death of the pulp- The writer fails to see wherein such a hyperemia differs in conse- quence from that produced by the surgical removal of a pulp aijd denominated with favor as surgical pericementitis. In his hands such teeth have given quite as good results as when other methods have been employed. By this it is not meant that there has been no difficulty in devitalizing some pulps, particularly some of those in which repeated applications of cocain under pressure failed to anesthetize, but that when carefully handled and sufficient time for pulp death has been allowed, careful filling of the canal has been successful. Action of Arsenic upon the Pulp. — Arkovy- was the first to point out the details of the action of arsenic upon the dental tissues: "1. AS2O3 brought into contact with the tooth pulp acts in the following way: A certain degree of inflammatory hyperemia, total or partial, depending upon the quantity of the agent applied, sets in; the bloodvessels become expanded, and here have a tendency to thrombosis. This latter effect may dlso be in connection with embolism of the capillaries, when the agent is quickly taken up into the bloodvessels. "2. AS2O3 produces no coagulation of tissue whatever. ' Introduced by Spooner in 1836. 2 Transactions of the International Medical Congress, London, 1881. 32 498 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING "3. It has a specific influence upon the blood corpuscles, combining with the hemoglobin to form a compound of arsen-hemoglobin, and of this chemical process there seems to be evidence in the profuse yellowish tinge of the whole pulp tissue and in the discoloration of blood in several of the bloodvessels. "4. In nearly every case it is taken up in substantia (in form of molecules) into the blood-ways; when there it produces, besides the above-mentioned changes, granular detritus of the contents and anemic collapse — shrinkage, the latter effect being brought about nearh'^ exclusively in cases where greater doses were used. "5. The bulk of the pulp tissue — viz., connective-tissue fibers and odontoblasts — undergoes no change whatever; not so the connective- tissue cells, which increase three or four times their normal size. " 6. The special action of arsenic trioxid upon the nerve elements consists in the following: the neurilemma is only so far influenced that its nuclei are somewhat increased; a more essential change takes place in the axial part, where, after the application of more than 1 mg., granular destruction of myelin sets in, and the axis-cylinder commences here and there to disappear. A very surprising alteration may be seen in the notchy tumefaction of the axis-cylinder, described heretofore almost only in cases of central lesions. "7. All these alterations occur in and among normal-looking tissue. "8. The action of arsenic trioxid is macroscopically exhibited by a brownish red-tingeing of the whole or of certain parts of the pulp body, as well as of the neighboring dentin and the cementum, this latter in cases treated with greater doses — viz., 2 to 5 mg. This alteration is most expressed at the top of the crown pulp and at the apical one-fourth to one-third part. This circumstance may be considered as an external evidence of the devitalization being completely attained to." In some cases the pinkish discoloration of the dentin may be marked; the broken-down corpuscles of the extravasated blood have their coloring matter taken up by the odontoblasts, and being dis- tributed through their protoplasmic processes produce a condition technically known as suffusion. The same result may be an attendant upon injury to the vessels from other causes, producing hyperemia, as when teeth are moved too rapidly in regulating. IMiller's experiments^ upon the tails of mice (made without and with rings at the root of the tail to simulate the surroundings of the apical vessels of a tooth; made without and with encasement of the 1 Dental Cosmos, 1894. DEVITALIZATION OF THE PULP 499 tails in plaster of Paris to imitate the rigid surroundings of the dental pulp) showed that in the absence of the plaster encasement enormous edema of the tail was produced and a sensory paralysis of the hind limbs; complete anesthesia of the tail occurred in forty-eight hours. "The action of arsenic appeared somewhat accelerated when a glass ring was applied close to the root of the tail. In more than forty cases there was not one in which the action of the arsenic extended beyond the ring, and the action was not appreciably affected by enclosing the tails in plaster casts. The action of the arsenic is of a progressive nature, beginning at the point of application and extending gradually in each direction." Flagg' devitalized ten pulps and removed them, cut off the portion of the bulb of each which had contact with the arsenic, and tested the ten pulps together by Reinsch's test. Arsenic was found, estimated at a one-hundred-thousandth part of a grain or one-millionth of a grain for each pulp. Allowing for possible mechanical introduction or contact of arsenic during extirpation, the quantity of arsenic introduced by the circulation must be very minute indeed. Flagg argued that as the pulp subsequently putrefies it cannot have died as the result of arsenical poisoning alone. In the roots wdth large foramina arsenic may be absorbed, as areas of devitalization of the apical and overlying gum tissue have been noted. In several apparently authentic cases the pericementum of a mature tooth has been said to be destroyed from the apex down and the tooth lost. I have never seen such a case resulting from the arsenical method alone in either clinical or private practice, although cases of marginal gum, alveolar, and pericemental death, beginning as the result of leakage or application to perforations, have been noted. It is probable that as stasis proceeds the apical portion of the pulp becomes involved in advance of arsenic absorption. Miller's experiments show that arsenic does not pass the point of constriction. Variations in the Action of Arsenic— In most cases of fully formed, single-rooted teeth in young adults an application of arsenical paste directly to the exposed pulp will be followed by the complete death of the organ in forty-eight hours. At the expiration of that time a sterilized broach may be passed almost to the apex of the root and the pulp removed en masse without pain. Pulps of molars require a longer time, often a week, before the filaments are dead. The finer filaments resist longer than the larger ones. If pulp nodules exist, the action of the arsenic may be delayed or in some cases be almost nil. In calcareous and other chronic pulp degenerations the action is also delayed. If arsenical applications are made over a layer of 1 Dental Cosmos, 1868. 500 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING dentin, the same delay is noted, and is increased in very dense teeth. There is also a greater tendency to suffusion. Some pulp, irrespective of the pulp condition, exhibits a peculiar idiosyncrasy in resisting the action of arsenic, requiring large doses and long applications before succumbing. Second applications often require more time to kill the balance of the pulp than the first appli- cation would have required. The time used in investigation is practically lost. The editor, therefore, allows plenty of time; about ten days for molars, five for single-rooted teeth, and prefers to find the pulp entirely dead. The rational objections to arsenic, aside from its escape upon the gum, are: (1) The possible production of pain. (2) Possible suffu- sion of the tooth. (3) The time required. The production of pain may largely be obviated by observance of certain technique. The pulp should ordinarily be exposed and be slightly bled to relieve any hyperemia or inflammatory engorgement present, as this seems to prevent the absorption of the arsenic. A powerfyl sedative, such as thymol, menthol, cocain hydrochlorid, or morphin acetate, should be employed as a corrective, and the menstruum should be sedative rather than coagulant. All pressure on the pulp should be avoided as this produces pain. Sufficient time for complete death should be allowed, say, from a week to ten days. If, upon examination with a fine smooth broach, vitality be discovered, a sedative should be applied and pulp death awaited. Leaving the dead portion against the vital part of the pulp is even better than making a second application, as its removal relieves the congestion by opening the vessels, and the congestion is necessary to the end in view. If the pulp give but little response upon probing it may be removed. Sometimes the diapedesis of red corpuscles, associated with the venous hyperemia, causes a staining of the pulp and dentinal fibrils with the liberated hemoglobin. This is unfortunate, but can be treated by bleaching with 25 per cent, ethereal pyrozone sealed in the pulp cavity for about twenty-four hours after the pulp is removed. The third objection, the matter of time, does not apply to the cases of prompt devitalization, as the time spent in pulpal anesthesia and checking hemorrhage is in the aggregate no less than in the arsenical cases. In the delayed action of arsenic the objection is valid, but the apical injection and general anesthesia methods are still open to trial. The arsenical method, of course, requires a longer period of treatment. Pulpal anesthesia can be tried when arsenic does not act well, but should be avoided when it originally failed. As stated, these considerations apply mainly to posterior teeth. DEVITALIZATION OF THE PULP 501 Forms in Which Used. — The following is an excellent formnla for arsenical paste: I^ — Arsenici trioxidi gr. xv CocaiiiEe hydrochloridi gr. xx Thymolis (vel mentholis) pr. v Olei caryophylli (I. s. ft. pasta — M. This should be finely ground in a mortar and spread over the bottom of a wide glass jar so that some of the paste may be taken up from the bottom. The arsenic settles to the bottom. Buckley recommends the following formula: ^ — -Arsenic trioxid gr. clxxx Cocain alkaloid gr. xxx Thymol gr. xv Petronal tU xv — M. Either of the above may have the powdered ingredients mixed. The cotton pellet may be wet with the menstruum and then dipped into the powder. Lamp black added to the paste colors it so that it is easily distinguishable in a cavity. The following are other formulae: The analgesics included are intended to dilute the arsenic and quiet the pulp, and thus both directly and indirectly modify the pain. I^ — Acidi arsenosi, Morphinse sulph aa gr. x Acidi carbolici q. s. ft. pasta — M. (J. D. White.) I^ — Acidi arsenosi gr. x Morphinte acetatis gr. xx Olei caryophylli q. s. ft. pasta — M. f J. Foster Flagg.) Creosote may be substituted for oil of cloves. R — Acidi arsenosi gr. x Cocainae hydroch gr. xx Olei cinnamomi q. s. ft. pasta — M. (E. C. Kirk.) I^ — Arsenic gr. x Alum gr. X Thymol gr. x Oil of cloves q. s. ft. pasta — M. As the ordinary pastes tend to separate into layers of arsenic, morphin, etc., and menstruum if made thin, they should either be made into stiff pastes or spread over the bottom of a wide jar, so that some arsenic may be scraped off the bottom at each application. ]\Iiller offers the following general rules as deductions from his observations : 502 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING "1. The rapidity and intensity of the action of arsenous acid depend, under certain circumstances, to a very considerable degree upon the substance or substances with which it is incor- porated. "2. Where there is but a small point of exposure, and in particular where extensive calcification has taken place in the pulp, escharotics should be avoided, since the coagulation of the tissue retards the absorption of the arsenic. This retardation is but slight where there is a broad surface of exposure. In stubborn cases, where applica- tions of the ordinary paste fail to effect the devitalization, a paste consisting of arsenous acid in oil of cloves, glycerin, or salt solution should be employed, undiluted by any third constituent. "3. Thymol is worthy of a trial as a substitute for morphin, on account of its anesthetic and antiseptic properties. "4. For devitalizing pulps of temporary teeth or remains of pulp tissue in root canals, arsenous acid, if employed at all, should be diluted with two or three parts of some other constituent (thymol, zinc oxid, morphin, iodoform)." Cobalt was introduced by Robert Arthur as a devitalizing agent some forty years ago. Within recent years it has been employed, notably by the Herbst method, to destroy pulps. The cobalt paste of Herbst was analyzed b}^ E. C. Kirk, and found to consist of metallic arsenic and cocain hydrochlorate. Kirk suggests that free acids which cocain salts may contain, or the chlorin from the chlorid, may combine with the metallic arsenic and form soluble salts. Com- mercial cobalt will certainly devitalize the dental pulp, but it is in consequence of the arsenic contained in it. There are some advantages in the so-called devitalizing fiber introduced by J. Foster Flagg. To make this, absorbent cotton is cross-cut with scissors to a fine lint. This is dusted into the paste or ground up with it in the mortar. It may then be dried on a blotter and be bottled for use. As it lacks long fibers, a small portion may be detached and be placed upon the pulp. There are cases, however, in whicli the paste should be carried to the exposure upon a probe and gently inducted into a fine exposure. Here its tendency to spread or penetrate is valuable. The fiber has no such tendency, which makes it less dangerous in use. In making the application a minute portion of paste is to be laid upon the pulp, or a pin-head pellet of cotton is rolled in it, the excess of menstruum removed, and it is then applied to the pulp, or a portion of devitalizing fiber is used. This is then sealed in. The cavity should be prepared for the reception of arsenic, decay being removed as far as practicable, and the cavity dried. Any DEVITALIZATION OF THE PULP 503 Fig. 436 redundant gum must be pressed away or saturated with trichloracetic acid and ablated. There are two good methods of sealing the arsenic. In cases not approaching the gum, or where dryness can be maintained, the application may be accurately made and quick-setting cement flowed over it. This cement is capable of being fairly dropped into a cavity or led around the periphery by a probe, and should be very adhesive, also be readily removable. A still safer method consists in applying a pellet of amadou over a part of the pulpal wall. The cement is then introduced about the periphery of the cavity, the amadou being left largely uncovered. When hard, any cement over the amadou is removed and the latter lifted out, thus leaving a box-like receptacle for the arse- nic and a pellet of amadou partly wet with eugenol in which menthol is dis- solved. When placed, the orifice is dried and more cement added. This method of first making the covering is of special advantage when the cavity cervix is near the gum and prevents the forcing of arsenic toward the gum in the act of making the covering. Amal- gam or facing amalgam^ or temporary stopping may be used in place of th'e cement (Fig. 4.36). Temporary stopping is not very safe against masticatory force. The rubber dam is generally insisted upon, but cannot be used in the worst cases, hence an expert may dispense with it. There is a tendency among students to rely upon the rubber dam alone to prevent accidents. This is a fallacy, as the same results may occur with it as well as without it. The chief danger lies in the use of temporary stopping after placing paste. Capillarity and pressure often carry the paste to the cervical margin. Making the covering first or using fiber constitute the best precautions. In case of a very dangerous cavity, as a distocervical one, a special drill pit known as a "pocket" is to be made at some other point extending in the direction of the pulp horn and as near to it as can be made without too much infliction of pain. In this the arsenic is to be sealed while antiseptic sedatives are to be placed on cotton in the cavity of decay. This method is also valuable when the pulp is Diagram showing method of first making the covering for an arseni- cal or sedative application. (See text.) EP, exposed pulp; AA, ar- senical application; C, sedative covering to same; A, amalgam placed before these applications; A', amalgam to seal them in; E, enamel. • Facing amalgam is silver 40, tin 55, zinc 5 parts, and mercury. 504 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING very irritable and permits devitalization through a more or less healthy portion of pulp. The presence of pulp nodules may necessitate an application after lifting away the nodule (Fig. 386). The arsenical method may be used after a preliminary general anesthesia and bulb removal, or may even be used against an obdurate pulp canal filament. When pulp removal is intended the applica- tion may be removed through the opening and a probe may be passed into the pulp to test the progress of the devitalization. If needed, a second application may be made or the tooth may be temporarily closed. In case the pulp be found partially dead, it is better to allow more time for complete devitalization than to make a second application, as removing a portion relieves the congestion. Symptoms. — The large majority of pulps die under arsenic with but little pain. Sometimes throbbing pain results, passing into a heavy fulness as congestion supervenes. If too great, the pulp should be uncovered and bled slightly, then a sedative should be applied, iodin used as a counterirritant upon the gum, and pulp death awaited. Ordinarily the pain passes away as the pulp becomes more fully congested. Apical irritation may result and may be ignored if slight, or if severe be treated in the same way as the pulp irritation (Fig, 394). A guard to prevent overocclusion is sometimes useful. Accidents from Arsenical Applications. — If a portion of an arseni- cal application escape from beneath its covering, it may destroy much or a little gum tissue, according to the amount which escapes. The teeth should be seen early in doubtful cases and the condition of the gum observed. The arsenic may attack the gum festoon, inducing in it stasis followed by necrosis. The gum assumes a purplish turgidity, which later changes to a dirty yellow slough. The bone is usually devitalized for a distance. If the necrosis be self-limited, as is usually the case, a small sequestrum comes away after a few weeks. In some cases the arsenic may follow the festoon of the gum of one or more teeth, causing disagreeable sloughs and ulcerations. It may follow the pericemental tract, kill the pericementum, and the tooth drops out. The alveolar process about one or several teeth may be devitalized and a sequestrum occur which includes the teeth. Cer- tain toothache nostrums are sold which contain arsenic. Dr. G. C. Chance^ records a case of arsenical necrosis occurring from this source. Dr. J. E. Powers^ records a case in which extensive necrosis 1 Proceedings of the Academy of Stomatology, Philadelphia, 1898. - International Dental Journal, November, 1902. DEVITALIZATION OF THE PULP 505 occurred from the use of colored woolen yarn (as a cleanser of inter- dental spaces) which contained arsenic used in the dye. From the infirmary of the Philadelphia Dental College was referred to the oral clinic a case of extensive coagulation necrosis, resulting from the rubbing of "toothache drops" upon the gum. Analysis showed the preparation used contained arsenic. Collapse from blood poisoning being the immediate danger, the child was operated upon by Prof. Boenning for drainage of the parts. During the recovery, the teeth from the right lower cuspid to the left lower second temporary molar, and the gums over the process, were lost, leaving a blackened alveolar process, to be later removed surgically (Fig. 437). Fig. 437 Boenning's case of coagulation necrosis due to arsenic; shows exposed and blackened alveolar process. Arsenic is liable to pass through the apical foramina of unformed or much resorbed roots. It may possibly pass through mature roots when an application is placed high up in the canal, rarely when applied under normal conditions (as recorded by some), or, as occurred in one case, by the application being pushed through the apex. It may be forced through in the act of broaching, or through the sub- sequent use of the cataphoric current or pressure anesthesia without the preliminary precaution of removing the arsenic. In some cases arsenic has been applied to perforations made through the sides of roots under the impression that the vital tissue found was pulp tissue. In such case its necrotic effects will be noted upon the gum overlying the root apex or over the perforation, the tooth being loosened and extruded and may possibly be lost. 506 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING E. C. Kirk^ has recorded several eases of loss of teeth from arsenical necrosis of the pericemental tissue following the use of mummifying paste to pulp stumps previously impregnated with arsenic. His theory is that the arsenic was liberated by the affinity of the ingre- dients of the mummifying paste for the proteid constituents of the pulp tissue. Such dangers as these demand that extreme precautions be taken against the careless use of quantities of the agent. The rules laid down should be adhered to. The only cure of the condition consists in the thorough removal of every particle of the arsenic. Any projecting masses of edematous gum should be cut away, as they are dead and will slough at any rate, and a freer access to deep parts is had — ^the blood-flow may itself wash away the arsenic. The forcible washing should be pro- longed and repeated, or 10 per cent, silver nitrate should be used to form arsenite. Dialyzed iron or tincture of iodin might be applied with a view to possible neutralization of the arsenic. The editor, in a case of known application of arsenic to an obscure perforation, succeeded in causing regeneration of tissue by removing surgically the dead tissue and inviting repair. It may, therefore, be that after minute portions of arsenic, forced through foramina, exert their full effect, the resulting dead tissue may be removed by resorption or even exfoliation; indeed, this result has been noted in which no other explanation seemed possible. If the teeth are loosened and lost as the result of arsenical necrosis, either beginning at the gum margin or at the apical space, the alveolus will exhibit a>bare periphery and even some odor of putrefaction may be present. The alveolus should be sterilized and the walls burred away to a tissue capable of healthy granulation. If suffusion occur, essential oils or phenol should be avoided in the subsequent treatment, as they tend to set the color by' acting as a mordant (Kirk), rendering bleaching difficult. After the pulp is removed it is well to fill the apical portion of the canal, and then at once bleach with 25 per cent, ethereal pyrozone, after which the balance of the canal and the cavity may be filled. (See Moist Gangrene of the Pulp.) Special Methods of Preparing Pulps for Removal. — A fully exposed pulp in a single-rooted tooth or single root of a multirooted tooth, may be suddenly "knocked out" by means of a delicately pointed orange-wood stick or Portuguese toothpick. The point is dipped in carbolic acid and suddenly and boldly driven into the pulp, either by 1 Dental Cosmos, October, 1903. DEVITALIZATION OF PULPS IX TEMPORARY TEETH 507 hand or mallet force. The method is not so agreeably delicate as pressure anesthesia, but is effective. It must not be used in partial exposure, as, not reaching the apex, it may cause pain. A vital remnant of pulp may be removed after instilling a strong cocain solution, or carbolic acid, or a paste of carbolic acid and acetate of morphin, into its substance by means of a "puncture probe." This instrument may be made by filing down a Donaldson bristle to a fine point, which is further whetted on an oil stone. The sides of the probe are polished by folding a cuttle-fish disk upon itself, holding it between the thumb and forefinger of the left hand, and drawing the probe through it. The pulp canal is flooded with the carbolic acid, and gentle thrusts are made into the pulp until the probe is stopped at the apex. If it pass through, that must be judged by the sense of touch. At times a small end of pulp filament may be seared with a hot Evans' root drier, which is quickly thrust into it. This does not necessarily give much pain. A slow but effective method of disposing of these filaments, when hyperirritable or when patients are timid, consists in packing a cotton twist saturated with carbolic acid containing cocain hydro- chlorate in solution into contact with the pulp, and then gently com- pressing the pulp. The cotton is to be left in position for a day or two, when, as a rule, the pulp may be removed. It induces throm- bosis, and carbolic acid may be used with pressure to produce anesthesia at the time of operation. A dressing of tincture of iodin has been suggested for the purpose. Devitalization of Pulps in Temporary Teeth. — All of the anesthetic measures are as applicable to temporary teeth as to the permanent ones if the little patient will tolerate their apphcation. If the child present an exposed pulp in a tooth the roots of which are not resorbed, arsenic much diluted, may be applied for twenty- four hours and then be removed, the pulp being then allowed to die. When roots are resorbed it is better to cap the pulp with Jodo- Formagen cement, or if necessary, apply a pellet of cotton wet with phenol, then touched to iodoform, and seal in with temporary stopping, making a slight pressure. This may remain a week or more and be renewed if necessary. Darby has used cantharides, 2V grain in carbolic acid, with success. It must be carefully sealed, as strangury is a possibility.^ Figs. 104 and 111 are guides as to the condition of the end of the root. * Dr. J. Foster Flagg had such a case. 508 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING THE EXTIRPATION OF THE PULP After the pulp is prepared for removal or the patient is anesthe- tized, free access to all parts of the pulp cavity and canals must be obtained. This is usually best accomplished by an opening made in direct line with the axis of the pulp canal. In general terms this involves for sound teeth an opening upon the lingual surface of incisors and cuspids and upon the occlusal surface of bicuspids and molars. This access may consist of a new opening or an extension of a cavity, or at times the cavity and canal may simply be made continuous. Fig. 438 Fig. 441 Fig. 442 Fig. 443 Fig. 444 Fig. 445 When a cavity of decay exists the pulpal wall should be perforated and a large bud bur should be used to cut away the dentin over- hanging the pulp cavity. It is usually necessary to extend the cavity in the central occlusal direction, so as to permit direct access to each canal (Figs. 438 to 445). When a tooth crown would be irremediably weakened by such a course, a slight indirectness is permissible when flexible cleansers can be used instead of drills. This leaving of tooth structure should THE EXTIRPATION OF THE PULP 509 be done with judgment. The canals must be cleansed. In cavity approaches the outer wall of the pulp cavity should be cut away to permit an obtuse-angled approach rather than a right-angled one (Figs. 443, 445, A). All pulp cavity corners should be burred to a shape that obviates retention of pulp debris, the subsequent decom- position of which would lead to discoloration. The opening shown in Fig. 441 is faulty for this reason, and is better if extended more toward the incisal edge, making an oblong opening with rounded ends. Fig. 446 \ H Kerr or Downie broaches. Various finer sizes of these broaches and reamers may be had. They should have accurate taper. In sound teeth the entrance to the canal is made with a small spear drill, after the enamel has had a "spot" made in its surface with a sharp dentate bur. This centres the spear drill and prevents its slipping about. After it has entered the pulp cavity dentate burs are used to enlarge the opening to the desired size and shape. A sawing motion creates more rapid clearance and cutting of tooth tissue. One should not always suppose that the spear drill will drop into an appreciable pulp cavity. The careless driving of a drill into a tooth may cause a perforation. Secondary dentin or a large nodule, and, in previously treated teeth, zinc phosphate may occupy the pulp chamber. Therefore, when doubt arises, open well that portion of tooth or filling which has been drilled through, and note the conditions, then go ahead carefully. In opening a located pulp 510 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING chamber with burs a bud bur is very useful, but all burs once placed through the drill hole and into the pulp chamber must be used laterally or the heel of the bur used with an outward sweep toward the occlusal aspect for the sake of safety. The canal (or canals) is now to be explored, and if of operable size a Donaldson cleanser or barbed broach is passed to the canal Fig. 447 Fig. 44S Fig. 449 Fig. 450 Fig. 451 Dr. Donaldson's pulp-canal cleansers. apex, twisted so as to engage its teeth with the pulp substance, and the pulp extirpated. If there be any difficulty in finding the canals after this preparation, by reason of the broach catching on the edge of the orifice, the mouth of the canal should be made contin- uous with the wall of the pulp chamber by means of a small bud bur. The wall then leads the broach into the root lumen. In single-rooted teeth with finer apices a fine Kerr engine root reamer (Fig. 446) may be passed by hand to the apical portion of the root and gently rotated. It is then mounted in the hand piece, passed gently to the apex, slightly withdrawn, and then operated by engine power. It is pressed lightly laterally to enlarge the canal slightly. The next larger size is then used in like manner, and finally the larger admissible sizes. This gives a beautifully tapered canal form useful in canal filling and for the adaptation of dowels. The pulp is simultaneously removed, generally being churned out Dr. Donaldson's spring-tem- pered nerve bri.stles. THE EXTIRPATION OF THE PULP 511 of the root, and danger of false openings is avoided. A final explor- ation and apical scraping may be given with a fine Donaldson cleanser (Figs. 447 to 460), and the pulp cavity corners rounded out with burs. This technique is only admissible in cases of openings in line with the pulp axis. Those almost in such line may have the flexible sizes of Kerr reamers so used, all apexward pressing and reaming to be done by hand at first. When general anesthesia is employed it is better to open roughly, then pass a fine Donaldson cleanser, which has been previously dipped in carbolic acid and laid aside in readiness, to the apex of the root canal. It is given a few turns to engage the pulp, and the latter is lifted away. The other work is to be done upon return to consciousness. As the Kerr broaches and reamers are made of a variety of forms, it should be stated that only those which have a gradual taper from point to shank can be relied upon to satisfactorily carry out this technique. In these the successive sizes follow one another without danger of perforation of the canal walls. It is sometimes better to drive a fine hand Kerr broach to the canal apex, and, if the engine broach be not permissible, to continue with the different sizes of hand broaches. One soon obtains a familiarity Avith the canal curve and size when working with the hand which gives confidence and safety when later working with engine power. In molar teeth and upper first bicuspids, after the pulp chamber has been prepared, the canals are to be located with a fine smooth broach or a Kerr broach. The finest root reamer is then used by hand and gently twisted and forced apexward into each canal in turn. The next smaller is then used. As these canals are normally somewhat curved, only flexible forms should be used unless the larger size follows readily the rather curved canal made by the previous one. Following this, Donaldson cleansers are operated by hand to scrape the sides and inequalities of the somewhat flattened canals which the reamers have not reached (Figs. 452 to 455). When the finest Kerr reamer does not explore the canal properly, owing to constrictions, a drop of 50 per cent, sulphuric or pure lactic acid in water is introduced into the canal and a smooth, fine, spring- tempered Swiss broach is used to gently enlarge it by drawing it back and forth in the canal. Then a fine Donaldson cleanser is to be used in the same manner; later the larger sizes are used. If feasible, the Kerr reamers may now be used, when direct access is had. If the access be indirect the Donaldson cleansers only should be used. 512 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING Some operators prefer the use of the alloy kahum-natrium, used on the broach as a means of facihtating the opening of the canals. In place of drills the process of canal enlargement devised by Callahan^ may be employed. The general cavity wall is varnished to prevent the action of the acid upon the dentin, and by means of a Fig. 452 Fig. 453 Fig. 454 Fig. 455 pair of Flagg's dressing pliers or a minim dropper a drop of sul- phuric acid (50 per cent, solution) is deposited at the mouth of the canal to be operated upon. The finest size of Donaldson's canal cleanser is then passed into the canal as far as it will go, using a 1 Proceedings of the Ohio State Dental Societj', 1894. THE EXTIRPATION OF THE PULP 513 pumping movement to carry the acid farther into the cahal and to scrape the canal walls softened by the action of the acid. The acid chemically destroys any organic matter — i. e., pulp tissue^present, releases the calcium of the dentin from its combination, and forms calcium sulphate, which is mechanically removed by scrapers. Care must be observed not to strain the broaches too greatly, as they may break. The operation is continued until the apex of the root is reached. F. T. Hayes suggests the use of aqua regia as less injurious to broaches; lactic acid is also less injurious. When the cleanser will not enter readily it is well to file away the barbs from an old cleanser and leave it roughened, and to use it for a time with the acid until the cleanser proper can be employed. Iridioplatinum or gold broaches may be used for this purpose. In the canals of posterior teeth short cleansers are mounted in a chuck handle and the shank sharply bent at a right or obtuse angle. If the cleanser bind in the canal, it should be grasped with the thumb and forefinger and given a straight pull to relieve it. ^''^- ^^^ If acid be used it should be neutralized with sodium bicarbonate or sodium dioxid. The improved Gates-Glidden drill (Fig. 456) has some use in the enlargement of canals the lumen of which has been determined by the above methods. They should not be used for the preliminarv opening of fine improved Gates-Giidden ^ (• 1 1 I nerve-canal drill for engine canals, as they tend to rorm raise channels work. in the side of the canals which constantly catch even fine bristles and may render a canal into a form even less advantageous than that it already possesses. The canal filament of pulps in molars and upper first bicuspids may be lifted away with barbed broaches or cleansers if the canals are large, but it is ordinarily a waste of time to attempt it in the finer canals, as the other work must be done in the apical regions. The use of 5 per cent, formalin, tannin, or alum, to be specially applied about two days after the application of arsenic, has been suggested for the toughening of pulps. Their use necessitates a visit for their special application. They toughen the pulp, and, while the advantage in pulp removal is offset by the special visit needed, may, in fine canals, mummify inaccessible portions of pulp tissue. The point of importance is the removal from the pulp canal of all removable portions of pulp tissue and an enlargement sufficient to admit a satisfactory root filling. It is an open question whether in multirooted teeth this is ever complete, or whether it is necessary that it be made absolutely so, regardless of other dangers. 33 514 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING A perfectly safe rule for mechanical procedures is as follows: Use drills only when they advance readily into the root lumen; prefer Downie Broaches and Donaldson cleansers under other circum- stances. Advance no large reamers into delicate apical portions of roots, as a lateral perforation may be made. If a fine broach cannot be passed through the apical foramen, do not attempt its enlarge- ment ; and it is better to preserve a normal foramen, as large foramina present greater difficulty of filling than normal ones. If doubt exist as to the presence of a portion of pulp in the apex of the root, papain paste may be placed in the canals for a few days to digest the remaining pulp tissue. (See Pulp Digestion.) If the pulp be removed as far as possible by careful work and the canal sealed to that point with a mechanically perfect and anti- septic root filling, it is improbable that any future trouble will arise, and it is better that any such trouble should be subsequently treated than that immediate trouble should be set up by perforation in an endeavor to force a finding of canals which a very fine Downie or Kerr cleanser, or broach, will not explore. This technique is, as a rule, bes^^arried out under rubber dam, to prevent the septic contaminatioj^B canals by entrance of infected saliva; but if this be impossible ^K wise to sterilize the mouth and napkin it, and to place a drop oFcarbolic acid or formocresol in the canals and continue the work under antiseptic precautions. It is wise to have the patient first brush the teeth, using soap or a tooth paste or powder. After application of the dam or napkin the cavity is cleansed of the ddg|^ of decay if any be present. Then the cavity is to be wiped OL^Kth phenol camphor. Next the appli- cation of cocain, etc., is mad^ Before entering the pulp chamber or just after, a drop of formocresol is to be placed on the field of operation and a clean bur used to enter the pulp cavity. The debris is removed, the canals located, and a fresh drop of formocresol placed before continuing with the canal work. As the napkins become wet they may be removed, the cavity douched with a jet of warm water, the patient rested for a moment, and then the napkins are reapplied, the cavity dried, and the opera- tion repeated. .^|gjAapkins may be renewed without disturbing the treatment, bu^^is often desirable to wash out the debris, and the rest is often agreeable to the patient. The scraping ovthe canals removes the possible remnants of pulp tissue, odontoblasts, etc., adhering to the dentin walls, and also a part of the wall with the large ends of the fibrils. All these are decomposaMe media, may become septic, and are wisely removed. - -'*' THE EXTIRPATION OF THE PULP 515 The final removal of all pulp debris, coagulated blood, etc., is best done with a fine Donaldson cleanser, moved to and fro in the canal with one hand, while with the other a stream of warm water is gently introduced by means of a Moffat syringe. A large cottonoid roll or a napkin may be held by the patient or assistant to absorb the excess of moisture when the rubber dam is in position. If the operations have been done under antiseptic precautions, the root is ready for filling, unless irritation of the apical tissues be severe, in which case a sedative antiseptic — e. g., menthol in chloro- form — on cotton should be sealed in the canal. The gum should be painted with iodin as a counterirritant, and the subsidence of the symptoms awaited. (See Aseptic Apical Pericementitis.) Rhein recommends for the treatment of inaccessible portions of recently devitalized pulps the use of a chemically pure zinc point, to be placed in the root moistened with a 1 to 500 mercuric chlorid in hydrogen dioxid (3 per cent, solution) and the anode of the cataphoric appliance applied to it, the cathode sponge to be placed under the dam on the cheek. P'rom 1 to 5 milliamperes of current are used and maintained for from three to seven minutes, according to the exigency. Zinc oxychlorid is produced and carried into the tissue. It is always, perhaps, safer to introduce a sealed dressing of phenol camphor plus menthol or thymol until all possible hemorrhage or irritation has subsided. In case of pressure anesthesia with free hemorrhage a little alum and thymol, equal parts, is well added to the phenol camphor, or even a dry dressing, to absorb any secondary hemorrhage. (Ottolengui.) Sometimes it is desirable to mummify any possible irremovable portion of pulp or the fibrils by the use of formalin solutions which are usually tolerated. The carrying out of canal treatment involves a knowledge of the topographical anatomy of the teeth and their pulp canals. As an aid to this Figs. 457, 45S, and 459 are introduced, showing the normal outlines of the teeth and their pulp chambers; Fig. 459 shows the appearance and locations of the pulp canal openings at their coronal ends. It is to be borne in mind that the roots are not always normal as shown in Fig. 458, and that various degrees of lack of development or resorption may cause the root canals to be unusually open or short, with the treatment complicated by the presence of vital tissue at the root ends. In a general way it may be stated that much resorbed roots, as indicated by the age in deciduous teeth, or largely incom- plete roots, as indicated by the age in permanent teeth, indicate a pulp capping operation rather than extirpation; in the permanent 516 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING teeth, to permit better root formation. If unavoidable, one must do the best possible. In the penetration and enlargement of canals the larger and straighter canals may be cleansed thoroughly to the apex, but in very fine and tortuous roots (Figs: 461 to 489) the operator is often con- fronted with the option of taking the chances of perforation by forcing further entrance or of leaving some doubtful apical portion DESCRIPTION OF FIGS. 457, 458, AND 459.1 Fig. 457. — Fig. 3 gives in contrast a sectional view of deciduous and permanent upper teeth divided through their lateral diameters. Pig. 4, a sectional view of the corresponding lower teeth divided through their anteroposterior diameters : a, b, c represent respectively the deciduous and permanent front incisors in contrast ; rf, e,f, the lateral incisors; g, h, i, the canines; k, deciduous molars, upper and lower; I, m, the successors to the deciduous molars, the bicuspids; 7i, o, represent permanent molars; c, f, i, m, o, have dotted lines indicating the thickness of enamel removed by wear, atrophy of the cementum, and reduction in the size of the pulp due to progressive calcification, these changes being incident to old age. Fig. 458 represents in Fig. 1, letters _o to h and a to h, the longitudinal or vertical sections of the sixteen upper teeth, showing the labiopalatal diameter of the pulp chamber and canal in crown and roots, the section of the molars being through the anterior buccal and palatal roots, while the bicuspids d e and d_e illustrate the result of such a compression of the root as to divide the pulp chamber into two canals — a condition which so frequently exists in these flattened roots. The double-lettered series, d d to h h and d_d to h h, represent in the molars a section through the posterior buccal and the palatal roots, from which is quite readily recognized the slightly greater lateral diameter of the pulp chamber in the crown and the larger canal in the posterior buccal root over that in the anterior buccal root, while the bicuspids lettered e e d d and dd e e illustrate modified pulp chamber and canal, with bifurcation of the root in one, the.se being cut through a different axis or plane from the single-lettered series. Fig. 2, letters a to h and a to ^ represent the sixteen lower teeth with the section through their long diameters, as in the upper series. These incisors illustrate the compressed or flattened con- dition of their rooty in contrast with the cylindrical character of the roots of the upper incisors, while the bicuspids d e and d_e illustrate the singleness of their pulp chamber and the cylindrical condition of their roots as in contrast with the flattened or compressed condition of the roots of the upper bicuspids. The molars /, g, h and /, g, h represent sections through the anterior root, illustrating its compressed condition and divided pulp chamber in the first and second molar, and a somewhat flattened one in the anterior root of the third molar; f f, g g, h h and f f, g g, h h represent the single and cylindrical pulp chamber in the posterior root of the lower molars, while b b. c c and a a, b b represent the incisors and canines of the same series, with modified pulp chambers arising from modified development. Fig. 459. — Fig. 1, from a to h and a to ^ represents the upper teeth, with transverse or hori- zontal section through the base of the pulp chamber in the crown, viewing the entrance to the canals of the several roots, while the same letters in Fig. 2 represent the lower series in the same m.anner. Fig. 3 represents the upper teeth, with the transverse or horizontal section made below the largest diameter of the pulp chamber and through the canals after they have diverged from the central chamber, but before the roots into which they run have in the molars bifurcated. Fig. 4 in like manner represents the lower series, well illustrating the flattened or compressed condition of the canal in anterior roots of the molars and the di\'ision of the chamber, as is fre- quently found in the roots of the lower incisors. The letters a a, b b, c c, d d,ff, dd, and e_e (Fig. 3) represent the relative shapes, whether cir- cular, oval, or flattened, of the pulp canal in the roots of the upper central and lateral incisors, the canines, the first and .second bicuspids, and the first, second, and third molars, while the same letters in Fig. 4 represent the relative shapes of the pulp canal in similar teeth in the lower series. ' These figures are taken from v. Carabelli's Anatomic des Mundes. ^ c THE EXTIRPATION OF THE PULP 519 '/ 5£ */i .0 ^^04 520 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING uncleansed. To further perfect the operation of canal cleansing a radiograph may be taken as indicated by Rhein, and the cavity extension made so as to permit as direct an access as possible (Fig. 460). In very bad cases the decision should be that the danger of Fig. 460 Fig. 461 Fig. 462 Fig. 463 Distal -mesial Diagram illustrating the inaprovement In access C, to the deeper portions of enamel by cutting in accordance with a radiograph. The dotted line shows the ordinary opening permitting the access 6 b. (Rhein.) Upper lateral incisors. (Ottolengui.) Fig. 464 Fig. 465 Fig. 466 Fig. 467 Upper canines. Fig. 468 Fig. 469 Upper first bicuspids. perforation is the greater evil, and agents of a mummifying character should be employed to render any such filament into a state lessening the danger of subsequent putrefaction. THE EXTIRPATION OF THE PULP Fig 470 Kig. 471 \2\ h a Upper second biouspid. Fig. 472 Upper molar. Fig. 475 Fig. 473 ' > Fig. 47G Fig. 479 h a Upper fir.st molar. Fig. 474 h a Upper second molars. Fig. 477 Fig. 480 Upper molars. (Ottolengui.) Fig. 481 Upper third molars. 522 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING The writer regards the use of formocresol (equal parts of 37 per cent, aqueous formaldehyd solution and cresol) as especially valu- FiG. 482 Fifi. 48(j a Lower first molar. Fig. 488 Fig. 483 Fig. 484 Lower bicuspids. Lower first molars. Fig. 487 Lower first molar, immature. Fig. 489 Lower second rjiolar. Lower third molar. able where immediate root filling is not indicated. If the patient be of a nervous and irritable type this may be diluted to 5 or 10 per cent, formaldehyd strength by the use of cresol or camphophenique without ACCIDENTS IN CANAL OPENING 523 impairing its value. Often the full strength may be used on cotton as a temporary dressing. This hardens any remaining pulp and also probably the fibrils in the tubules. It also permits the apical tissue to heal and resume its normal sensitivity when the pulp has been entirely removed, which is of value in determining the extent to which pressure may be applied in filling the canals. In anterior teeth it is better to use aqueous formaldehyd solutions, as the cresol may cause discoloration, but in these situations more perfect mechanical work can be done. In a few cases in which cervical cavities obliterate the canal or cause annoying approach to it, it is desirable to remedy the condition. In such case the canals are opened as usual and enlarged, and the Fig. 490 Method of restoring lost canal continuity. The cavity should have more retention form than shown: a, amalgam. cavity prepared with suitable retentions for filling. The last-used reamer is then to be placed in the canal and the filling inserted. The filling is then supported by pressure while the reamer is slowly twisted to the right and withdrawn, leaving a canal through the filling. This may be done with amalgam or with zinc phosphate if a later removal be required. If the root be much weakened, a tapering dowel may be cemented through the crown and canal, thus attaching the root to the crown more firmly (Fig. 490). ACCroENTS IN CANAL OPENING The chief accidents that may occur are the perforation of the root wall and the breaking of the instruments used. If the technique laid down be carefully followed the danger of perforation is practically 524 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING eliminated. In fact, the greatest danger is the penetration and enlargement of the apical foramen. To avoid this the Kerr reamers should always be passed to the apex of the canal by hand or while the reamer is not revolving. It is then withdrawn a trifle and revolved, and one may always judge the distance the reamer was withdrawn. Accidents are usually the result of thoughtless forward pressure of reamers and drills, and care will reduce this to a minimum. Sometimes one must take the chances with the Kerr engine reamer. When doubt exists as to canal locations, the desiccation of the pulp chamber is of great assistance by bringing them into view, and if secondary deposits exist one should always use a small bud bur and keep well within the limits of the dentin of a root while gently seeking a canal lumen. Frequent exploration should follow gentle advances, and, as a rule, the canal will be found of fairly normal size just beyond the point of constriction. In some cases 50 per cent, sulphuric acid should be sealed against the suspected canal and the operation deferred to another sitting. If a perforation be accidentally made it should be covered as in any case of perforation (which see). Always one should be able to diagnosticate such an opening and arsenic should never be apphed to such. Cases of extensive necrosis have occurred from carelessness in this direction. The breakage of broaches is largely avoidable through the use of new instruments and by adhering to the rule of using the smaller sizes until the canals are sufficiently enlarged to permit the use of larger sizes, and, in case of engine reamers, of starting the power with the reamer loose in the canal. The engine broach seems to be of better temper than the engine reamer. Accidents of this sort usually occur with barbed instruments of the Donaldson cleanser type, especially when used with force. Sul- phuric acid tends to disintegrate the broach, so that lactic acid is often better used with it, or the alloy of sodium and potassium with a smooth broach will open the canal so that the cleanser will not bind. If it does it should be grasped with the thumb and finger and given a straight pull. While avoidance is far better than the application of the remedy, if the accident occur, the broach should be removed if possible. If lying loosely in the canal a new cleanser may be passed to one side of it and then be pressed against it. It should engage the barbs and jig it out. Cotton wrapped on a small Swiss broach may be pressed down at one side of the broken broach and its fibers made to engage its barbs. THE FILLING OF ROOT CANALS 525 Moving the broach back and forth while sulphuric acid, sodium dioxid, or sodium and potassium is about it, will sometimes loosen it. One may sometimes drill to one side of a broken instrument with a Kerr hand broach in order to more readily engage it with a barbed instrument. If very loose a magnetized probe will attract it and draw it out. Fig. 491 If the broach be tightly fixed in the canal, ?> sodium chlorid, tincture of iodin, sulphuric acid, aqua regia, or 25 per cent, pyrozone may be sealed in, in the hope of chemically disintegrat- ing it. The head of a Gates-Glidden drill or Kerr reamer is treated in the same manner. Some- times in straight roots the How appliance shown in Fig. 491 is useful. If any broach be irremovable, iodoform paste or embalming paste should be packed over it and sealed in, in order to keep the part perma- nently sterile. In a septic case the formocresol treatment should precede such root filling. THE FILUNG OF ROOT CANALS In all cases in which the removal of the dental pulp from the canals is necessary, it is imperative that the pulp canals shall be filled with some substance that shall mechanically obliterate it by sealing it throughout its length in order to prevent the ingress of fluid either from the mouth or apical tissue. Such fluid is liable to putrefaction, and the results of putrefaction follow. If made antiseptic, it also tends to kill out any bacteria which may find a partial entrance. The mechanical sealing may be defective, even when the best possible eflFort is put forth to make it perfect, so that the addition of more or less permanent antiseptics is valuable. It matters little whether a canal filling is hard or soft provided it seals the canal permanently, that it is permanently antiseptic, non- irritating, and that it is not disturbed by any subsequent work. It is better that it be capable of removal with a reasonable amount of safe work. Split and threaded in- strument for engaging the shank of a Gates- Glidden drill. 526 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING It also makes very little difference whether the pulp has been removed while aseptic or has been in a septic state, provided the canal has been rendered sterile by appropriate means. In other words, when the canal is aseptic and the apical tissues sterile and healthy, the canal is ready for filling. The length of time this may require also makes no difference. Therefore, what is here said applies to all cases requiring root filling. The size of the apical foramen, the presence of inaccessible apical portions of canals, the presence of perforations and some other conditions, however, indi- cate a choice of some root filling rather than others, so that there is no absolute rule for all cases. The following root canal fillings are useful. Gutta-percha. — This is usually the ordinary, low heat, pink gutta- percha base plate containing vermilion and zinc oxid. Cones may be rolled or left with fiat sides. Prepared cones may be purchased which have an accurate taper and are either round or fiat-sided. The fiat side permits any adjunct plastic filling material or solvent to fiow down the side of the cone rather than be forced toward the apex. Temporary stopping may be melted in a spoon and aristol added to it. It is then rolled into cones for use. Instead, a stick of it may be warmed at a point away from the end and then be pulled out into two cones which may be further rolled out. They may be rolled in powdered aristol if desired. Chloro-percha. — This is a solution of gutta-percha base-plate in chloroform. Usually a quantity of aristol or iodoform is added to make it antiseptic. As it shrinks in hardening it should be used in conjunction with gutta-percha cones or carried upon cotton twist or upon fioss silk, which it saturates, transforming them practically into a solid mass when the chloroform evaporates. Eucolypto-percha (euca-percha) .— The basis of. this substance is a solution of gutta-percha base-plate in eucalyptol. To this various antiseptics may be added. There are various modes of making this substance. B. L. Cochran'^ suggests the following: I^ — Gutta-percha base-plate §ss Dissolve in chloroform q. s. to a thin solution. Add saturated solution of thymol in eucalyptol f.^ss. Let the chloroform evaporate. Euca-percha Compound (Buckley, Lilly) is a simple solution of base-plate in eucalyptol made by aid of heat. Formo-percha (Blair) has paraform and oil of cassia added. » Dental Review, 1905. THE FILLING OF ROOT CANALS 527 This material may be warmed into a creamy paste and be used either on cotton or be used in conjunction with gutta-percha cones. Zinc Oxychlorid. — This consists of the ordinary zinc oxychlorid cement, which consists of modified calcined zinc oxid for the powder and diluted zinc chlorid as the fluid. It is antiseptic for a time at least, and may have iodoform incor- porated with it if desired. It is carried to place on a thread of cotton, or may be used with gutta-percha cones. The addition of a trifle of glycerin retards setting. A so-called embalming paste is prepared as follows: ft — Paraform 1 part Thymol . 1 part Glycerin . 1 part Zinc oxid 1 part or more. Or, R— Paraform 1 part Thymol .2 parts Alum .1 part Zinc oxid .... 2 parts Creosote to a thick or thin paste. This is used as a temporary germicidal canal dressing on cotton or as a root-filling with gutta-percha or temporary stopping cones which are pressed into it. Fig. 492 Fig. 493 Radiograph of a perfect gutta-percha root filling. (Rhein.) Root-canal filling: .1, gutta-percha; B, zinc oxychlorid. Wax or Paraflftn. — Either of these may have a third of its bulk of salol, aristol, or iodoform, or a fifth of paraform added to it while melted in a spoon. It is then rolled into cones or small pellets. In use a pellet is dropped into the dried pulp chamber and a hot Evans root drier point applied. As it melts, the metal point is carried down into the root and the fluid material pumped to the apex. Capillarity does part of the work. It adjusts itself to the tissue and the canal 528 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING walls. The pulp chamber is then cleared of excess wax, etc., and filled without pressure. Salol. — This is a solid antiseptic, melting at 104° F. It is used much as paraffin is. A gutta-percha cone may be thrust into it while fluid. It often seems to disappear from canals, and unless used with paraffin is to be used only as a temporary root filling. Canada Balsam. — A solution of Canada balsam in chloroform to which hydronaphthol is added (Williams) makes a useful solution in which to saturate cotton twists or to moisten canals previous to the introduction of a cone of gutta-percha. Balsam of Peru is now on trial, but its soft condition is liable to render it a failure. Fig. 494 Fig. 493 A, perforation through side of apex; D, cone of gutta-percha passing through; B, portion to be cut off; C, portion of canal not treated. Lateral perforation due to holding a bur at a wrong angle to the axis of the root: A, root canal subsequently filled with gutta- percha; B, perforation filled with a fitted cone of gutta-percha; C, zinc oxychlorid. Normal Tapering Well-opened Canals. — In these canals gutta-percha is admirable; a little eucalyptol is applied to the canal walls and a section of a suitable cone mounted by heat on the end of a canal plugger which will go to or nearly to the canal end is gently but firmly pressed into the apex of the canal. Temporary stopping cones are more readily adapted, and as they can be made antiseptic, are valuable. The rest of the canal is then filled with other sections or with zinc oxychlorid made thin and carried to place on cotton twists. The latter may be used for the entire canal, and should then be preceded by a tiny bit of cotton saturated with an essential oil to prevent irritation of the apical tissue. It is claimed that this cotton is acted upon by the zinc chlorid being transformed into an amyloid condition. If used alone a slight degree of moisture aids in carrying to the apical foramen (Fig. 495). A variant consists in moistening the canal with chloro-percha or eucalypto-percha, and using the section of cone or pressing in an entire cone. A second cone may be placed at the side of the first and THE FILLING OF ROOT CANALS 529 both compacted after warming with a hot air blast, or the first cone alone used. Ottolengiii advises the use of bits of floss silk an inch long to be saturated with chloropercha and dried. These are to be pressed into chloro-percha previously placed in the canal and crimped to place. An end is left projecting into the pulp chamber. If necessary this may be caught and the dressing withdrawn. Another variant is the use of chloro-percha on cotton, which makes a very accurate and easily introduced root filling when carried to place on a properly formed and tempered Swiss broach or prepared Donaldson bristle. When the broach must be bent to enter canals, loosen the broach first before introducing into the canal, thus leaving the cotton loosely mounted on the broach. To prepare a Donaldson bristle cut oft' the hook and flatten the end upon an Arkansas stone, then lay upon a glass slab and burnish thoroughly to remove any bur left. In use the cotton and broach are rolled with the left forefinger and thumb only. It is obvious that to do this the broach must be per- fectly straight. The writer believes the prepared Swiss broach not only more facile but economical in use. To prepare broaches, select accurately tapering Swiss or English broaches from which the temper has not been drawn. Xext, draw the temper by placing a few in a test-tube and heating first at the shank, gradually drawing the tube over the flame toward the points. The blue color seen on the shank should be run out to the tip; let cool on any open surface. The soft broaches usually sold are nearly useless. The point is left if canal exploration is intended. For carrying cotton twists, cut the end off with scissors. To wind the cotton lay a wisp on the left forefinger, lay the broach upon it, close down the thumb, then quickly revolve the broach with the right forefinger and thumb, stroking the cotton with those of the left hand into a symmetrical cone. To use as a swab, rotate in the canal to the right. To leave the cotton in the canal, rotate to the right as the twist is pressed to the apex. Then turn the broach once or twice to the left to loosen it from the cotton, withdraw a little, then press in again. Thus the cotton is crimped upon itself. Roots with Open Foramina. — These may be incomplete roots with very large apical openings, in which case wax with aristol is the best filling used, as previously stated. It should be said again, however, that if possible the pulp of such a tooth should be capped to permit root formation to be completed. If the foramen is of moderate extent and either natural or unfor- tunately made with drills, gutta-percha cones are valuable. To 34 530 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING determine the size of the cone, one of two methods may be employed. Perhaps the more accurate is the employment of a series of gradually increasing sizes of canal pluggers. One should be selected which will just fit the apex or be a trifle too large. By placing this in the hole of a draw plate, a specially rolled cone or even a slightly tapering size may be made to fit the hole in the plate. The canal is moistened with eucalyptol or chloro-percha and a quarter-inch section of the cone is carried on the plugger to its place in the root-canal apex. A slight protrusion is not ordinarily productive of injury. A cardboard per- forated by the respective plugger mil do instead of the draw plate. If the root length was previously measured with a piece of rubber dam slipped over the plugger shank and some known point on the tooth used as a guide, the cone should be seen to go do^^Ti until it chokes the foramen, when the dam should be above the guide point a distance equal to the length of the cone section used. Fig. 496 Fig. 497 Manner of measuring the length of a root and fitting a gutta-percha cone. -a Manner of tapering a canal to fit a cone of the same size. --(^ In the second method a long, tapering cone is prepared. Some point on this must fit the foramen. It is tried in and as often as sensation is felt it is cut off a trifle and tried again until it chokes the foramen without sensation. In case of abscess, especially if filling is a means to a cure, this may extend beyond the apex of the tooth. The cone should be marked at a point corresponding to the guide point chosen and be laid aside. Next, a fine hook made by bending the tip of a fine broach to a right angle, then cutting it close to the shank, has a piece of rubber dam slipped over it and is passed through the apex and hooked upon the edge (Fig. 496). The dam is slipped THE FILLING OF ROOT CANALS 531 to the chosen guide point. The probe hook is withdrawn, the dam laid at the mark on the cone, and the cone cut off at the lower edge of the hook (Fig. 496, h). In use, a little solvent, preferably chloro- percha, is placed in the canal and the cone slowly slipped to place until the mark coincides with the guide point. The cone is then cut off with a hot instrument, warmed, and gently packed into the canal. When the canal has been reamed with a small engine reamer, and the apex enlarged, the hook may be placed and have a bit of rubber dam on it as a guide. Then slip a bit of dam over a larger tapering root reamer at a corresponding length. Drive the reamer in until at the guide point. This gives a tapering cone shape to the canal and is a guide in the construction of the cone (Fig. 497). In some cases of large foramina or perforation a bit of grafting sponge may be introduced into the apical space and the filling placed against it.^ Canals with Inaccessible Apices. — Any tissue in such apices should have been mummified or sterilized with formocresol or be treated by Rhein's method^ of filling a canal with mercuric chlorid in hydro- gen dioxid (1 to 500), passing in a zinc probe, then applying the anode of a cataphoric outfit with from 1 to 5 milliamperes of current from three to seven minutes (the cathode at the cheek). The object is to form zinc oxy chlorid in the apical root canal through electro- lytic action. The canal must be regarded as doubtful, but if well opened to the inaccessible portion a trifle of formo-percha may be placed on cotton at this point and the balance of the canal be filled with antiseptic temporary stopping. The paraform and cassia in the formo-percha are active agents. A variant consists in the use of embalming paste or Soderberg's mummifying paste, either made stiff and introduced with successive sizes of pluggers, beginning with the largest admissible and proceeding to the smallest, or moistening the canal with the thinner paste and packing a cone into it. The use of such a paste in connection with a cone of gutta-percha is valuable as an agent embalming the fibrils in the dentin of teeth from which living pulps have been removed, or of keeping sterile the tubules of those teeth in which the pulp is gangrenous. If conditions admit of it, provision for future entrance of the canals should be made, and it is always well to divide the operation of canal filling and crown filling by a short period of time. Iodoform paste with or without cotton may be placed in the upper third of the canal. ' G. Brunton, England: Dental Cosmos, 1900. 2 Dental Cosmos, 1905, p. 1196. 532 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING Root Canals in Temporary Teeth. — These may at times be well filled with gutta-percha points, which, if aseptic, do not interfere with resorption, but a material of easier adaptation which absorbs with the root is preferable. The waxes meet the indications, as they can be pumped while fluid from the action of a hot root drier into all inequalities, where they adjust their relation to the soft tissue. Buckley recommends in cases of chronic abscess the use of a stiff mixture of calcium phosphate and formocresol (formalin, 1 part; cresol, 2 parts), to be packed into the pulp cavity and zinc phosphate flowed over it. Johnson recommends eucalypto-percha to be pumped into the canals and pressure with temporary stopping to be exerted until the solution appears at the fistula. Such temporary stopping as does not interfere with filling integrity should be left. There are various other methods of filling root canals, such as driving wood points saturated in carbolic acid into the canals; the use of iodoform paste, with or without cotton, or of creosote on cotton (preferably raw cotton) ; the use of balsamo del deserto, etc., which have had advocates, but the methods given are those which have had long-continued and successful use. The Covering of the Root Canal Filling. — The Jbulb of the pulp chamber may be filled with any of the more solid materials. In case of a strong crown, temporary stopping makes a good occupant of this cavity, though gutta-percha is often used; oxychlorid of zinc aids in keeping good color. In the weaker teeth or sometimes for other reasons the final filling may extend into the pulp canal to assist in anchorage. Fig. 498 Herbst's method of preserving pulp stumps. Partial Removal of Pulp. — The Cobalt method of pulp treatment has been alluded to. Wm. Herbst, of Bremen, advanced the idea that if the bulbous portion of the pulp be devitalized by cobalt and removed, leaving the root portions, the latter will remain vital if protected after a manner described by him. The bulbous portion of the pulp is cut away and the pulp chamber enlarged by means of MUMMIFICATION OF THE PULP 533 large rose burs. Over the pulp stumps a cylinder of tin-foil is laid, and burnished to fit the floor of the pulp chamber without pressure upon the pulp stumps (Fig. 498) . Over this a filling is placed. Herbst claims that the pulp stumps will remain vital. Were this to be depended upon, it would be a marked saving of time and trouble and would lessen the chances of pericementitis subsequent to pulp removal; but when it is known that the cobalt of Herbst is metallic arsenic, the ultimate death and decomposition of the pulp remnants seem almost inevitable, and in fact does occur. The method should not be employed. MUMMIFICATION OF THE PULP Many experiments have been performed relative to leaving in situ portions of pulps and covering them with substances having for their object the chemical alteration of the pulp tissue, so that no peri- cementitis shall result from its putrefaction. The first effort in this direction is credited to Witzel in 1874. INIiller,^ after many experiments w^th various materials, has shown that none but the most powerful and penetrating antiseptics have value as permanent sterilizers. These are the cyanid, bichlorid, and salicylate of mercury, sulphate of copper, and oil of cinnamon. Orthocresol, carbolic acid, trichlorphenol, and zinc chlorid penetrate the pulp tissue rapidly, but are too diffusible, their effects disappear- ing in a few weeks. He classifies salicylic acid, eugenol, camphophenique, hydro- naphthol, a-naphthol and /S-naphthol, aceticotartrate of aluminum, and some essential oils, resorcin, thallin, sulphocarbolate of zinc, etc., as being of doubtful value. Those nearly or quite worthless are iodoform, basic anilin coloring matters, borax, boric acid, dermatol, europhen, calcium chlorid, hydrogen dioxid, sozoiodol salts, tincture of iodin, spirit of camphor, and naphthahn. The preparation giving the best results consisted of mercuric chlorid, 0.0075 gram; thymol, 0.0075 gram, in tablet form. The pulp is devitalized; the crown portion and all the root portion readily accessible are removed; one of the tablets is placed in the pulp chamber, crushed by means of an amalgam plugger, and co^'ered with gold-foil. The mercury salt tends to discolor the crown of the tooth, so that its employment should be restricted to the posterior teeth; 1 Proceedings of Columbian Dental Congress, 1893. 534 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING indeed, the necessity for its use would be, as a rule, found with these teeth, being those from which it is most difficult to extract pulp remnants. Miller expresses faith in the power of oil of cinnamon to permanently sterilize pulp fragments. Soderberg^ recommended a paste composed as follows: ^ — Alum exsic, Thymol, Glycerol aa 3J Zincioxidi q. s. to make a stiff paste — M. It is preferable to add the zinc oxid as needed or to make a small quantity of the paste frequently, as it gradually hardens. To the paste used a crystal of cocain is added to prevent pain. Bennette, of England, has advised the use of paraform incorporated in the paste, for its well-known antiseptic and hardening effects. Greenbaum suggested the use of a drop of 40 per cent, formaldehyd solution to be incorporated with the paste. Both reduce the pulp to the consistence of catgut. Soderberg reopened cases months after application of the paste to pulp stumps, and found them shrunken and with an odor of thymol about them. He applied the paste in the manner shown in Figs. 499 and 500. In 1900 Soderberg reported the use of the paste in about 900 cases, Fig. 499 Fig. 500 a, caries exposing a horn of the pulp. a, root portion of pulp; &, mummifying paste; c. zinc phosphate; d, gold or amalgam. of which 220 were test cases of from two to six years' standing. He claims that in no case did apical pericemental disturbance arise from the use of the paste as described. This method has met with much opposition from prominent oper- ators, who prefer the thorough cleansing and filling of the canals. 1 Dental Cosmos, November, 1895. MUMMIFICATION OF THE PULP 535 No doubt the rational method of procedure is to cleanse the canals as well as possible, and to use the paste against unrem()val)l(i pulp stumps. The best results were obtained when arsenic was applied for a limited time only in order that the arsenic should not penetrate too deeply. In view of Kirk's observations (p. 506) this would seem wise. While the paste may effect mummification of entire canal filaments of pulp, leakage is always imminent about shrunken pulps, and the only safeguard is the antiseptic effect of the paste. This is much enhanced if the bulk of putrefiable material be replaced with the anti- septic paste used as a root filling. Many such root fillings have done good service for many years. A certain percentage of failures would be no argument against the employment of the method when indicated, as no method is infallible in all circumstances, and particularly in those in which the method is indicated. Pulp Digestion. — Harlan recommended that the following paste be applied to unremoved portions of dead pulps as a means of digesting them preparatory to root filling: I^ — Papain ,. . . . gr. v Price's pure glycerin TTliv Sol. 1 to 200 hydrochloric acid TRv — M. This is applied in the pulp canal, covered with blotting paper soaked in liquid vaselin, and the whole temporarily sealed for a few days. The pulp is reduced to the consistence of jelly and can be readily washed out. The method, on the whole, does not seem preferable to either mum- mification or the Rhein treatment or the formocresol treatment of inextricable portions of pulps in curved roots, etc., inasmuch as the occupancy of a canal by a sterile pulp remnant is better than leaving an empty root canal apex or filling only a portion of it in such manner as to render subsequent treatment almost impossible. In fact, it is better that dentists recognize their limitations and put themselves in position to do future good to the patient, than to blindly obstruct efforts in that direction. Perforations and Resorptions. — The same accidents that occur in canal opening in the case of the removal of anesthetized or devitalized pulps may occur in all gangrenous cases with somewhat increased liability to infection of the pericemental tissue. In old cases the pericemental tissue may hypertrophy, causing the condition of hyperplastic (fungoid) gum. This should be sterilized 536 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING and then may be frozen with ethyl chlorid and ablated with sharp instruments, or it may be saturated with trichloracetic acid and ablated, or it may be pressed away (resorbed) with cotton saturated with tincture of iodin or an antiseptic oil. The perforation is then covered. The Filling of Perforations. — Perforations made high up in the canal, after being appropriately sterilized with formocresol, should be jBlled with wax or with gutta-percha cones, which have been accurately fitted to the openings. It is often difficult to do this accurately, but the effort should be made. When ready, a little antiseptic chloro-percha is to be placed in the perforation or upon the cone, and the latter packed to place. In low perforations without a fistula associated, the opening of the perforations should be enlarged inwardly and a ball or plaque of aseptic, warm, low- heat gutta-percha, or even temporary stopping, adapted to the opening. A piece of pure gold plate may be burnished over an accessible opening, and be adapted with thick chloro-percha or temporary stopping. Any of these may be fixed in place with oxyphosphate of zinc. Quick-setting oxyphosphate of copper in its soft, gummy, state may be painted over the tissue and root opening by means of an instrument, or the perforation may often be satis- factorily closed with copper amalgam. When in posterior teeth a pin must be used, the pin may be made smaller than the root canal and be coated with wax, soft oxyphosphate of copper is put in the canal, and the pin gently thrust in. When the cement has set the pin may be heated and withdrawn, and when included in the intended superstructure, the pin may be again cemented in place. When a perforation threatens to produce an abscess an artificial fistula should be made and the case treated accordingly. If a perforation have a fistula associated with it, the oxyphosphate of copper or zinc oxychlorid may be allowed to go through the fistula, by way of which any excess may be removed. In case of resorption of the roots of permanent teeth great difficulty may present, the soft, absorbent tissue having grown into the cavity in the root side which it has made. A radiograph will aid in deter- mining the extent of the lesion which usually renders canal treatment impossible and extraction imperative. CHAPTER XVIII GANGRENE OF THE PULP Definition. — By gangrene of the pulp is meant its death through an interference with its nutrition. It may be partial, as when an abscess in the pulp or violent irritation causes the bulbar portion to die, the canal portions being found alive; or when only one canal portion is dead, the others being alive. Either dry or moist gangrene may occur. Causes. — It is probable that a construction of apical root tissue (hypercementosis) about the pulp may so constrict it as to bring about its death. (For the primary causes of this see Hypercemen- tosis.) Sudden shocks, such as occur from thread, string, or cigar biting, or blows or rapid movement in regulating or wedging, or non-fixation after regulation, may cause torsion or tension of the bloodvessels entering the apex of the pulp. These influences may either cause pulp hyperemia or strangulation of the apical bloodvessels, or, possibly, an area of apical thrombosis, cutting off the nutritive supply to the pulp. Septic or aseptic inflam- mation of the pulp may cause its total death. Death of pulp tissue due to arsenic produces results in nowise diftering from gangrene, provided the pulp be left in situ. (See p. 456.) DRY GANGRENE OF THE PULP Definition.^By dry gangrene of the dental pulp is meant its death in toto and its subsequent transformation into a dry, shrivelled mass occupying the pulp chamber and canal. Causes and Pathology. — If the pulp die and remain under conditions which exclude bacteria from contact with it, the water of the pulp may be removed, leaving the organ as a tough, shrivelled mass (Fig. 501). The conditions most favorable seem to be: (1) Pulp death from some aseptic cause, e. g., the hyperemia resulting from a blow on a sound tooth; (2) constriction of the apical foramen, due to hyper- cementosis, the result of thread biting or other mild irritation of the pericementum; (3) the presence of secondary dentin over the bulbar portion of the pulp, causing pulp exhaustion yet protecting it from infection; (4) the capping of the pulp with zinc oxychlorid or formagen 538 GANGRENE OF THE PULP paste, the pulp being permeated with the drug or dried by it; (5) the covering of pulp stumps with a paste containing a tannifying sub- stance, such as alum, formaldehyd, or tannin. The water necessary to putrefaction is abstracted, either naturally or chemically, and probably bacteria are at the same time excluded, either mechanically or because the chemical substances used have penetrated the pulp tissue, acting as antiseptics. Symptoms. — The tooth has a nearly normal color, but under re- flected Hght is seen to have lost perfect translucency. There is no response to thermal or electric tests for pulp vitality. The dentin is insensitive to cutting instruments, and the cuttings upon the bur have no odor. There is no odor or fluid in the pulp canal when this is entered, and the pulp is found as a tough, dry mass not unlike that seen in a dry extracted tooth which contained a vital pulp at the time of extraction. These cases as spontaneous occurrences are relatively rare. Tests for Pulp Vitality. — The diagnosis of pulp vitality or death being in practice almost daily required, the decisive tests are here indicated. A tooth containing a vital pulp is translucent and pink; that con- taining a dead one always opaque to transmitted light, and usually clouded to a gray or bluish black. The ordinary appearance by reflected light often corresponds to this, but sometimes a tooth is clouded by fillings, or looks dead, but is vital. An electric mouth lamp with or without a reflector so arranged as to reflect the light upon the Ungual surface of the tooth wiH supply the means for this test. In its absence strong sunlight may be re- flected by means of a mouth mirror, but is not nearly so good a means as the electric light (Fig. 357). If the tooth be isolated by means of rubber dam and, first, cold water be thrown, or, later, ethyl or methyl chlorid be sprayed upon it or upon the filling contained in it, absence of response will indicate either partial or total pulp death or the formation of a -quantity of secondary dentin. In the latter case the test must be renewed as the excavation proceeds. A hot burnisher or hot gutta-percha applied to a filling or dentin, or very hot water thrown upon an isolated tooth, should provoke at least a delayed response from a vital pulp. Woodward has shown that if a few cells of a cataphoric apparatus are in action and the positive electrode be applied to the dentin or metal filling in a vital tooth, while the negative pole is at the cheek or wrist of the patient, a distinct sensation should be felt, while in case of a dead pulp there will be no response; usually even a small DRY GANGRENE OF THE PULP 539 filling will transmit a distinct shock in a vital tooth which is absent in a devitalized tooth, A mild interrupted current has also been used for the test. There may be no response through a metal filling, while such response may be obtained by packing wet cotton against the dentin after some drilling. A mild current should always be used unless there is no response, when the strength of the current should be increased. It is generally possible to test some evidently vital tooth nearby as a control. If the filling reach the gum, the current may be transmitted by it. The possibility of contact of the filling with another in a vital tooth is to be remembered. Insulation with rubber dam is indicated in such a case. Fig. 501 Fig. 502 Fig. 503 Dry gangrene of the pulp: PN, pulp nodule; DP, shrivelled pulp. (From a speeimen of pulp extracted intact in this condition.) Caries; moist gangrene in imprisoned temporary molar. (Skiagraph by Hagopian from editor's case.) Mo'st gangrene. Skia- graph of unfilled root canals with large mass of filling material built in over them. (Price.') In doubtful cases, such as that shown in Fig. 503, the a;-ray skia- graph is valuable, and indicates at least the removal of the filling for further diagnosis and treatment. When dentin is insensitive, pulp death should be suspected. A strong odor of putrefaction may be obtained from bur cuttings in cases of moist gangrene only. This must be differentiated from the odor of decayed dentin, which usually also has an acid character. In case of partial death of the pulp not discoverable by the tests given above, a fine, sharp probe passed into contact with the pulp remnant will demonstrate its vitality. Treatment.^ — If septic matter be introduced a violent pericementitis may be lighted up; but if aseptic precautions be employed in opening the canal, and this be kept under the influence of a germicide, such as 5 per cent, formaldehyd or sodium dioxid, the root may be filled by the immediate method — i. e., when opened and sterilized it is to be 1 Items of Interest, 1901. 540 GAXGREXE OF THE PULP dried and then moistened with eucalyptol and the excess of this removed; previously prepared cones of temporary stopping are then packed into the root or another root filHng employed. The method of moistening the canal with forma-percha and then placing the cones, or the use of cotton, silk, or asbestos fibers saturated with forma-percha, has all the advantages of the temporary antiseptic filling, with the added merit of permanency if the indications declare a success. A temporary filling of pink base-plate gutta-percha is to be inserted in the crown cavity until all irritation, if any, subsides. Slight aseptic apical irritation may be anticipated as a matter of precaution by the use of iodin as a counterirritant at the time of root filling (see p. 451). Such irritation is either mechanical or due to the chemical substances used. MOIST GANGRENE OF THE PULP Definition. — By moist gangrene of the pulp is meant death of pulp tissue en masse and its subsequent decomposition by the action of putrefactive agencies. As putrefactive decomposition is the essential feature in these cases, and that which gives the process its patho- logical significance, the causes, nature, effects, and treatment of putrefactive decomposition of the pulp are included under this subheading, (See p. 86.) Causes. — The causes of moist gangrene are such as may cause the death of the pulp and its subsequent decomposition by bacteria. Without bacteria putrefaction cannot occur. Among these the Bacillus gangrense pulpae (Arkovyj figures prominently.^ Four ti^es of cases are seen: (1) In teeth apparently sound; (2) in teeth filled, but the canals not treated — i. e., death of the pulp has occurred after filling; (3) in teeth filled with canals partly filled; (4) in teeth having open cavities and canals. In the first type of cases the bacteria may enter by way of the blood channels, but it is not improbable that slight cracks or histo- logical defects in the enamel may admit to the dentinal tubules the necessary bacteria, or that they may gain entrance by way of the cementum and dentin at the neck of the tooth. (See Caush's Tubes.) The inference is similar in case of trimmed crowns of teeth underlying gold caps. 1 Siberth and Goadby regard this microorganism as a variety of Bacillus mesentericus, prob- ably "niger." Mycologj- of the Mouth, p. 148. MOIST GANGRENE OF THE PULP 541 Pigment. Fig. 504 Sulphur + hemoglobin. A case presenting some analogy to these teeth is that of an egg with apparently perfect shell, but in which intense decomposition has occurred. That the gases and other odorous products are somewhat confined the author proved to his dismay as a boy by smashing with a hatchet one found in the brush. Many of these teeth do not develop abscesses even after the tooth has become dark in color; perhaps the bacteria are killed by their own products. If the dentin be exposed, as at the incisal edge, the abscess may develop. The entrance of air or beginning of treatment often starts an abscess unless treatment is instituted. In the filled cases crevices about crown and root fillings may admit bacteria, which may pass through the tubules of even secondary dentin in some amount. On the other hand, it is irrational not to admit the possibility of an infection via the circulation. In cases of obvious pulp infection beneath fillings — e. g., suppuration of the pulp — the bacteria necessary are iji situ. In the open cases the infection ob- viously arises from the mouth. Pathology and Morbid Anatomy. — The pulp being wholly or partly dead from any cause whatever, sapro- phytic bacteria gain access to it, and the serial decomposition it un- dergoes is in exact correspondence with that of moist gangrene or putre- faction in other localities. In this serial decomposition albuminous substances are first transformed into peptones and allied substances, some of them being very toxic. Compound ammonias, known as ptomains, or animal alkaloids, such as putrescin, neuridin, and cadaverin, are probably next formed. Next the nitrogenous bases — leucin, tryosin (amido- acid), and the amines (methyl, ethyl, and propyl) — make their appearance, together with organic fatty acids. Next aromatic products, indol, phenol, cresol, etc., and finally, hydrogen sulphid ammonia sulphid, carbon dioxid, and water. By alternating pro- CO2, NH,; H-.O and H3S. Aromatic and fatty prod- ucts. Ptomains. Peptones. Diagram illustrating the more complete decomposition of the pulp at its coronal end. 542 GANGRENE OF THE PULP cesses of hydration, reduction, and oxidation, bodies of increasing simplicity of chemical composition are formed. "Fermentation and putrefaction can only occur where the fungi concerned live and the Fig. 505 t -''S^:^ Fig. 506 Fig. 507 .X Fig. 508 ^o <^mfM Fig. 509 :f^. Fig. 510 Fig. 511 Fig. 512 Uf'X • • HH)tO J 1 _ X '• I extent of decomposition is conditioned by the number of fungi. "^ The contents of the tubules (fibrillpe) also are putrefied. These Zieglcr: General Pathology. MOIST GANGRENE OF THE PULP 543 products are derived from the following chemical constituents found in normal pulps, according to Hodgen: Proteins and albu- minoid, fibrin, hemoglobin, collagen, elastin, fats, tripalmitin, stearin, and olein. The irritant bodies are probably the gases and ptomains which have experimentally been found capable of producing suppuration in the absence of bacteria. INIiller^ found, in the deepest portions of the degenerating, putrefy- ing pulps, where inflammation and suppuration were in progress, a preponderance of small cocci and diplococci, and proceeding toward the open pulp chamber an increasing number of large cocci, several forms of bacilli, vibrios, and other spirilla, spirochetse, and long thread forms (Figs. 505 to 512). Figs. 511 and 512 are from the same pulp; Fig. 508 was taken from the radicular portion of a pulp which was alive and suppurating; Fig. 505 was from the putrid crown portion. INIiller found that bacteria of pulp putrefaction cultivated in gelatin, with and without the access of air, exhibited a difference in the poi- sonous properties of their products. Those developed with free access of air produced stronger reaction, and more extensive suppuration than those developed without the access of air. Arkovy,- in an examination of 43 cases of chronic apical abscess, pulp gangrene, etc., found the Bacillus gangrense pulpse present in 41; the Staphylococcus pyogenes aureus in 15; Staphylococcus pyogenes albus in 8; Staphylococcus pyogenes citreus in 2; Strepto- coccus pyogenes in 10, and Bacillus pyocyaneus in 4. He found the Bacillus gangrene pulpfe in mouths free of caries as well as in mouths containing carious teeth, and established the fact that it is pleomorphous (bacillus and coccus form) . He inoculated healthy pulps with this bacterium, and found that in pure culture it produced total gangrene without suppuration; while mixed cultures, and even the mixed pleomorphic forms of the same bacillus, produced chronic pulpitis. On gelatin cultures a putrid, cheese-like odor was perceptible. The germ is subject to the antiseptic effects of strong acids, alkalies, car- bolic acid, and tincture of iodin, which explains, in part, the success of the treatment hereinafter mentioned. Arkovy's demonstration seems a satisfactory explanation of cases of quiet death of pulps under fillings. The hydrogen sulphid combines with the HN3 of proteid origin, to form ammonium sulphid (NH4)2S, which, again, combines with the iron in the hemoglobin of the red corpuscles, producing ferrous 1 Dental Cosmos, 1S94. - Synopsis by Soderberg: Dental Cosmos, IS'J'J. 544 GANGRENE OF THE PULP sulphid, Fe2S, which darkens the decomposing tissue, and, entering the tubules, stains the dentin a slaty gray or bluish-black color. Other derivatives of hemoglobin may be responsible for the yellowish brown discoloration often seen in cases in which bacteria have not reached the pulp until long after pulp death. The color is, therefore, not due to the presence of hydrogen sulphid. Fig. 504 is a diagram illustrating these changes; it being assumed that the decomposition is most advanced at the crown portion of the pulp, owing to the entrance of bacteria at that point. In the early stage of the process the gangrenous pulp resembles a yellowish mass of sloughing tissue, with reasonably tough con- sistence, which can be easily removed. In the later stages it is more decomxposed and dark and jelly-like, and yields to the broach. In the final stages nothing but fluid, or even an almost dry canal, may be found. Naturally the greatest number of fungi will have, by multiplication, invaded and putrefied that end nearest the source of infection, while the more consistent (less putrefied) portion of the pulp will exist at the apex. This last condition must not be confounded with dry gangrene. If fluid, or odor without fluid, be present the case is one of moist gangrene. Gangrenous pulps do not necessarily produce abscesses at once, but often clinical history shows that a year or two, or even more, may elapse, though as short a time as two or three weeks has some- times been sufficient. In one case of a boy, aged ten years, the time between a capping of a bleeding pulp with Jodoformagen and the presence of a fistula upon the gum was but two weeks. It was, however, in a temporary first molar, and the cement covering the cap was found to be loose. The forcing of gangrenous pulp tissue by instrumentation into apical tissue generally results in an abscess, even when extraneous bacteria are presumably not introduced. The irritating substances in a decomposing pulp are presumably the bacteria, the ptomains, and the expanding gases. Many decomposed pulps produce no pain, but in these cases the gases may escape via dentinal tubules and leaks about fillings (Fig. 503). Clinically, putrefactive pulps may be found in sound teeth, in filled teeth, and in teeth the pulp cavities of which are open to the oral fluids, either actually or through the medium of open tubules in the dentin over them, or in apical portions of poorly cleansed or partly filled canals. A cotton dressing having a bad odor, or an apparently empty apical portion of canal or a leaky gutta-percha canal filling associated with a bad odor, even though the pulp has MOIST GANGRENE OF THE PULP 545 been successfully removed, have a similar pathology. There is little difference in principle between putrefactive serum or tubule contents and a putrefactive pulp. Any of these may cause abscess or remain quiescent. Symptoms. — The symptoms are opacity of the tooth evident to the eye or noted by transmitted light, bluish or brownish discolora- tion of \arying degrees, odor, and discoloration of the dentin in a cavity. There is a lack of response to cutting, thermal, and electric tests. Sometimes a bad taste due to leakage about fillings is present. Upon drilling out a filling the odor of putrefaction may be clearly noticed even before entrance of the canal, and sometimes rises to the operator's nostrils. The odor of the bur cuttings is diagnostic in less pronounced cases. The gases may be present in quantity without symptoms of pain. Looseness, tenderness to percussion, incipient and acute abscess, or a chronic fistula are evidences of pericemental irritation. Pain to heat, while usually indicative of pulp irritation, also some- times occurs, and is explainable upon the same theory of the expan- sion of gases against vital tissue — in this case the apical tissue. These symptoms are all explained by the pathology of the condition. A confusing condition clinically is found where one-half of a pulp has died and undergone decomposition, as in molars, the other half remaining vital, although the seat of infection and inflammatory action. So far may this condition go, that abscess, acute or chronic, may be present upon the root of one tooth long before the second segment of the pulp has succumbed. The diagnosis of such cases is made by the light test, by obtaining the painful reaction to heat and perhaps to electricity, and usually some tenderness upon percussion upon some particular portion of the tooth; upon opening the tooth the peculiar condition described is found. The a--ray should show the condition. In one case of a lower molar with a fistula related with the distal root I found the pulp apparently vital upon entering the pulp chamber with a bur at a point about midway between the horns. There was apparently a persistence or hypertrophy of the pulp bulb attached to the mesial filaments. The distal canal was found to contain only the fluid remains of a dead pulp filament. In cases seen at the right time the bulbal half of a pulp may be gangrenous without positive putrefaction, while the apical half is still vital. J. H. McQuillen^ recorded a case of longitudinal fracture of a bicuspid tooth extending from the sulcus to the bifurcation of the > Dental Cosmos, J871. 35 546 GANGRENE OF THE PULP roots, and which was apparently due to the expansion of the gases of decomposition. Poinsot^ records a similar case, and states that several teeth containing decomposed pulps confined in a glass tube caused the latter to break. Observations previous to that of McQuillen have recorded a sound, as of an explosion, to have occurred simultaneously with the fracture of the tooth. I have looked all my professional life for such a case, but have never been able to eliminate the possibility of fracture from ordinary causes. Treatment. — The pulp being presumably infected, all quiescent gangrenous pulps or putrefactive conditions under any conditions discovered indicate a similar treatment, namely, first disinfection to remove or kill bacteria which might cause an abscess and at the same time to destroy the chemical nature of the gases and ptomains. After this the canals are to be thoroughly opened, cleansed, further disinfected for the sake of surety, and later filled. Three substances are preeminent in this direction — (1) formal- dehyd, (2) nascent oxygen, (3) iodin or its derivatives. At the present writing no substance equals formaldehyd because of its rapid diffusion as a gas through all canals, tubules, and even abscess tracts. The first and best treatment consist"; in opening the pulp cavity and gently removing the bulk of decomposed pulp from the pulp chamber and canals, care being employed to avoid forcing any putrid material into the apical tissue by broaching or plunging of the bur. Also, no bacteria should be introduced from outside. The opening should not be too freely made, and should be funnelled or countersunk out- wardly to secure the seal against being plunged into the pulp cavity in mastication (Fig. 513). This being done, the canals are dried with cotton and hot air, and a small pellet of cotton saturated with formocresol or 10 per cent, aqueous formaldehyd solution, or geranium formoP is to be placed in the pulp chamber. Any that has come in contact with the orifice should be removed with alcohol. The orifice is then dried and a small piece of dry spunk placed over the application, but not so as to interfere with the seal. Quick-setting, adhesive, hydraulic cement is now flowed into the orifice, air bubbles being avoided by flowing it in with an instrument (Fig. 513). A bit of paraform accomplishes the same purpose as the solution, namely, the liberation of formal- dehyd gas. 1 Dental Cosmos, 1901. 2 Geranium-formol introduced by Andr6 and de Marion, I'Odontologie; abstract by Inter- national Dental Journal, 1901. MOIST GANGRENE OF THE PULP 547 When opportunity for self-relief seems proper, as when the operator is leaving his practice for a short time, or may otherwise be inacces- sible, hot temporary stopping may be used and the patient instructed as to the proper procedure to obtain relief. An ordinary pin crooked at the point by striking it across any hard surface will serve to pick out the stopping and cotton. In all cases tight coverings must be made, as the object is to concentrate the action of the formaldehyd gas upon the canal and tubular contents. In some cavities it is well to make the covering first, as done for arsenic (see Fig. 43G), and to seal the dressing in with a further addition of cement or temporary stopping. The latter does not permit mastication like the former. Fig. 513 Fig. 514 a, cotton and formocrrsol; 6, spunk; f, cement. Cervical wall built up with amalgaia to permit canal sterilization and treatment. If there be a broad cavity extending beneath the gum, it is well to press the gum away with cotton pellets, then to form the cavity and open the canal orifices. Then a retention at the cervical portion of the cavity should be made, even if it be necessary to drill a series of pits along it with a No. 1 bur. Spunk is now placed over the pulp canals and quick-setting amalgam is to be permanently built in at this part of the cavity. When set the spunk is withdrawn, formocresol in cotton is placed instead of the spunk, and the covering completed with cement. The amalgam is finished as far as practi- cable at the one sitting, and the case dismissed. At future sittings the rubber dam may be applied and the canal work done (Fig. 514). When cavity walls are frail, spunk may be placed in the pulp cavity, and a permanent cement lining built into the cavity. This can be perforated to the spunk, thus leaving the walls supported during the treatment. Formocresol, introduced by Buckley, consists of equal parts of 37 per cent, aqueous formaldehyd solution and cresol, which combine well. 'Bf — Formaldehyd 40 parts Essence of geranium, distilled 20 parts Alcohol SO per cent 40 parts 548 GANGRENE OF THE PULP According to Buckley, the formaldehyd not only acts as a germi- cide, but combines with the ammonia of ammonium sulphid to form urotropin and water, 6CH2O + 4NH3 = (CH2)6N4 + 6H2O, and with hydrogen sulphid to form sulphur and methyl alcohol 2CH2O + 2H2S = 82 + 2CH3OH. The cresol is supposed to act upon the fatty compounds, changing them into a compound resembling lysol. Thus, antiseptic substances are formed from poisonous ones. This does not necessarily represent all the reactions occurring, as many other compounds may result from putrefaction. The probability is that the thoroughly bactericidal action is the one of greatest value. This action has been shown by Mayrhofer to be true only for the first twenty-four hours; thereafter the bacteria in the tubules may grow back into the canal and the dressing, in spite of the fact that the odor of the dressing is present. The canal should therefore be mechanically cleaned after twenty-four hours, and a fresh application be made.^ Mayrhofer claimed inability to sterilize permanently with formocresol. Nevertheless the editor treats such cases at wide intervals ordinarily with impunity. In a few cases an abscess has supervened after the first dressing, but none as yet after the second. Leakage of the formaldehyd gas may have been the reason, but a chronic apical abscess in the third stage (which see) has been a suspicion. Cleansing and reaming the canals at the first sitting is another danger, even when formaldehyd is subsequently used. Some persons do not tolerate formaldehyd well, so for them it is well to reduce formocresol to 5 per cent, strength with cresol or phenol camphor, or even abandon it for menthol or thymol in phenol- camphor or other sedative, or iodoform may be tried. Formaldehyd is so efficacious in the writer's hands that it has displaced other methods in his practice. All other methods of dis- infection produce results less certain than those produced by it, and are more cumbersome, therefore they will be here dispensed with. While this is true for a great majority of the cases, occasionally a patient is met with whose tissues do not tolerate formaldehyd well. Formocresol then should be reduced to a 5 per cent, solution with cresol or phenol camphor, and in some cases abandoned for more sedative antiseptic remedies, such as eugenol or phenol camphor with menthol. This first dressing may be left for from twenty-four hours to a week or longer if the patient is comfortable. At the second sitting the rubber dam is to be applied and the canal opening thoroughly made under formocresol influence, just as though ' ViuUeumier: Items of Interest, March, 1910. MOIST GANGRENE OF THE PULP 549 the pulps were vital, the technique differing in no respect. (See pp. 508 to 526.) A second dressing is introduced into the canals. Whether this shall carry the full strength forniocresol or it shall be modified by the addition of cresol or phenol camphor depends upon the history of any irritation or perfect comfort as a result of the first application. The object of a second dressing is to determine whether the odor (gases) has been discharged from the tubules. When the dressing has absence of putrefactive odor, no pus can be detected, and the patient is comfortable, the canal is ready for filling. Less than this result is too soon, and delay beyond this is a loss of time. When one pulp filament is gangrenous and another vital, the treat- ment is the same, it being the writer's experience that forniocresol loosely placed is not incompatible with ulcerated pulps, and, indeed, is an excellent dressing for suppurative pulps when modified to a 3 to 5 per cent, strength; even full strength has been acceptably used. Later, the vital portion is appropriately /removed. ^Mien apical pericementitis of a subacute nature is present on a filled tooth, as when a tooth shows some looseness and tenderness, with some injection of the gum, all faulty root canal fillings should be removed with barbed broaches, cleansers, or root reamers, and the case is then resolved into one of moist gangrene and treated accordingly. If a cotton root filling be found it sometimes allows the broach to tear loose. Li such case a Kerr broach is driven into it to create a central opening, after which the fibers become engaged by the barbed broach. Eucalyptol may be used to soften gutta-percha root canal fillings, and at times the smallest Kerr or Downie broach is to be bibevelled at its end and used as a drill cutting its way. Oxychlorid and other cement fillings may have 50 per cent, sulphuric acid or strong ammo- nia water applied to them to assist in breaking up the bond of the cement by chemically destroying either the zinc oxid or the acid. The drill will tamp the fluid into the cement and cut the cement at the same time. All root fillings of cement nature are apt to be faulty when used as such, because the air in the canal prevents ingress, though it may appear to be well filled. This fact is of importance in diagnosis in filled teeth, giving evidence of chronic pericementitis, i. e., there is probably an unfilled portion of root canal containing putrefied pulp or serum. It is a weakness of many good operators, if not all, to think that their individual canal fillings are perfectly made. The writer was 550 GANGRENE OF THE PULP once associated with a most conscientious man, and possesses a gutta- percha canal filling of his in a molar now successful for twenty years. On one occasion he declared that he had filled perfectly a canal of an upper second bicuspid because the material had been felt by the patient as it reached the apex. Two weeks later the tooth was extracted, though comfortable, for orthodontic purposes. Its well- opened canal was empty for a quarter of an inch at the apex. To remove pins from roots a bibevelled Kerr broach may be driven into the cement or dentin about it and the drifts united. The pin may often be forced to one side and then jigged loose.. If there be sufficient pin extending above the face of the root a "pin puller" may be used. If the pin cannot be loosened it must be drilled out bodily. A sharp round bur should be used to countersink the end of the pin, and then by the aid of oil it is cut into shavings. Frequent desiccation and examination to observe the presence or a metal remnant is necessary to avoid the accident of perforation. In drying with the compressed-air syringe, care should be employed to avoid extensive emphysema of the cheek, which may be induced by intense pressure. If it occur, the emphysema should be reduced by manipulation, with a view to gently forcing the air back through the root. Christensen^ and L. Greenbaum have each reported a case, and I have recently had my first case when desiccating an accidental lateral perforation. This occurred even without close application of the syringe nozzle, 35 pounds' pressure being used. The immediate treatment of canals containing gangrenous pulps may at times be necessary. The mechanical work should be done while the canal is flooded with, formocresol, and embalming paste containing paraform should be used with gutta-percha canal points or sometimes on cotton twists. If any inaccessible portion of root canal remain it may be treated according to Rhein's method of placing a zinc probe in the canal, which should be filled with a solution of mercuric chlorid in hydrogen dioxid (1 to 500). The positive pole of the cataphoric current should be applied to the probe, with the moist negative spoiige electrode at the cheek. From three to seven minutes with a force of from 1 to 5 mi. of current are required to form oxychlorid of zinc which occupies the inaccessible portion of the canal.^ (See p. 515.) Root sterilization may be immediately attempted after the rubber dam has been placed and the crown washed with 5 per cent, formalin or alcohol and water. A little dry sodium dioxid is placed upon a slab with a drop of 1 Dental Cosmos, 1904, p. 151. 2 ibid.. 1905, p. 1196. MOIST GANGRENE OF THE PULP 551 water near it. A broach is drawn through tlie water, then through the powder, and the adherent powder carried to the canal and gently passed into the moist putrid contents of the canal; a reaction occurs between the water and sodium dioxid as follows: Na202 + 2H2O = H2O2 + 2NaOH, producing hydrogen dioxid and sodium hydrate. The sodium hydrate or lye saponifies all fatty matters and destroys organic matter, even living matter, and the hydrogen dioxid liber- ates nascent oxygen, which is a disinfectant. No oil or phenol should be used with dry sodium dioxid, as an explosion may occur. The use of the alloy kalium natrium in a moist canal causes an oxidation of the metals by the O of the water, flame being the result of ignition of the hydrogen. Sodium and potassium hydrate are formed. The result of the reaction should be washed out with a gentle stream of warm water, while a broach is gently passed to and fro through the mass. The action is then repeated as far as it can be carried. The danger in the use of these material lies in the possibility of the production of a chemical inflammation of the apical tissue, due to the nascent hydrates, if the foramen be open, which inflammation may be severe, or in the possibility of a non-sterilization of the contents of inaccessible canals. For this reason it may be well in fine roots to follow with the Rhein method, or to use a fornralin solution for the purpose of completing the sterilization in the more open roots, and 20 per cent formalin or 25 per cent, ethereal pyro- zone (H2O2) for the finer roots. Following this the root filling is either attempted immediately with removable antiseptic root fillings or a dressing of 5 per cent, formalin introduced into the dried canal for a few days. Any irritation of chemical nature may be treated in anticipation by the use of counterirritants applied to the gum. While this may be done in some cases the occasional production of an abscess leads the editor to strongly advise the first treatment suggested. The writer on a Monday lanced an acute abscess on a cuspid treated with this alloy by a clinician at a clinic on Saturday. Opening the canals under antiseps is with formocresol kept in them while broaching, etc., is an even better immediate method, but still not so good as twenty-four hours' sterilization, then free opening. The filling of canals by driving wood points saturated in carbolic acid into the infected canals, forcing carbolic acid by pressure into the apical tissue, and the filling with gutta-percha are all successful in many cases; but there is much likelihood of a.pical abscess, or, at least, of traumatic or chemical irritation, which it requires much 552 GANGRENE OF THE PULP courage not to undo, with a patient complaining, and some doubt as to whether an abscess will result, so that more gradual yet thorough work is advisable, at least for the young practitioner who must retain the confidence of the patient. Hoffendahl,^ of Berlin, has extended the demonstration of Zierler and shown that the constant galvanic electric current from a battery of from 30 to 40 Leclanche cells to overcome the resistance of the tissues will electrolytically decompose 0.75 per cent, sodium chlorid solution and drive nascent chlorin, H2O2, and oxygen through even fine root canals and into the infected tissue about an abscess cavity. Thus, electrolysis and cataplioresis are brought into play. The current does not pass through the side of the root ; a street or central direct current with a rheostat attachment reducing the current to from to 80 volts is equally effective. The tooth should be rubber dammed to insulate the gum. The canal should be carefully cleansed, so as not to permit ptomains to pass into the apical tissues, and then filled with a sodium chlorid solution. A fine platinum electrode is introduced into the moist canal, and must be attached to the positive pole of the battery. A large moist negative electrode is to be applied to the hand to lessen resistance and conduct the current to the negative pole of the battery. The size prevents uncomfortable sensations about the tooth. The rheostat should be manipulated so as to introduce the current gradu- ally until about 1.5 mi. is recorded on the meter, and should be continued for five minutes. An antiseptic dressing is then inserted, and a few days later the current is repeated to destroy any bacteria developed in the interim, when the root may be filled. Hoffendahl employs a paste of paraform, thymol, oil of cloves, and zinc oxid packed by means of asbestos fibers. In experiments in conjunction with W. D. Miller they found 0.6 mi. passed for ten minutes through a putrid pulp to which pure cultures of germs were added, sterilized the pulp so that agar cultures failed; canals of multirooted teeth are best treated separately. The principle involved in immediate sterilization is the destruction of all septic matter within the canal and beyond the apex at the first sitting. After the canal disinfection is accomplished by one or more of the various immediate means suggested, its walls should be desiccated and made absorbent by means of hot air, then moistened with euca- lyptol or forma-percha, and a root filling of temporary stopping or gutta-percha packed in. If aristol be added to these the effect is 1 Dental Cosmos, 1905. MOTST GANG RENE OF THE PULP 553 increased. Cotton and tor ma-perch a make a readily removable filling suitable to cases in which some doubt exists. I have had excellent results in molars with this material. (See p. 52().) A tem- porary filling of l)ase-plate gutta-i)ercha is then placed in the crown cavity as a test filling, or, in case of need, the filling may be inserted. Any apical irritation may be attri])nted to the disinfectant and be treated by counterirritation, or the counterirritant may be applied as a precaution at the time of operation. Refrigeration of the gum over the root liy means of ethyl chlorid is a valuable means of reducing inflammation in these cases. This traumatic irritation is often mistaken for acute septic pericementitis. Any irritation not too severe is to be considered as due to non-septic causes and treated accordingly. A few of these cases may, of course, result in failure owing to imperfection in the application of the method. The great majority of cases are successful. Still, if one desire still fewer failures, employ the first method. The withdrawal of the cotton dressing in the tentative method should be done under aseptic precautions. There may be found no collection upon cotton. In such case a fresh twist on a Swiss broach should be passed to the apex to determine its condition. If nothing be found the root may be dried and filled unless odor be present, when the root should be resterilized before filling or the dressing renewed. Active hemorrhage may ensue or serum may ooze from the apical tissue. This may be checked with 25 per cent, pyrozone, adrenalin chlorid, 1 to 1000, or, preferably, alum and thymol, and the root filled. If the apical foramen be a large one, and if a pus flow follow the removal of the temporary dressing and be but slight, the pyrozone or zinc chlorid (or both) should be used and the root filled. The con- dition is one of apical abscess without fistula, and is often amenable to immediate root filling. If, however, this be not considered advis- able, the temporary dressings may be renewed, though often without benefit. Sometimes a thick, glairy fluid will ooze from the apical tissue. This is coagulable lymph, and the parts require treatment in the same manner as when a slight amount of pus is present. The principle involved in the departure to an immediate method of treatment is based upon the thorough sterilization of the apical tissue, the sealing of the canal to prevent infection from the mouth, and the prevention of effusions from the apical tissue into the canal. This done, the apical tissue is expected to care for itself. In order to prevent apical irritation in so far as possible, the gum is to be painted with ordinary tincture of iodin or spotted with the 554 GANGRENE OF THE PULP dental tincture of iodin, both lingually and bucally, as a counter- irritant. I^ — Iodin Siij Alcohol BJ Shake frequently for a week or two. (Flagg.) If infection of the apical tissue by any chance ensue, either as the result of the operation of canal cleansing or previous to operative interference, the disease known as septic apical pericementitis is established. Pericementitis following the opening of teeth containing gangrenous pulps has been explained upon the ground that the bacteria in the absence of free admission of oxygen have lost their virulence, which is restored when the air is admitted. It is quite likely that either this is true or that extraneous bacteria are introduced during the course of treatment. In case of partial moist gangrene in which a portion of a filament is gangrenous and the balance of it vital, or in which one root filament is dead and the other vital, the treatment must be varied to suit the requirements. The dead portion is removed as described and the living portions treated as. ulcerated pulps. (See p. 470.) In a few cases the continuity of the canal has been lost because it has become involved in caries upon one side of the root. To remedy this, if the root be still salvable, the cavity should be excavated and then a tapering probe run through the tap in the crown and into the apical portion of the root canal. Around this a non-shrinking amalgam filling may be built. The probe is then withdrawn, leaving a canal in the amalgam through which when hard the canal may later be treated and filled (Fig. 369). As a means of preventing the effects of sepsis under cement through the absorption of septic matter, powdered thymol in about 5 per cent, should be added while mixing the cement. Discoloration of the Teeth by Moist Gangrene. — In the final decomposition of the pulp a pigment molecule is formed, which, entering the tubules or formed in it, stains the dentin and imparts an abnormal color to a portion or nearly all of the crown, which ranges from an almost imperceptible loss of translucency to a yellow brown, slaty gray, or bluish-black color. Also in conditions of venous hyperemia or pulpitis, with which venous hyperemia (stasis) is associated, the escape of the red corpuscles into the tissue, their disintegration, and the solution of the hemoglobin then occurs, and the solution enters the tubules, staining the dentin a pink color, which soon passes into a purplish rose, and finally becomes bluish black or slaty gray. MOIST GANGRENE OF THE PULP 555 Those cases resulting in the yellowish or brownish coloration are usually associated with the loss of the pulp in comparatively sound or totally sound teeth, the loss occurring probably through trauma- tism or through slow atrophic changes, such as occur in the forma- tion of pulp nodules, secondary dentin, ai)ical constriction, etc. Apical abscess is often much delayed, but sometimes occurs, showing that pulp decomposition or a later infection has occurred. The demonstration by Ilopewell-Smith of fibrosis of the pulp and the obliteration of vascular structures may account for a lessened vas- cularity, and the absence of the production of iron sulphid because of the absence of necessary putrefaction and the production of the hematoidin products, as shown below\ The first class of cases occurs either in sound teeth in which the pulps have died by traumatism!, or in filled teeth with pulps not exposed, or in teeth the pulps of which are exposed to the fluids of the mouth, permitting putrefactive agencies and extraneous coloring or color-setting materials to enter. The discoloration is most rapid in the exposed cases. These color changes are rationally explained by Kirk^ as due to the decomposition products of hemoglobin existing in the pulp at the time of its death, and having an analogue in the pigmentary degeneration occurring in the hemoglobin in a bruise (extravasation of blood), in which the part becomes, first, "black and blue," then passes through a series of color changes, in which yellow, green,^and bluish black are notable. These are due to new chemical compounds which crystallize in the tissue. These compounds are divided into two classes: Hemosiderins, or those containing iron, and hematoidins, those without it. Each class of these has several distinct substances in it, each having its own color molecule. Kirk states that methemoglobin is brownish red, hemin bluish black, hematin dark brown or bluish black, and hematoidin orange. Jakob (Stengel) gives light pea green and brownish red as the colors of hematoidin for an old hemorrhagic focus, showing a probable slight chemical variation in the composition of the color molecule. As the color changes in a bruise are effected under aseptic con- ditions, and usually the colors finally produced are lighter than the "black and blue" first resulting, it is rational to suppose that the yellowish or brownish discoloration of teeth results under such conditions of aseptic decomposition (probably autolysis). These colors, as remarked by Kirk, are more or less permanent. When a permanent or progressively darkening slaty gray or 1 American Text-book of Operative Dentistry. 556 GANGRENE OF THE PULP bluish-black color is produced, it is considered by Kirk to be due to the formation of iron sulphid or an analogous product in which iron and sulphur are constituents, and that it is analogous to the black discoloration occurring in the visceral walls of animals undergoing putrefactive decomposition. The iron is liberated from the hemo- globin present by putrefaction, and combines with the ammonium sulphid which is formed from the ammonium and hydrogen sulphid produced by the putrefactive decomposition. Treatment.^ — The treatment of discolorations consists in what is known as the bleaching process, which means the reduction of the color molecule to another chemical molecule which is colorless, and then washing that out of the tubules. This is usually done by the use of chemicals which directly supply a molecule of nascent oxygen when coming in contact with the putrefactive material or its product, the color molecules, or which, as chlorin, abstracts hydrogen from the water present and so liberates a molecule of nascent oxygen, which combines with the color molecule. These are direct or indirect oxidizing agents, the effect being the same, i. e., an oxidation of the color molecule. A second class, as sulphurous acid, which abstracts oxygen from the color molecule, is called a reducing agent, and may be effective when the oxidizing agents fail. In the use of bleaching agents the canal should have been cleansed and disinfected with a simple aqueous solution of formalin or 25 per cent, ethereal pyrozone, or an aqueous solution of hydrogen dioxid, or with sodium dioxid, all oils or other materials likely to complicate the color molecule being avoided. V/ith the exception of formalin, these are also bleaching agents and to an extent aid the subsequent operation. Formalin would best be avoided in cases of recent pulp death, as it may harden the undecomposed fibrils in the dentin. The upper half or two-thirds of the canal should then be filled with gutta- percha or oxychlorid of zinc, leaving the crown and one-third of the root dentin to be bleached. After accurate rubber damming the most valuable and facile method consists of placing a pellet of cotton saturated with 25 per cent, ethereal pyrozone in the pulp chamber and sealing it after careful drying of the lingual tap or cavity orifice by dropping soft, quick-setting cement upon the margin and sealing the entire tap. The rubber dam should not be removed until the cement has set, as the ether or oxygen gas may cause it to bulge or blister. This is then allowed to have twenty-four or even more hours of action, when, if necessary, it may be removed. The operation may be watched at the first or the second sitting if desired, though it may be somewhat prolonged. MOIST GANGRENE OF THE PULP 557 Aqueous 25 per cent, pyrozone may be made by shaking together in a test-tube one volume of distilled water and two volumes of 25 per cent, ethereal pyrozone and evaporating the ether, the H2O2 being left in aqueous solution; the addition of sodium acetate or sulphate assists the passage of the current. This is introduced by means of the cataphoric current, the positive pole being in the tooth, the negative at the hand. Occasionally the reversal of the pole succeeds after failure, the tubular contents probably being discharged with the H2O2 present in them. Oxygen may be liberated from sodium dioxid (Xa202) by sulphuric acid. A saturated solution of sodium dioxid is made by surrounding a small beaker containing about 2 drams of distilled water with cracked ice. When cold the sodium dioxid powder is to be slowly dusted into it until it assumes a semi-opaque appearance, indicating saturation. In use the dried dentin is saturated with it, asbestos fiber being used to carry it to place, and 10 per cent, sulphuric acid is used to produce the liberation of oxygen with the following equation: NaoOo + H2SO4 = Na2S04 + IW2. The effervescence forces the tubular contents out. The sodium dioxid acts upon putrefactive material, decomposing it, and also saponifies fatty matters. If the operation fall short of success, this is due, in Kirk's opinion, to the formation of iron oxid, which can be removed with oxalic acid by sealing a crystal of it in the pulp chamber for twenty-four hours. The tubular contents being entirely removed by the sodium-dioxid method, the tooth is more translucent than by other bleaching methods in which the bleached organic debris remains in the tubules. The chlorin method, introduced by Truman, depends for its efficiency upon the affinity of chlorin for hydrogen, forming hydro- chloric acid (HCl). Finding this in the water, it liberates nascent O, which oxidizes the color molecule, or, possibly, it abstracts H from the organic matter. The chlorin is usuall.y evolved from chlorinated lime, that sold in paraffined paper cartons or glass bottles being the best. That sold in metal cans is often contaminated by the metallic chlorids. The dry powder is packed into the cavity, moistened with 50 per cent, acetic acid, and sealed in with oxyphosphate or temporary stopping for one or two da}s, and repeated if necessary. Only vul- canite, bone, ivory, or wood instruments should be used, as metal instruments are acted upon by the chlorin. All gold or metallic fillings should be removed for the same reason, and if their removal 558 GANGRENE OF THE PULP would cause hardship or so render the tooth into a condition indicating crowning, either this should be done or the direct oxidizing method tried. The liberation of sulphurous acid may be induced from a powder consisting of a mixture of sodium sulphite, 100 grains, and boric acid, 70 grains, separately desiccated and afterward ground together in a mortar, by acting upon it with a drop of water. The cavity is stopped by a plug of gutta-percha previously prepared and warmed. The following reaction occurs: 2H3BO3 + SNasSOs = 2Na3B03 + 3H2O + SSO^. In all the methods, except the use of Na202, the apex of the canals should be sealed before and after bleaching; at least 1 pint of hot distilled water should be forcibly injected into the tooth to dissolve out all products of chemical action remaining in the tubules, a towel being used to catch the drip. The tooth is then thoroughly dried, and if any organic matter may be present in the tubules the pulp cavity should be thinly hned with oxychlorid of zinc to coagulate it. If it has been removed, as in the sodium dioxid method, leaving the tubules empty, they should be filled with cavitin varnish after desiccation to promote absorption, and the thin lining then placed. A temporary filling is to be inserted over this until success is evident, when the permanent work is completed with zinc phosphate and a metal filling. The removal of metalHc stains has been referred to on page 317. Moist Gangrene of Pulps of Temporary Teeth. — The same con- siderations pertain to moist gangrene of the pulps of temporary teeth, but as the roots are resorbed to some extent or are to be resorbed, the root filling should be of such a character as to permit its resorption. Probably a combination of paraffin and aristol will best fulfil the indications. An iodoform paste is preferred by some. (See Root Canal Fillings.) If the roots be much resorbed, it is better to use a material which will permit venting of the tooth if necessary. The canals and pulp chamber may be filled with a combination of vaselin and aristol, and this covered by a filling. If trouble arise, a spear drill is driven into the pulp cavity from a point beneath the gum margin, establishing a vent. The patient should be instructed to keep this open, and be furnished a Swiss broach for the purpose. At an age when the permanent tooth will shortly thereafter erupt, extraction of the temporary tooth is often to be preferred to treat- ment. MOIST GANGRENE OF THE PULP 559 Root-canal Work in Cases of Gangrenous Pulps Involving Future Consideration. — In some cases of doubtful root sterilization or filling, and in wliich crowning by means of dowelled crowns is a necessity, ])rovision may be made for future relief or treatment by the employment of one of two excellent methods of procedure: 1, Kirk has suggested that the post and band of a Richmond crown be painted while warm with a solution of gutta-percha in chloroform. The solvent evaporates, leaving a coating of gutta-percha. The crown is then set with cement. By warming the crown with a hot crown-setting tool (How) or forceps, it may be removed without destruction of the piece. Bridges so set are very firm. The crown may be set with gutta-percha alone. 2. Girdwood (Edinburgh) has suggested root intubation, the tube being closed at the end with temporary stopping and then set with cement. Immediately thereafter the temporary stopping and soft cement are removed with Donaldson cleansers, leaving the root lumen free to the apical foramen or root filling. The tube and canal are then treated as a continuous root canal would be. The idea is also applied to a Richmond or all-porcelain crown, the tube being used in place of the pin, and allowed to extend through the backing, to be later filled as desired. SECTION V DISEASES OF THE PERICEMENTUM CHAPTER XIX SEPTIC APICAL PERICEMENTITIS (ACUTE) Classification. — The dental periosteum and ligament, or the peri- cementum, is the seat of numerous nutritive and functional disturb- ances, which may be grouped, according to their causes, into septic and non-septic. The term pericementitis has been indiscriminately applied to all affections of the pericementum, and in some cases erroneously, for in not all affections of this structure do the phenomena of inflammation appear; in some hyperemia alone may exist. However, most of the acute and chronic degenerations are accompanied by evidences of inflammation. Bcdecker's division of the affections of the, pericementum into purulent and non-purulent is misleading. Cases may be due to septic causes without pus formation; pus formation represents but one form of sepsis. The most convenient clinical classification of these disorders is that offered by G. V. Black .-^ (1) Diseases of the pericementum beginning at the apex of the root; (2) those beginning at the gum margin; (-3) those beginning in some intermediate portion of the pericementum. These may again be divided, according to their causes, into septic and non-septic. Another clinical classification would be into localized and general disturbances — another into acute and chronic. Evidences of Pericemental Disturbance.— It was noted in the study of the diseases of the dental pulp that the diagnostic signs of pulp disturbance were exaggerated or diminished response to thermal stimuli; reflected instead of localized pains; and, except in rare cases of advanced hyperemia, no tenderness upon percussion. Disturb- ances of the pericementum are accompanied by entirely different ' American System of Dentistr\ , vol. i. 36 562 SEPTIC APICAL PERICEMENTITIS symptoms which serve to distinguish between them and diseases of the piiip. They are, in general, tenderness upon percussion. As shown by Black,^ the pericementum is the touch organ of the tooth, its tactile organ, through which a tooth locates force applied to the tooth. The pains of pericemental disturbance are, therefore, in the majority of cases, exactly localized, instead of not being localized, as in the case of the pulp. A tooth tender upon percussion has its pericementum as the seat of disturbance. Most cases of peri- cemental diseases are accompanied by vascular reactions ranging from an increased blood flow or grades of hyperemia to pronounced inflammation, and have the corresponding symptoms. The increased volume of the pericementum causes the protrusion and loosening of the tooth, heightened sensitivity being the accompaniment. As the vascular supply of the pericementum and that of the gum are in a degree collateral (see p. 181), evidences of vascular engorgement are seen in the gum overlying the affected tooth. Owing to the altered density of the parts surrounding the tooth root, percussion upon the tooth elicits a different sound from that observed in health — the sound is dull. The general symptoms of pericemental affections are, therefore, tenderness upon percussion and a dull percussion note, more or less protrusion, and looseness of the tooth and a deepening of the local gum color. DISEASE OF THE PERICEMENTUM BEGINNING AT THE APEX Diseases of the pericementum beginning at the apex of the root are of two classes, septic and non-septic. The septic cases are almost invariably the sequel to diseases of the pulp, namely, suppuration and gangrene, or arise in consequence of infection through the canals of pulpless teeth. The non-septic cases are due to mechanical and chemical irritants, and in rare cases to undiscovered causes. Acute Septic Apical Pericementitis ; Acute Alveolodental Abscess ; Dento-alveolar Abscess. — Definition.— By septic apical pericementitis is meant an inflammation of the apical pericementum due to the entrance of septic organisms into the tissue lying in the apical space. Causes. — The most common causes of septic apical pericementitis are: 1. Septic organisms engaged in the putrefaction of a gangrenous pulp. The gases and toxic products evolved by the process also cause much irritation. ' American System of Dentistry, vol. i. DISEASE OF PERICEMENTUM BEGINNING AT APEX 503 2. Pyogenic organisms engaged in the production of suppuration of the pulp in its later stages. 3. Septic organisms introduced into the otherwise aseptic tissues of the apical space by means of instrumentation or other lack of aseptic precautions. 4. Infection of an apical space by an abscess arising in some con- tiguous part and extending in the direction of the apical space under consideration. 5. Septic infection from a pyorrhea pocket located upon the side of the tooth in question, the deepest portion of which approximates the apical space. 6. Possible infection by way of the pericemental tract from the gum margin or by way of the circulation, which infection may cause a pericemental abscess located in the apical tissue. The last two conditions would be septic apical pericementitis, but are to be considered separately as pericemental abscess. (See Pyorrhea Alveolaris.) As a cause of apical abscess it is rare, but has been seen. Apart from these causes infective inflammation of apical tissue does not seem to occur. It is to be remembered that a small portion of gangrenous pulp beneath a root-canal filling is equivalent to an entire gangrenous pulp as a cause of pericementitis. The vast majority of cases occur as a sequel to moist gangrene of the pulp, either before or after instrumentation, or as a result of infection of the apical tissue by instruments either unsterilized or reinfected by contact with the oral fluids. The organisms found in acute apical abscesses are those usually found in gangrenous and suppurating pulps, and in a certain per- centage of even healthy mouths. (See p. 46.) Schreier found the Diplococcus pneumoniae in 15 out of 20 cases examined. He also found Staphylococcus pyogenes albus and aureus, and occasionally Streptococcus pyogenes. Arkovy found the Bacillus gangrenae pulpse in a number of cases. (See p. 513.) These are virtually the same organisms that are found in the deeper portions of a suppurating or gangrenous pulp; this fact in itself is enough to show the continuity of infection from the pulp canal. It is a well-known clinical fact that acute outbreaks of septic apical pericementitis are most liable to occur under those conditions when patients "take cold." Schreier points out that these atmospheric states produce a bodily condition which favors the development of the Diplococcus pneumoniae (Pneumococcus), and finds in the association of these factors the reason why this diplococcus should be pathogenic in the dental condition. 564 SEPTIC APICAL PERICEMENTITIS Pathology, Morbid Anatomy, and Symptoms. — The Inflammatory Stage. — As in abscess elsewhere there is first infection by pyogenic organisms which produce the phenomena of infective inflammation within the substance of the apical tissue, and in the later stages in the contiguous tissues. Following the infection, arterial hyperemia is produced, sensation is exalted, and the tooth becomes tender upon percussion; but if forcibly pressed upon — i. e., if the arteries be compressed — the hyper- emia is momentarily lessened and the pressure brings a sense of relief. At this stage the gum over the apex looks normal, but^may respond to pressure. Fig. 515 Showing the morbid anatomy of septic apical pericementitis (acute): A, pus; B, area of dying leukocytes; C, septic matter in root canal; D, inflammation of process (osteomyelitis; area of lesser inflammation); E, swollen periosteum and gum, hyperemic; F, alveolar bone in a state of hyper- emia; G, pericementum at edge of necrosis. Following the arterial hyperemia, the venous obstruction which ends in stasis is inaugurated and diapedesis of leukocytes and fibrin- ous exudation into the intervascular tissue occurs. The fixed cells undergo proliferation. As this condition of inflammation becomes established the pain due to pressure upon the sensory nerves becomes of a violent throbbing character, accompanied by a sense of fulness. The swelling of the tissue about the apex of the root, due to the excess of fluid, blood, leukocytes, and tissue cells, of necessity pushes the tooth from its DISEASE OF" PERICEMENfUM BEGINNING AT APEX oGo socket, so that it feels and is longer than the other teeth. Moreover, as it is bitten upon the apical tissue is further irritated. The tooth is Fig. 516 A B A, method of accurately determining length of root; B, a cyst extending from left lower second bicuspid to the central of same side. The central has a root filling. In absence of other things this may be regarded as the origin of the cyst. Fig. 517 Acute abscess in second stage. Tooth opened at 6 for treatment, making an abscess, discharging via the canal. (Black.) Fig. 518 Fig. 519 Abscess on crowned root. (Skiagraph by Lodge.) Abscess on incomplete root. (Skiagraph by Lodge.) 566 SEPTIC APICAL PERICEMENTITIS Fig. 520 loosened and percussion induces pain and elicits the dull note which is diagnostic of the increase of bulk in the pericementum. The color of the gum over the root becomes deepened. First Stage of Pus Formation. — The central area of the apical tissue — i. e., that next the apical foramen — is broken down into pus, some of which enters the root canal (Fig. 515, A). As the area of pus formation widens, all of the apical tissue is liquefied (Fig. 517, a). From a clinical point of view the abscess is incipient when inflamma- tion of the apical tissue next to the foramen is profound, and pus formation has just begun (Fig. 515). The first stage continues while the pus is in the apical tissue. Second Stage of Pus Formation. — The bone cells become involved in the process and are destroyed (osteitis). The throbbing pain, the extrusion, looseness, and dulness to percussion, and the inflammation and edema of the con- tiguous tissues are marked. The gum is widely inflamed, reddened, and swollen, but no demarcation of an abscess may be noted upon the gum at this stage. The mem- branes of the adjoining teeth be- come irritated and hyperemic, and they may exhibit tenderness upon percussion (Fig. 517). Third Stage of Pus Forma- tion. — The pus continues to form in all directions until the bone is perforated at some point — i. e., usually through the labial alveo- lar plate — that being the thinnest and most readily perforated. The periosteum is now destroyed and the gum tissue directly involved as a boundary to the pus, which collecting beneath it, raises it into a distinctly demarked tumefaction (Fig. 520, h). The pain becomes less acute, owing to the binding resistance of the gum being less than that of the bone. At first the swelling is hard, and this represents a mass of gum tissue over- lying pus; later, it softens at its highest point, pus appears as a yellow spot beneath the mucous membrane. The mucous mem- Acute alveolar abscess of a lower incisor in the third stage, with pus cavity between the bone and the periosteum: a, pus cavity in the bone; 6, pus between the periosteum and bone; c, lip; d, tooth; e, tongue. (Black.) DISEASE OF PERICEMENTUM BEGINNING AT APEX oG7 brane bursts and a discharge of pus follows. The inflammation and tenderness then largely subside, but some degree of looseness and protrusion remains. During the latter part of the second and in the third stage of pus formation, instead of the swelling extending but little beyond the overlying gum, the tissues of the lips, cheeks, or neck may be very much swollen and with upper teeth the eye of the affected side injected. In some cases the outer skin may become reddened and dusky, exliibiting the evidences of extension of the inflammatory process far from its original site. The inflammatory process spreads out from the central focus of pus formation, there being around the pus a zone of active inflamma- tion or stasis; about this one of a lesser degree of inflammation, also full of leukocytes; about this an area of arterial hyperemia or the first stage of inflammation, and around this normal tissue. These areas are not sharplv defined, but merge into one another (Fig. 515, A,D,E,F). In this way the contiguous area of the alveolar bone and the soft tissues of the face become involved in the process, being discolored and tumefied in proportion to the extent of the pus formation and the inflammatory reaction thereto. While in the vast majority of cases the direction taken by the pus, and the point at which it finds exit, is the buccal or labial aspect, and immediately over the root apex of the aflfected tooth, or near it, these being the directions of least resistance, other anatomical con- ditions or histological peculiarities may make the direction of least resistance in some other path (Figs. 521 to 524). Instead of the circumscribed suppuration described as the ordinary course of abscess formation about the apices of roots (septic apical pericementitis) which accompanies infection by the staphylococci, clinical evidences of infection by streptococci occasionally appear. The inflammatory process, instead of being circumscribed, is diffuse; the inflammation extends along the lines of the connective tissues and of the lymphatics; the connective tissues are swollen, the swelling extending to the tissues of the cheek, down the neck, and even to the shoulder — a phlegmonous inflammation. Instead of the com- paratively free flow of pus which follows incision of the swelling in ordinary abscess, pus formation in streptococcus infection is seen, upon incision, to be limited and seropurulent. While in alveolar abscess of the ordinary types evidences of septic intoxication or poisoning are unusual, the lymphatics being blocked, as a rule, by the inflammatory exudates, septic intoxication and poisoning are the rule in the erysipelatous cases, those probably due to streptococcus 568 SEPTIC APICAL PERICEMENTITIS infection; bacterial poisons being taken up by the lymphatics find their way into the circulation. The symptoms of the absorption of bacterial products from the circumscribed abscesses are: Fever, often ushered in by a distinct chill. The pulse increases in volume and tension; it is full, hard, and frequent. The tongue is coated, the bowels constipated. The patient is also weakened and made irritable by pain and attendant loss of sleep and appetite. In the streptococcal infection there is danger that these may change into the more profound symptoms of septicemia — i. e., a soft, frequent pulse, repeated chills, diarrhea, clammy skin, general depression, and a disordered nervous system. In multirooted teeth the inflammation and abscess frequently appear on only one root. If the case be seen early, before the active exudation period of the inflammation sets in, the symptoms may be clearly localized in one root, the tooth exhibiting tenderness upon pressure over the affected root, but not upon the opposite side. After spontaneous discharge of the pus from an abscess, the condition remaining is that of an ulcerous surface (the abscess boundaries) which is being continuously infected from the putrescent pulp remnants. The conditions, it is seen, are not like those of ordinary abscess, where the infective material is largely discharged in the pus evacuation, and the cells bounding the abscess wall dispose of remaining bacteria, so that regeneration of tissue occurs. Spon- taneous healing of an apical abscess is the exception; the embryonic tissue lining the abscess walls, being continuously infected, degener- ates and dies as fast as it forms, leaving a condition known as chronic apical abscess, or chronic purulent, apical, septic pericementitis. Clinical History. — The clinical history of acute alveolar abscess may be divided into three stages: (1) That of initial inflammation and pus formation; (2) the destruction of the alveolar process; (3) the passage of pus through the periosteum and mucous membrane. The second stage is usually the longest. The duration of the disease depends upon the readiness with which the tissues between the point of beginning pus formation and its exit yield. When the pulp chamber is open pus may find exit by this path, constituting the condition known as blind abscess — a misnomer, because a blind abscess is one without a point of discharge, without a fistula leading to it; in the cases discharging via the canal, the latter may be considered a fistula (Fig. 517). Acute abscesses usually run a short course, the inflammatory symptoms being severe and the tissue destruction limited. Notably upon lower molars, and upon the palatal roots of upper molars, DISEASE OF PERICEMENTUM BEGINNING AT APEX .509 the density and thickness of bone overlying the roots may make paths of greatly increased resistance, so that the destruction of tissue proceeds along the line of the pericementum, the pus finding exit at the neck of the tooth. It is rare in cases of lower second molars, and still more rare upon the third molars, that pus finds exit over the apex of the root, the dense bone of the external oblique line offering the greatest resistance (Fig. 521). Over any teeth the outer fibrous layers of the external periosteum may present unusual resistance to the perforative advance of pus, so that when the fibers of attachment of the periosteum have been softened by the inflammation, and pus gains entrance between bone and peri- osteum, it may travel or burrow along the course of this membrane (Fig. 522), depriving the bone of its main nutritive source, so that Fig. 522 Abscess upon lower third molar, showing the usual paths of pus exit, A and B. Abscess upon palatal root of an upper molar dis- charging at the neck of the tooth. limited necrosis threatens. The roots of the central incisors may lie unusually close to the floor of the nose, and be overlaid externally by an unusually resistant layer of bone; in these cases the path of least resistance may be in the direction of the floor of the nose, the abscess opening at that point (Fig. 523) , or the pus may perforate the lingual alveolar plate, and, raising the periosteum and mucous membrane, form a large swelling upon one side of the hard palate. The root apices of the posterior upper teeth, particularly of the first and second molars, may, after the age of twenty-five or thirty, be encroached upon by the enlarging maxillary sinus, so that any or all of the roots of these teeth may be separated from the floor of the sinus by but a very thin lamina of bone or only by periosteum and mucosa; should abscess arise upon any of these roots, pus discharge into the antrum would necessarily follow. In these cases the acute 570 SEPTIC APICAL PERICEMENTITIS symptoms may rapidly subside, but later symptoms of antral empyema may follow (Fig. 524). Resort to the use of poultices upon the face, for the relief of the pain of abscess formation, may induce such a softening of the tissues over which they are applied that the passage of pus is invited toward the exterior; the abscess may thus open upon the face or neck, producing permanent, disfiguring scars (Fig. 554). Fig. 524 Alveolar abscess at the root of a superior incisor, discharging into the nose: a, large abscess cavity in the bone; 6, mouth of fistula on the floor of nostril; c, lip; d, tooth. (Black.) Alveolar abscess at the root of an upper molar discharging into the antrum of High- more: a, abscess cavity in the bone; 6, mouth of fistula on the floor of the antrum; c, pus in the antralcavity. (Black.) In patients who are in a cachectic condition, who have an evil heredity, or whose tissue resistance is markedly lessened in conse- quence of tuberculosis, or more frequently of syphilis, septic peri- cementitis may run a riotous course; the bone suffers extensively by direct action; the periosteum is undermined, is stripped from the bone over large areas, and breaks down readily; so that while in the healthy person alveolar abscess formation may run a direct course and find prompt outlet, in the syphilitic patient extensive pus infiltration, with necrosis, may occur. In cachectic persons lym- phatic involvement is common; waste products of bacterial origin find their way into the lymphatics, and set up secondary irritative processes in the nearest lymphatic glands — lymphadenitis. In persons whose oral hygiene is neglected the third stage of alveolar abscess is frequently violent and the inflammatory process widespread. Diagnosis. — In incipient apical pericementitis the symptoms may consist of reflex painSj but, as a rule, are distinctly localized in the teeth affected, which are tender to the touch. The discoloration of DISEASE OF PERICEMENTUM BEGINNING AT APEX 571 the tooth crown and other evidences of moist gangrene are usually present unless the tooth has been previously partially treated, when the color may be good, but by transmitted light opacity is noted. In a few cases the tooth has had almost a normal color even under the transmitted light. In the pronounced cases the symptoms are as described. Upon a sound tooth the evidences of pulp vitality or death should be observed — i. e., the pink translucency or the opacity to light transmitted by an electric mouth mirror, or the thermal tests of great heat or cold applied Fig. 525 Fig. 526 Diagnosis of apical abscess by x-rays. (Price. 1) Skiagraph of perforation and apical abscess; wire thrust through same. (Lodge's method.) If the tooth be filled, or the dentin uncovered at any point, the interrupted electric current or the galvanic current, with the anode applied to the tooth, the cathode at the hand, produces a slight shock. In case of exposed dentin, dryness may interfere with the test. When a sinus is present a soft silver probe may often be passed toward the tooth affected. A timid patient will often unintentionally confuse pericemental tenderness with the pain of sensitive dentin. In very doubtful cases, as when molars have deep amalgam fillings, or pins have been placed in root canals, or gold crowns cover the natural crowns, either the covering must be removed or a skiagraph be taken. After high inflammation has existed for twenty-four hours, pus is generally present in the apical tissue. Of two pulpless teeth surrounded by a zone of inflammation, the most tender and loosened is the one affected, though both may be acting at once. It is to be remembered that adjoining, otherwise 1 Items of Interest, 1901. 572 SEPTIC APICAL PERICEMENTITIS Fig. 527 normal, teeth may show some evidence of pericementitis, due to extension, so that differentiation is necessary. The various stages of inflammation and pus formation are judged by the appearance of the gum or by the a:-rays (Fig. 525). The greater the swelhng and injection of the gum, the more advanced is the pus formation. The inflammatory action precedes the advance of pus, which furnishes a guide to the direction the pus is pursuing — viz., where the most intense coloration and the greatest swelling appears will be the point at which the abscess will point or discharge. A sudden subsidence of inflammation without an immediately discoverable point of pus exit should lead to the suspicion that the discharge has taken place in an unusual situation. The direction pus may take is often determined by gravity, but the resistance of certain tissues may cause the pus to seek the easiest path. Thus, by discharging into the an- trum it goes rather counter to gravity. In such cases as discharge into the an- trum there is liable to be a collection of pus in that cavity which may cause destruc- tion of the mucous membrane and bone. This condition is known as empyema of the antrum. The sudden subsidence of an acute abscess upon a tooth located beneath the antrum should create a sus- picion of discharge into that sinus. If a fine probe can be passed an unusual length into a root canal it indicates this form of sinus involvement. An abscess originating about an im- pacted tooth, or one due to subperiosteal inflammation, must be differentiated^ (Fig. 527). A pericemental abscess must also be considered. It is always more lateral and there is less facial involvement, also there is usually a pyorrhea pocket leading to it. An acute abscess of the pulp in its most pronounced stage may simulate incipient or even pronounced acute apical pericementitis. (See p. 473.) An abscess sometimes forms beneath the flap of gum overlying a third molar. This begins as an ulceration of the under side of the flap, but the pus burrows between the tooth and the gum, and when well confined may develop laterally, causing the formation and at least partial retention of a quantity of pus in the tissues of the cheek. Non-descended cuspid and lat- eral. These teeth were entirely enveloped in pus. The cuspid and lateral shadows overlie each other. Between these and the first bicuspid may be seen three tiny supernumeraries. (Lodge.) ' Black: American System of Dentistry, vol. i. DISEASE OF PERICEMESTUM BEGINNING AT APEX oTS This condition more nearly simulates the lateral abscess associated with a pyorrhea pocket, and as by extension it sometimes involves the tonsil, the case may be mistaken for an amygdalitis. The last three conditions are usually associated with suspected teeth containing vital pulps, so that tests for pulp vitality are to be applied. In certain cases of pulp gangrene part of the pulp only may be dead — e. g., the lingual filament of the pulp of an upper molar; while the balance may be vital (the buccal filaments). This fact may con- fuse the response to tests and is to be borne in mind. A broken root covered more or less by gum or carious bone must be taken into account. Prognosis. — In the majority of cases the prognosis of acute apical abscess, as to the future retention of the tooth, is favorable; and usually very favorable if the case receive intelligent therapeutic aid. The future of the tooth depends upon the thoroughness with which sources of infection may be destroyed and permanently removed, and the completeness with which regeneration of tissue can be induced. Treatment. — In the initial inflammation and first stage of pus for- mation the treatment should be abortive, to afford relief from the pain. The cause of the inflammation should be removed, if possible, and the pus formed be removed or, at least, permitted to escape by way of the pulp canals. The promptness of relief from pain depends upon the thoroughness with which this is accomplished. The pulp chamber should be opened to an extent w^hich permits the free passage of broaches into the canal (Figs. 517 and 522). If the cavity of decay be open, the pulpal wall is to be perforated. If a filling be present, it is in part or entirely removed. If the enamel be entirely sound, or if subsequent treatment require a new opening in line with the pulp canals, it is at least in part made. These openings are usually begun with a small, spear-pointed drill (Xo. 100 S. S. W. Catalog) revolving in a perfectly true hand piece. To centre the drill, first spot the enamel with a dentate bur. The opening made is enlarged with successive sizes of sharp, round, dentate burs until of sufficient size. According to the amount of tenderness, the tooth will require a counterpressure to that of the drill. If the entrance be made through the occlusal face of the tooth, or in a direction which would cause direct pressure on the apical pericementum, a ligature of linen thread with long ends may be placed around the tooth, and traction be made by drawing on the loose ends of the ligature.^ EfTective • J. Foster Flagg: Lectures on Dental Therapeutics. 574 SEPTIC APICAL PERICEMENTITIS counterpressure against lateral entrance to the pulp chamber may be made by softening a small roll of modelling compound and mould- ing over the face of the affected tooth and several of those adjoining it, and hardening with cold water. This temporary splint is held in place by the index finger of the left hand. In case the inflammatory process is marked, or if the patient be in bed, it may be necessary to make a vent opening by the easiest path, especially when using a hand drill — i. e., at the junction of enamel and cementum — directly into the chamber. As soon as entrance to the pulp chamber is effected, the cavity is syringed with a strong antiseptic. Fine probes are passed and repassed into the opening to free the outlet, so that gases and pus may escape and fresh portions of the antiseptic be worked into the cavity. The escape of blood from the canal is a sign that all the pus is vented. The quickness with which relief is secured will depend upon the thoroughness with which the canals are entered and their putrid contents given vent. A tedious class of cases are those in which a canal of a molar is filled or partially filled. Unless entrance to and cleansing of the canal be accomplished, the inflammation will proceed until the pus finds external vent. An hour spent in gaining access to and cleansing such canals is well spent. The canals may be dried and an anodyne antiseptic, such as phenol camphor plus menthol, pumped into them. If, now, pro- vision against mastication upon the elongated tooth be made by means of a guard, relief is tolerably certain. Watkins^ has used "blue Hght" apphed from a 16-candle power blue-globed electric lamp through a funnel directly upon the part. He claims relief from the pain, enabling him to open the tooth previously too painful to be operated upon. He also claims that swelling is much reduced by it, in some cases in twenty minutes. Patients do not ordinarily tolerate the rubber dam in these cases, and as the tooth should be left open it need not be used. A guard may be made from a strip of rubber dam two inches long and of a width corresponding to the distance from the buccal to the lingual gum margins and folded into a pad of the width of the occlusal face of the tooth to be covered. Floss silk is then sewed through this in such a manner as to cause it to tie the pad over the tooth, the silk itself encircling the neck of the tooth.^ This should be attached to a nearby tooth, and will insure rest of the affected pericementum by preventing occlusion upon the crown (Fig. 528). Cold antiphlogistics, such as lead water and laudanum or cata- I Dental Cosmos, 1905. ' Flagg. DISEASE OF PERICEMENTUM BEGINNING AT APEX 575 plasma kaolini, should be applied externally. No hot external applications should be used in abscess cases, as they may cause an external fistula to be formed. The mouth is to be frequently washed with an antiseptic. In simple cases with prompt relief this is all that is necessary; in marked cases the reduction of the inflammatory engorgement should be attempted in addition. Swedish leeches may be applied to the gum, or a cut or two made in the gum over the apex of the tooth will allow free bloodletting and drainage of the excess of blood in the pericementum. A hot pedi- luvium and a saline cathartic conjoined are useful as counterirritant derivatives, and the latter is also depletive, reducing the volume of the blood. The hot pediluvium with mustard added and diaphoresis conjoined are also useful. Ten grains of Dover's powder in divided doses in hot lemonade are given, in part, while the pediluvium is being administered, and the patient is later well covered up in bed. Fig. 528 Rubber dam guard for use in pericementitis: A, roll of dam threaded; B, guard fitted over tooth; tooth eliminated to show the manner in which the silk encircles it. Quinin in doses of gr. vj is given as a febrifuge and to limit exu- dation, and tincture of aconite, two drops at first, and one-half drop each half hour is given until the volume, tension, and frequency of the pulse are reduced. If syphilis be a complication in these cases, potassium iodid, in doses of 10 grains each three hours, is useful as an antagonist of its influence and as a nervous sedative. Unless Dover's powder is used, morphin sulphate in blondes and morphin bimeconate in brunettes (especially those with blue eyes), or any persons wath known idio- syncrasies to morphin, should be administered in | grain doses, repeated each hour up to f grain. When great suffering renders it necessary, a h\"podermic may take its place. When used, a saline cathartic should be given the following morning. These several measures are to be regarded as the abortive treat- ment of alveolar abscess; they apply to all cases if seen early enough, and will in the majority of cases prevent the disease of the peri- cementum passing the early inflammatory stages. In all cases the 576 SEPTIC APICAL PERICEMENTITIS severity of the inflammatory process is lessened in proportion to the thoroughness with which the antiseptic measures are apphed, provided that in the attempt at such apphcation no septic matter be violently thrust through the apical foramen, especially of the one of a multirooted tooth not involved. While this is true, marked relief is so often given in even severe cases by the simple opening of the pulp chamber by means of a spear drill, thus permitting the gases and pus to find vent, that in those cases in which tenderness of the tooth prevents thorough opening, or when patients are confined to bed by illness, such an opening may be made, either at the neck of the tooth or through a filling. If the patient admit a marked relief upon venting, further relief may be expected, as a rule, even though the tooth be still painful. The Second Stage of Acute Apical Abscess. — In very mild stages the pus is in the bone and the infection considered more virulent, i. e., the germs are specially active. The abortive treatment should first be tried, and if free venting of pus is obtained relief is usually given. If not given the case continues to the third stage. If bearable, or the surgical method be impracticable, a dental capsicum plaster may be applied to tt^e gum or a roasted half-raisin may be applied. Either causes an inflammation of the gum, which advances the tissue that much nearer suppuration. Thus it prepares a readily invaded tissue and hastens pointing. The contrary effect has sometimes been produced, and is explained upon the ground that the increased amount of blood has increased the phagocytosis and destruction of bacteria or his stimulated a restoration of the circulation, possibly both. Morphin is a useful adjunct when the pain is severe. For the purpose of hastening suppuration, calx sulphurata, | grain each hour, is useful. It also sometimes hastens resolution. It is proper to denominate this the expectant treatment, and while, perhaps, unsurgical, at times permits no alternative except extraction. When tolerable or imperative, the surgical method of venting the abscess through an opening in the gum is valuable. The apical region is located as nearly as possible by measuring the length of the tooth with a probe passed into the canal and over which a small piece of rubber dam is slipped as a guide. This is laid over the crown and gum and a tiny drop of carbolic acid is placed just above the point of the probe as a guide. A vertical cut is made in the gum down to the bone, and a broad spear drill is driven through it into the abscess tract. Whether this shall be done under ethyl chlorid refrigeration, cocainization, or short general anesthesia, the operator must determine. A gradual perforation is useful in some cases. This method, DISEASE OF PERICEMENTUM BEGINNING AT APEX 5/7 designed by Black, consists in gradually escharing and scratching the gum tissue. Successive applications of just such carbolic acid as adheres to the point only of a sharply serrated plugger are made, followed by slight scratching only so that blood shall not be drawn. In this way the bone is ultimately reached. A fresh drop of acid is applied, the periosteum scraped away slightly, and the drill then used. A Rollins tubular knife (Fig. 529) has been used with success to remove a piece of gum, after which the drill or a fine trephine (Fig. 530) is used. Some acute pain may follow this operation, but usually lasts only a short time. Fig. 529 P'ig. 530 A y Tubular knives. o O Walker- Younger trephines. If antiseptics are used to syringe out the abscess cavity, it is better to use a mixture of six parts hamamelis (aqueous) and one part Listerine as a partial sedative. The use of hydrogen dioxid is often very painful, owing to the rapid reaction with the blood present, and as it sometimes also drives the infective material into remote parts without disinfecting it, its use in this connection is not without danger, and should be avoided. It has been a subject of controversy whether a tooth should be extracted while the abscess is in the second stage. It has been claimed that the continuation of pus formation after extraction renders the state of the patient worse than before extracted. This occurrence is comparatively infrequently seen, and is, of course, due either to the retention of some pyogenic organisms beneath the clot which forms in the alveolus or the infection of the parts by extraneous organisms. The retention of the tooth until a fistula forms would also confine the bacteria for the time. 37 578 SEPTIC APICAL PERICEMENTITIS Unquestionably metastatic infections have appeared as the result of persistent local infection following tooth extraction, the avenue being the lymphatics; therefore, in cases of extraction during the second stage of pus formation the alveolus should be forcibly syringed for ten minutes with hydrogen dioxid, in every four ounces of which 1 grain of mercuric chlorid has been dissolved. If it be thought desirable to repeat the syringing, a tent of antiseptic gauze may be gently carried to the apex of the alveolus and left. This tent may be removed to permit syringing, and should never he left long at any one time, as septic inflammation of the alveolar walls may occur. It also does not drain pus readily, so it might cause an abscess if left too long. In cases of this kind oral sterilization and anti-infective systemic medication are of importance. As soon as improvement is noted the tent should be removed, the alveolus sterilized as before, and a new clot induced by a curetting of the walls. The case should now pro- ceed as any ordinary extraction; if not, it should be treated as for dry socket (which see). In a reply to a circular letter of questions regarding this point. Black, Kirk, Ottolengui, Hoffheinz, and Schamburg all favored extraction as a means of removal of the cause and as a less evil than allowing the tooth to remain enclosing the bacteria, which, if cap- able of producing septicemia, it would do if allowed to remain. They are therefore in agreement with the editor's position taken in the second edition of this work (1904). Brown argues the difficulty of decision in an individual case. All are practically opposed to the idea that pneumonia is more likely to result from post-extraction sepsis rather than septicemia, Morris^ having taken the position that pneumonia resulted from extractions in this condition. Each and all advised careful ante- and post-extraction antisepsis. The editor has had quite a number of cases of necrosis (necrotic dry socket) following extractions at the hands of specialists, and believes they and he should have been more watchful in these cases, and that in most cases a strong solution of potassium permanganate should be used before and after extraction, especially in cases requir- ing laceration of the gum. Antiseptic spraying of the alveolus, etc., is a reliable measure. In one case of extraction of a lower third molar operation under anesthesia for prevention of progressive necrosis became necessary. The making of a cautious diagnosis and awaiting the proper time, as recommended by Mitchell, is a physical impossibility unless one await the third stage or a fistula or general ' Mitchell: Dental Cosmos, 1907, p. 713. DISEASE OF PERICEMENTUM BEGINNING AT APEX 579 infection, as in this state the bacteria are considered virulent, especially while bone solution is in progress. The Third Stage of Acute Apical Abscess. — In this stage the pus has found its way through or beneath the periosteum on the outside of the bone; therefore its germs are engaged in liquefying the gum tissue or in unusual location the mucosa or muscular tissue of the part. Except in these cases the gum is tumefied, a hard, circum- scribed, inflamed nodule indicating pus near the bone, a soft, more generally diffused swelling indicating more superficially located pus, while a soft yellow or yellowish-pink tumefaction indicates pointing. In all these cases the indication is for a surgical opening of the gum rather than the opening of the tooth. The part should be gently disinfected with hydrogen dioxid on a ball of cotton, and a sharp bistoury should be boldly driven to the bone, with the cutting edge turned toward the occlusal. The lip or cheek is to be drawn well away to avoid injuring the coronoid, buccal, or facial artery. A cut about three-quarters of an inch in length is rapidly made by sweeping the edge and point downward occlusally. Too deep lancing upon the hard palate may injure the posterior palatine artery. As this is usually painful, it is better to refrigerate the gum or operate under short general anesthesia, e. g., nitrous oxid or the first impression of ether. Cocain is only useful in the case of deep-seated pus. Next, the abscess tract is to be gently washed out with a diluted hamamelis solution, preferably warmed. Fairly hot water containing an antiseptic also gives relief. If the abscess has been deep-seated it is well to introduce a fine tent of antiseptic gauze through the opening into the abscess tract to prevent the too rapid healing of the external orifice which is apt to occur, owing to the approximation of the lips of the wound pro- duced by cheek pressure. This healing permits a second collection of pus. The tent should be removed not later than the next day, the abscess tract disinfected again, possibly with a mercuric chlorid solution, and the tent replaced. At this time the tooth should be opened and disinfected if not tolerable at the first sitting. When this is tolerable the crow^n should be tapped and formocresol sealed in the pulp chamber, just before the operation of lancing, in order to permit disinfection and thus limit pus formation and to save time. Tents in alveoli should never be left long at a time, as they become septic and may cause necrotic conditions of the alveolus. The patient should always be cautioned to remove the tent if swelling return, as this indicates a stoppage of the vent, with collec- tion of pus. When dift'use cellulitis with marked febrile disturbance passing 580 SEPTIC APICAL PERICEMENTITIS into the adynamic type is produced, one should fear the infection with Streptococcus pyogenes and treat not only locally, but use blood germicides against a possible septicemia. In these cases there is little pus formed compared with the area involved. As a preventive of possible blood infection the following may be administered : I^ — Hydrargyri bichlOridi gr. j Tincturse ferri ohloridi f§j — M. Sig. — Twenty drops in water four times a day. The editor, while suffering from a very "severe abscess about the finger-nail, due to infection by the Streptococcus pyogenes and associated with lymphangitis extending as a bright red streak into the axilla, employed this remedy with markedly beneficial effect. If the adynamia and other symptoms be progressive, medical cooperation should be obtained to divide the responsibility and to afford every means possible toward the cure. The extraction of the tooth followed by sterilization and curettement of the part, and the use of streptococcus antitoxin conjoined with the sustention of the vital powers by nutritious predigested food and alcohol is logical. (See p. 142, etc.) In even ordinarily severe cases not of this variety there will be some fever due to the toxin absorbed, and the pain and loss of sleep and appetite will cause physical debility. For this there is nothing better than the following, as tonic, antiseptic, and antipyretic: B— Saloli, Quininse sulphatis (vel hydrochloratis) aa gr. Ix M. et fiant capsule no. xx. Sig. — Take one four to six times daily, before meals when near them. Or, I^ — Quininse sulphatis gr. xxx Acetanilidi gr. xxiv Cafleinse citratis gr. iij M. et fiant pil. no. xij. Sig. — One every hour. (Endelmann.) The facial swelling resolves with the cure of the abscess or its proper venting, but may be assisted by cold applications or cataplasma kaolini to the outside of the face and by gentle massage by the patient or nurse. As a means of reducing swelling, vibratory massage is useful. A simple appliance for this purpose, devised by W. H. Mitchell,^ con- sists of a cam-like piece of metal perforated at its smaller end for mounting upon a screw mandril; it is held in the dental hand piece ' Dental Brief, 1908; Academy of Stomatology. DISEASE OF PERICEMENTUM BEGINNING AT APEX 581 strapped to the hand as shown. Its centrifugal force imparts a vibratory motion to the hand which can be utilized for massage with the finger tips, or by holding in the hand an instrument containing upon its end a soft rubber cup. The part to be massaged should be lubricated with vaselin (Figs. 531 and 532). Fig. 531 Fig. 532 K .■?4 ^ ^H 1 i ^ p #■ ■ f r^ .'^ ',,. V ^M W. H. Mitchell's vibrator strapped to hand. W. H. Mitchell's vibrator and rubber cap applicator. The heat of a large electric lamp concentrated upon the face from a short distance and followed by massage is also useful in facial swellings due to cellulitis. Under no circumstances should hot poultices be applied to the outside of the face, as a discharge of pus in that direction will cause a disfiguring scar. If an abscess threaten to open externally, the abscess should be opened by an incision made from a point within the mouth, and, after sterilization of the tract, a drainage tent of antiseptic gauze should be introduced nearly to the bottom of the pus cavity. This should be removed daily, the abscess cavity steril- ized, and the tent renewed. An antiphlogistic compress should be applied to the face. The principal object sought is the mechanical apposition of the walls of the abscess cavity at the dependent or external portion, in order that these shall unite by granulation and that the fistula shall in this manner become an ordinary one. The patient should lie in a position to counteract the natural effect of gravitation. After lancing, the mouth should be kept well sterilized by frequent 582 SEPTIC APICAL PERICEMENTITIS sprays or gargles of hydrogen dioxid, which may be diluted to one- third strength with water — i. e., to a 1 per cent, solution. If, in connection with the lower third molar, marked swelling be observed in the submaxillary triangle, free incision of the tissues of the floor of the mouth should be made at the angle of Junction with the bone. The cut should be made close to the bone and toward it, but not too deep, lest the mylohyoid artery or nerve be injured. The deep lancing of an abscess upon the hard palate may cause a cut to be made in the posterior palatine artery. External to the jaws the facial and coronoid arteries are to be considered. Keeping close to the alveolar process while the cheek is pulled out renders the operation safe. It is ever to be borne in mind that so long as the cause of infection remains pus formation continues, and so long as pus forms tissue destruction is in progress; furthermore, in proportion to the amount of tissue loss perfect recovery after alveolar abscess is delayed or imperfect. While it is the clinical experience of nearly every operator that a tooth and adjacent structures may recover from inflammation which involves not only the first tooth attacked, but by an extension of the inflammatory process involves the general periosteum and neighboring teeth, provided the case receive prompt and decisive surgical treatment, yet the danger of necrosis and septicemia in prolonged cases is always imminent. When the general periosteum is involved, as shown by extensive boggy swelling in the mouth, if several free incisions carried to the bone do not afford prompt relief, the tooth which is the centre of infection should be promptly ex- tracted. If, in the continued course of the pericementitis, chills, followed by fever, a coated tongue, and much physical depression occur, a general infection is to be feared, and no time should be lost in sterilizing the mouth, extracting the tooth, and subjecting the socket to free spraying with antiseptics. In cachectic individuals acute abscesses may cause inflammation of the deeper tissues and of the periosteum as well, and extensive necrosis may occur. The after treatment of acute apical abscess which has been relieved by abortion is exactly that of moist gangrene or of chronic abscess without fistula (which see). In very mild cases the formaldehyd treatment may be instituted at once. In severe cases it is better to allow drainage for a day or two. When the relief has been afforded by lancing the treatment is as for chronic abscess with a fistula. Acute septic apical pericementitis may occur on a temporary tooth, most frequently a temporary molar. The symptoms and pathology DISEASE OF PERICEMENTUM BEGINNING AT APEX 583 are the same, except that the looser character of the alveohir struc- ture seems to frequently permit the abscess to assume the chronic form before the dentist is consulted. Children often hide these conditions from their elders out of fear of the dentist. In strumous children the inflammation may be spreading and the Ij^mphatic glands ma}^ be involved. There may also be some symptoms of septic intoxication evidenced by chills accompanied by fever, etc. These cases require an opening of the abscess, sterilization of the part, and attention to the systemic condition. If seen in the acute stage the treatment is the same as for the permanent teeth, unless the disease occur shortly before the date for eruption of the per- manent successor, when the temporary tooth should be extracted. If treated, the canals should be filled with materials which can be resorbed by the tissues, such as paraffin or wax with aristol or paraform. As soon as the pus escapes, the condition of chronic apical abscess is established. CHAPTER XX CHRONIC SEPTIC, PURULENT, APICAL PERICEMENTITIS (CHRONIC APICAL ABSCESS) By this title is meant a condition of apical pericementitis due to septic influences in which pus is continuously formed at the expense of the apical pericementum and contiguous tissues. It is the usual outcome of acute apical abscess, and is established as soon as the pus finds vent either through the gum as a natural or operative result, or through the root canal as the result of opening the canal. These two avenues of pus escape give the two clinical conditions of (1) chronic apical abscess discharging via the root canal; (2) chronic apical abscess with fistula; (3) a third condition of latent chronic apical abscess (true blind abscess) with absorption of pus by the tissue may exist. CHRONIC APICAL ABSCESS DISCHARGING VIA THE ROOT CANAL Pathology and Morbid Anatomy. — First Grade. — Upon abortion of an acute abscess in the first stage the pressure of pus upon the apical tissues is released, and, as a rule, the walls of the abscess cavity throw out granulations which fill it. This tissue tends to organize into more or less healthy tissue (cicatricial tissue). The bacteria are killed out except at that part represented by immediate contact with the root foramen; at this point the tissues are infected and some molecular loss of tissue as pus may occur. A limited loss of granulation tissue by pus formation is compensated for by the forma- tion of new granulations. The conditions are almost analogous to those existing in moist gangrene of the pulp, and require analogous treatment. Second Grade. — If the abortion of the abscess have only partly permitted the pus to drain, or the alveolar walls or crypts of the abscess wall remain infected, the pus will continue to form and escape in some degree via the canal. If the tooth now be extracted, a small abscess sac will be found upon the root end. If opened, this will be seen to be a mass of fibrous vascular tissue (inflamed peri- CHRONIC APICAL ABSCESS 585 cemental apical tissue) having a central lumen connecting with the root canal (the abscess cavity).* Third Grade. — With partial^vent to the pusjormed, the abscess cavity of the second grade may enlarge, involve the bony walls of the alveolus, and the soft tissues then prolif- erate to such an extent that they finally ^^°- ^^^ organize into a large, fibrous, vascular sac attached to the tooth. This sac has the central pus cavity before described, which is connected with the pulp canal. It may be a half-inch or more in length (Fig. 533), and may be extracted with the tooth or may be left attached to the bone. It necessarily occupies in the latter a cavity of a size cor- . Ill *•• "11 Chronic apical abseess> respondmg to its own bulk. As its inner walls third grade: b, abscess sac are infected, extraction without its removal containing a central pus . 1 • 1 11' cavity; D, apex of root; C, leaves an infected area, which must be dis- canai containing pug. infected or a secondary acute abscess may result. (See p. 577.) In one case which had given only slight uneasi- ness owing to partial vent, was treated at two o'clock and the tooth extracted at midnight, had the appearance shown in Fig. 533. Fourth Grade. — Instead of organizing, the fibro vascular tissue may be liquefied into pus. The root apex becomes denuded for a distance about the apical foramen. Pus collects about the apex of the root and rests upon the bone, owing to the influence of gravity. The bone is thus infected, inflamed, and further liquefied, while necessarily the abscess cavity enlarges. If a bistoury be thrust through the labial alveolar wall in such a case, as shown in Fig. 534, but slight resistance will need to be overcome. In the lower jaw the tendency is to burrow into the cancellated tissue of the bone away from the tooth, so that destruction of the pericementum may not be very extensive. In the upper jaw the tendency is to spread along the pericementum and into the cancellated bone, so that the cavities of chronic abscess upon the upper anterior teeth particularly may cause extensive excavation in the palatal process of the superior maxillary bone (Fig. 536). The pus may burrow in irregular and circuitous directions until it finds external vent. In long-established cases deposits of pus calculi (serumal) may form upon the root end (Fig. 537). The cement corpuscles of the apical cementum may die and the root tissue itself become infected. In other cases resorption of the root end occurs. (See Resorption.) Symptoms. — In all of these cases the formations are gradual, owing to the partial vent, and it may be that no pain beyond a slight 586 DISEASE OF PERICEMENTUM BEGINNING AT APEX gnawing or feeling of fulness or an occasional reflex pain may occur. If for any reason the vent^become occluded, the pus formation Fig. 534 Fig. 535 Chronic abscess of upper incisor, showing tend- ency of pus progressively to destroy pericementum, owing to the influence of gravity. Chronic abscess upon lower tooth, showing tendency of pus to sink into the substance of the lower maxilla, owing to the influence of gravity. becomes rapid and an acute abscess is set up, which may be painful or not, according to the amount of tension produced before discharge of the pus. Aside from this, the gum color at the apex Fig. 536 Fig. 537 Chronic apical abscess discharging through the hard palate and threatening to discharge labially. Chronic abscess, showing denudation of apex of root (a to 6), with deposits of calculi (a) upon cementum. is somewhat deepened, the tooth is slightly loosened, and slightly tender to percussion. Signs of previous moist gangrene are in evidence. CHRONIC APICAL ABSCESS 587 Diagnosis. — The passage, without production of sensation, of an undue length of fine probe into a canal is evidence of destruction of apical tissue and a guide to its probable extent. An extensively inflamed gum tissue over the apex indicates a prob- able approach of pus formation to gum tissue. The presence of pus in the canal or upon several dry cottons introduced for absorbent purposes is diagnostic. If pus be not seen, and the canal be thor- oughly sterilized and dressed with an antiseptic, the supervention of an acute abscess affords evidence of the presence of an abscess sac or cavity. The .r-rays afford a means of diagnosis (Fig. 550). Prognosis. — The prognosis is favorable to a cure in nearly all of these cases, provided thorough canal asepsis and filling can be attained and the abscess cavity can be drained and disinfected. In cases resisting this treatment, a fistula must be estabhshed. Treatment. — The first and second grades of chronic apical abscess discharging via the canal may be treated upon exactly the same principles which are involved in the treatment of moist gangrene of the pulp. The infection is considered as simply more deep seated, so that it is necessary to pass disinfectants into the abscess cavity with two objects in view: (1) To destroy the bacteria present; (2) to stimulate the tissues to granulative activity. The canal should be sterilized with sodium dioxid and the foramen very slightly enlarged if necessary with a fine Donaldson cleanser, the canal having been flooded with 10 per cent, formalin or formocresol as an antiseptic. If necessary the root canal may be otherwise enlarged. (See p. 510.) A dressing of 10 per cent, formalin or phenol-camphor to which a little menthol and a drop of formaldehyd, 40 per cent., have been added, or formocresol, should be loosely placed in the canal and the tooth sealed for twenty-four hours, or, if the tooth has been very troublesome and still tender, a soft temporary stopping may be used and the patient provided with instruments suited to the removal of the covering and the cotton. It is better that the tooth should be under the control of the patient. At the next sitting the stoppings are more tightly made. The Zieler-HoflFendahl method may be used to sterilize the root and abscess, then the dressing is sealed in for a few days and renewed as necessary, being made continuously tighter. (See p. 552.) When no pus can be found on the dressing or following it, or on an exploratory cotton twist, and there is no odor, the root may be filled ; in case of any doubt in fine roots, with a removable material such as forma-percha on cotton or the paraform alum paste (p. 527), which may remain if no ill-results follow. A temporary crown filling of gutta-percha should be used for a week or two. Each change of dressing should be preceded by sterilization of the cavity and bulb 588 DISEASE OF PERICEMENTUM BEGINNING AT APEX of the pulp chamber with a strong formahn solution to prevent reinfection of the apical tissue during the change, and it is well to use counterirritation directly after the root filling. It is always well when using an occlusal opening to close it with amalgam or cement after the first tentative dressing, while compres- sible dressings are in place, as even one heavy bite upon the covering may force the medicament into the apical tissue and renew the irri- tation. SHghtly countersinking the orifice of the tap will prevent an inward thrust of a rigid covering overlying cotton (Fig. 513). Some operators prefer to leave a small vent in the temporary covering, used to act as a drain. This, however, is apt to prevent the concentration of the action of the medicament upon the apical tissue. If formaldehyd be irritant, perforating the temporary stop- ping with a pin will sometimes relieve the pressure. If pus formation persist in any case, with large foramen the cotton may either be protruding from the root and keep up irritation or fall short of the root end and permit pus to enter the canal, and especially if no pain has been produced, good results sometimes follow a departure to the immediate method of root filling. The canal and pus cavity are resterilized, a little zinc chlorid or carbolic acid is pressed into the apical tissue, and the canal apex filled with gutta-percha or oxychlorid of zinc. The tissues are expected to care for themselves. A persistent discharge of serum or glairy lymph are indicative of inflamed aseptic but weeping tissue, and requires the same treatment. (See p. 553.) In a relatively few cases teeth cannot be closed at all without a recurrence of trouble within a short period, which trouble is usually relieved by opening the tooth. The repetition of this is annoying, and in some cases is due to the strength of medicaments such as formaldehyd, which should be modified or abandoned for sedative antiseptics such as phenol-camphor or eugenol plus menthol. In some of the cases the gases may accumulate more rapidly than dis- infection occurs. In other cases the irritability of the ti:ssues seems to produce intolerance of any remedial measures. What is known as "systematic stopping and unstopping" seems sometimes to over- come the irritability and accustom the tissues to being covered. The system consists of stopping with eugenol and menthol or modified formocresol for about eight hours, or from morning to afternoon, then venting and redressing until the following morning, then for twenty-four hours, then forty-eight, then seventy-two, etc., until the tooth stays stopped. There have been a few patients who cannot seem to have teeth "treated," nearly all cases being practical failures even when aseptic. CHRONIC APICAL ABSCESS WITH FISTULA 589 Some few may be kept in comfort for a while with permanent vents, l)ut this is objectionable. The making of an artificial fistula should be attempted. Cyst formation occurs owing to the projection of an aseptic root filling or to some not well understood cause; a cystic swelling may occur over the root of a tooth and have its origin in the pericementum. The swelling is apt to be bluish about its margin, and has a clear stretched look in the centre. It is probably due to a collection of fluid in some portion of the pericementum, or may have as its excitant a portion of calculus deposited aseptically in the peri- cementum. Indeed, apart from infection, it may be that cases of pericemental abscess, discharging merely glairy fluid, are cystic swellings. It may, however, be in relation with septic canal contents. (See p. 609.) In such a case, if swelling increase or be persistent, an artificial fistula must be estabhshed (see p. 576) and the case treated as a chronic apical abscess with fistula. In the third and fourth grades the prognosis for treatment by way of the canal is not, as a rule, good, but if desired may be attempted. If, however, an artificial fistula be established, the ease of treatment is greatly increased. The case is then treated as a chronic apical abscess with fistula. In no case should hydrogen dioxid be forced in quantity into the pus occupying such an abscess cavity until the fistula has been made, and it is better even then that the bulk of it be washed out with warm water before applying the drug. A neglect of this precaution may bring about great pain, owing to the rapid reaction of the hydrogen dioxid with the pus and blood present. In some cases hydrogen dioxid has forced pus into remote locations without destroying it. CHRONIC APICAL ABSCESS WITH FISTULA Morbid Anatomy and Pathology. — This form of chronic abscess occurs as the result of the discharge of an acute abscess through the gum or other part to the surface of the body, and whether the fistula has naturally occurred or been artificially established. (The interior of the mouth or other cavity exposed to contact with the air is considered external to the body proper.) If the acute abscess has been severe or long continued, the tissue destruction may be great, but, as a rule, granulation promptly sets in and the walls of the abscess cavity organize into cicatricial tissue. From the interior of this a canal (fistula or sinus) lined with cica- tricial tissue leads to the surface, the pus being almost constantly 590 DISEASE OF PERICEMENTUM BEGINNING AT APEX formed at the expense of the granulation tissue, which is as constantly renewed. The fistulous opening, as a rule, appears as a small teat of inflamed tissue located, in the majority of cases, upon the buccal surface of the gum, about a quarter of an inch below the apex of the root and slightly distal to it — a position probably determined by the density of the tissues surrounding the acute abscess. At times the only evidence of a fistula is a small spot of inflammation surrounding a minute opening, from which pus exudes. The fistula is sometimes located upon the lingual surface of the gum. It may perforate the Fig. 538 Fig. 539 Chronic apical abscess on mesial root. Ultimate result of a pulp capping. Editor's practice. (Skia- graph by Hagopian.) bone of the hard palate and open through the mucous membrane of the roof of the mouth (Fig. 536). Instead of finding exit by a direct path through the buccal or lingual alveolar plate and gum, the pus may burrow along the length of the pericementum and discharge at the neck of the tooth, and simulate a pyorrhea pocket (Figs. 521 and 522). One-half or more of the lateral aspect of the pericementum may remain vital, although involved in a chronic inflammation, the remainder being destroyed. Not infrequently the pus burrows along the surface of the bone and discharges at a point over an edentulous portion of the jaw. This is common to a lower bicuspid. It may burrow in the direction of the apices of other teeth, destroy their pulps and thus cause an abscess, having added causes for persistence. Chronic alveolar abscess of the root of a lower incisor, with abscess cavity passing through the body of the bone and discharging on the skin beneath the chin: o, very large abscess cavity; b, mouth of the fistula. (Black.) CHRONIC APICAL ABSCESS WITH FISTULA 591 When the apices of the roots of upper posterior teeth He in very close proximity to the floor of the antrum, perforation of this floor may occur before tissue destruction has proceeded far enough in other directions to afford escape to the pus (Fig. 524). Extensive pus accumulations may occur in the antrum in consequence, and when the tissues in the antral floor are affected, other teeth may be involved. It may discharge into the nasal cavity, in connection with acute abscess; at such points the discharge may remain per- sistent. Sometimes the discharge occurs through the canal of the affected tooth; the canal then acts as a fistula (Fig. 518). Upon a lower tooth, particularly the incisors, the pus may burrow downward through the cancellated tissue of the bone and emerge at the base of the bone and open upon the face (Figs. 539 and 541). Fig. 540 Fig. 541 Fistula passing down through the body of the lower ma.xilla. (Black.) In other cases the pus may per- forate the bone and find passage along the submuscular tissue, open- ing upon the face or neck (Fig. 541). The apices of the roots of teeth lying beneath the line of insertion of the mylohyoid muscle may cause an abscess to open in the neck cavity. Cryer records a case where an abscess opening upon the face immediately anterior to the line of the facial artery was traced to the root of a lower molar; the direction of the sinus is shown in Fig. 542. In a case having a similar anatomical associa- tion the pus penetrated the bone lingually, was encapsuled beneath Chronic alveolar abscess at the root of a lower incisor, with a fistula discharging on the face under the chin: a, abscess cavity in the bone; 6, b, b, fistula follow- ing in the periosteum down to the lower margin of the body of the bone and dis- charging on the skin. (Black.) 592 DISEASE OF PERICEMENTUM BEGINNING AT APEX the internal pterygoid muscle, and appeared as a swelling at the inner aspect of the angle of the jaw. Another case dissected along the muscles of the neck and discharged at the clavicle. Occasionally the apices of the roots of lower molars are separated from the inferior dental canal by only a thin lamina of bone, so that discharge into this canal may occur with infiltration along the vessels and nerves in the canal (Fig. 239). While discharge into the nasal chamber is most frequently associated with abscess upon the central incisors, abscesses upon molars may discharge into the same cavity. Cementum infection occurs as a sequence to death of the cement corpuscles from lack of nutrition. Pus calculi may also form on the roots in the long continued cases. The granulation tissue springing up about the parts has a resorbent action and the root ends are often resorbed, though this action is probably to an extent counter- acted by the alkalinity of the pus. The formation of the latter may, however, be in abeyance at times (Fig. 544). The extent of tissue destruction varies considerably, but is usually greatest in dependent parts, gravity influencing the burrowing of the pus. Symptoms and Diagnosis. — A fistula is seen upon the gum, visible as either a small teat of flesh (perhaps pedunculated), discharging pus, or as a tiny orifice in the gum surrounded by inflamed tissue, and from which pus may be squeezed (Fig. 523). As a rule, a soft silver probe may be passed to the apex of a nearby root, whether possessing a crown or embedded in the bone. In case of an external opening upon the face a similar procedure shows the trouble to lie with some tooth root. The a:-rays will sometimes be valuable in determining the exact location of the abscess cavity. Upon the teeth themselves but four conditions may cause a fistulous opening: (1) Moist gangrene of the pulp or its equivalent apical infection; sometimes the sinus is at the oral end of a bfoken root; (2) septic perforations, apical or lateral; (3) a pericemental abscess (see Pericemental Abscess); (4) a secondary abscess asso- ciated with a pyorrhea pocket. (See Pyorrhea Alveolaris.) Aside from these, the probe may lead to carious or necrosed bone, a cyst, an impacted tooth, or a subperiosteal abscess (maxillary periostitis) . In these cases the probe does not lead to a root. Carious bone will impart a honey-combed sensation to an excavator; necrosed bone will be exposed and firm, or the sequestrum will be in evidence as a movable body. There may also be several fistulas and extensive inflammation of the tissue. A cyst will be a tumor with certain characteristics, and an impacted tooth will usually impart the feel CHRONIC APICAL ABSCESS WITH FISTULA 593 of smooth enamel to the instrument, though the enamel may at times be rough at certain points. An embedded root will be movable, and will present the dentin and its central opening, the pulp canal, as diagnostic features. Maxillary periostitis will, as a rule, have a history of traumatism, or the previous use of a probably infected Fig. 542 Fig. .>13 Abscess with tortuous sinus, opening upon the face: A, tissue of cheek; B, floor of mouth; C, abscess tract. Fig. .544 Large abscess cavity in relation with a lateral incisor, complicated by an impacted supernumer- ar>' tooth beneath the nasal spine. (Philadelphia Dental College Museum.) hypodermic needle^ associated with it. In all cases not clearly due to other than dental causes, evidence of the four dental conditions men- tioned should be sought. Treatment. — In cases arising from sources not dental, surgical interference for the removal of the cause is necessary. This may require a minor or major operation, according to the case. In the purely dental cases the cause must also be removed. If due to pericemental abscess, this is to be treated. If due to a septic perforation not yielding to treatment by way of the root canal, the fistula may be enlarged, packed open with antiseptic cotton or gauze applied on successive days, and when the perforation is Abscess and resorption at apex. (Skia- graph by Lodge.) Boenning: Dental Cosmos, 1902. 38 594 DISEASE OF PERICEMENTUM BEGINNING AT APEX exposed it may be filled with amalgam. If properly done the fistula should heal. If this operation be impossible, the root should be amputated at a point between the perforation and the crown. If the perforation be in the middle or cervical third of the root, it may at times be treated from the root canal. A good method is to force root-filling material through the perforation and fistula and to smooth it off through the sinus. Stiff oxychlorid of zinc or oxyphosphate of copper are excellent. If incurable, the entire root must be amputated in case of a multirooted tooth. In case of a single-rooted tooth the tooth must be extracted, and if the con- ditions warrant the operation the root may be perfectly sterilized, properly filled, and then replanted after the associated abscess cavity has been surgically obliterated. (See p. 599.) In the cases due to moist gangrene of the pulp the canals must be freely entered, the apical foramen opened with Donaldson or other cleansers, and the canals and abscess tract thoroughly sterilized. The canals are flooded with a formaldehyd solution, mechanically enlarged, and if possible made continuous with the abscess cavity. It is then filled with hydrogen dioxid. With a Swiss broach upon which cotton is wound a plunging force is exerted upon the fluid in the canal. Antiseptic liquid soap may be used. This tends to drive it into the abscess cavity and out of the fistula, flushing and steril- izing the abscess tract. This is then repeated. If this simple pro- cedure be not effective, a thread of cotton saturated with hydrogen dioxid should be placed in the canal. Pressure is then exerted with vulcanizable rubber, as in pressure anesthesia. A third method consists of filling the crown cavity with gutta-percha or vulcanite rubber, forcing the nozzle of an abscess syringe through the mass, and driving down the piston of the syringe. In all these procedures except the initial sterilization, the unaffected roots of multirooted teeth are to be avoided so far as possible, as undue pressure may excite an abscess. The fistula will admit the nozzle of the syringe, which may be used to flush out the abscess tract with hydrogen dioxid. The nozzle of a hypodermic needle may be fitted to the canal by packing wax, temporary stopping, or raw vulcanite about it; a piece of flexible tubing may be previously stretched over the free end and later the other end of the tubing stripped over the compressed-air syringe. Medicaments or air may thus be blown through the fistula. The method should be cautiously used in fistulous cases only, except for reasons well known by the operator employing them, as very painful distention and even emphysema of the cheek may occur. (See Index.) CHROXIC APICAL ABSCESS WITH FISTULA 595 Fig. 54o Fig. 546 Q i!MlHI(lL"Mm]'niil!) Miiiiui syringe. J. X. Farrar's alveolar abscess syringe. Fig. 547 Bulb syringe. 596 DISEASE OF PERICEMENTUM BEGINNING AT APEX The rubber cup shown in Fig. 548 may be used as a vacuum pump to draw the pus from the fistula or to draw medicaments through the canals. All preliminary work having been done as well as possible, formo- cresol is to be pumped into the abscess tract and the canal tempor- arily stopped with the same antiseptic on cotton. With this treat- ment the discharge of pus should cease and be replaced by serum. It is good practice to resterilize the canal and fill it as soon as this result is noted, or, in emergency cases, the canal may be filled at the first sitting after prolonged germicidal work. The fistula then will probably heal uninterruptedly in the vast majority of cases. In a week or two the fistula should have healed if attached to treat- able canals; for the difficult canals subjected to germicides only more time may be required, but healing usually eventually occurs owing to the removal of the cause. If the abscess cavity does not heal, one of several causes may be assigned: (1) The crypts in the walls of the abscess cavity may require further disinfection; (2) the cotton in the canal may have absorbed pus formed after an interval of antiseptic influence and may keep up the infection; (3) the root canal may not be explorable; (4) the root end may be encrusted with calculus, or the cementum be infected, or dead bone may be present. For the first condition the canal and abscess tract may be treated with 10 per cent, zinc chlorid, or rnercuric chlorid may be added to hydrogen dioxid (1 to 500 or 1 to 1000) and the abscess cavity syringed out at intervals. For the second condition a non-absorbent dressing should be used, such as forma-percha, or the root apex may be permanently filled with gutta-percha. In the fine, unex- plorable canals 25 per cent, pyrozone may be used for twenty-four hours, as though bleaching the root, or Rhein's cataphoric method (see p. 515) may be employed. In some cases abscesses require some weeks to heal, but eventually do so, particularly^ if the abscess be syringed out with an antiseptic every third day via the fistula, and tlie abscess tract filled with balsam of Peru or paraffin and aristol. Beck's bismuth paste may be injected for skiagraphy or to stimulate the fistula. Tissues about abscesses have an inherent tendency to repair; cases of long standing frequently healing promptly, sometimes, though not often, in twenty-four hours. ^ In indolent chronic inflammation the use of a small gum dry cup with vacuum bulb attached may be used for five or ten minutes ' Darby: Proceedings of Academy of Stomatology, Philadelphia, 1899. CHRONIC APICAL ABSCESS WITH FISTULA 597 at a time several times a day, to draw fresh blood and effusions into the inflamed part. The opsonic index of the lymph drawn in is said to be raised to several times beyond that of the body lymph, thus rapidly increasing phagocytosis in the part. The rubber cup shown in Fig. 548 may be left imperforate and furnished the patient for this purpose. Fig. 548 Rubber cup to be used as a vacuum cup. Amputation of root apex: OG, opening in the gum made by packing fistula; /IC, absces.s cavity: RF. root filling. For the fourth class of cases the apical foramen should be sealed and the abscess tract syringed once a week with 25 per cent, sulphuric acid, the mouth and clothing being properly protected by using a pad of cottonoid over the fistula and needle to absorb the excess. This dissolves calculi and disinfects dead cementum. It also stimulates the soft parts to a granulative action. Phenol- sulphonic acid may be forced through the apical foramen and fistula in some cases. ^ If necessary the patient should receive appropriate systemic treatment, especially if anemic. (See p. 606.) In this way some old and somewhat obstinate cases may be induced to heal. In some cases gravity so retains pus in abscess cavities that granu- lation is interfered with. The instruction of the patient in the syringing out of the tract with a mild antiseptic several times a day is of great value in that it removes pus which if retained would destroy granulations. Hydrogen dioxid is often preferable. Many apparently desperate cases heal of their own accord after some months. Some success attends the packing of a root with a thick 1 Acid phenolsulphonic consists of 97 parts, by weight, of concentrated sulphuric acid and 93 parts, by weight, of phenol, kept at 100° C. for about twenty-four hours to produce a reaction, when sufficient distilled water is added to make the liquid assay about 80 per cent, of phenolsulphonic acid. (Buckley, Lilly.) 598 DISEASE OF PERICEMENTUM BEGINNING AT APEX paste of iodoform in any oil after opening the root as far as possible. Cases in which a canal was not explorable for any considerable dis- tance have healed after this treatment. The a:-ray application, made for ten or twenty seconds, or skiagraphy seems to aid the heal- ing of the fistula. If the abscess be incurable by the above method, or radical measures being considered better, the root end may be amputated, after canal filling as far as possible with gutta-percha. The fistula is enlarged and packed open with antiseptic gauze or cotton or sandarac varnish dipped into powdered orthoform applied until the root end is fairly in view. After sterilization of the abscess cavity and local anesthesia, a denta'te fissure bur or a Schamburg surgical bur is laid upon one side of the root at the level of the healthy tissue, and carried laterally with a sawing motion until the root end is separated. It may readily be picked out. If the root can be correctly located without packing the fistula the part may be anesthetized and a portion of gum may be cut away with a tubular knife, or an incision may be made, after which a fissure or surgical bur may be used to cut away the root. Any necrosed bone may be removed at the same time. A skiagraph to act as a guide is necessary when the fistula is not packed open. Fig. 550 Fig. 551 Fig. 552 A skiagraph of apical abscess cavity about two root apices; incurable by ordinary means. The same after root amputation. The same thirty days later, showing a certain amount of new bone formation. (Price.) Necrosed root ends may occasionally be seen projecting through the gum and alveolar process which have been lost above them. They should be removed as above indicated. Sometimes salivary calculus deposits on them. Antiseptic gauze or cotton saturated with balsam of Peru should be packed into the abscess cavity after operation to stimulate granu- lation. The quantity of gauze should be gradually lessened until CHRONIC APICAL ABSCESS WITH FISTULA 599 the cavity is nearly healed. It should thereafter be kept sterilized by means of hydrogen dioxid until the cavity has healed. An alternative is to inject into the cavity Beck's bismuth paste: ^ — Bismuth subnitrate 30 parts Vaselin 65 parts Paraffin 5 parts Wax 5 parts Mix while boiling. which excludes septic moisture, is antiseptic, and stimulates granu- lation. Stimulation by means of fused silver nitrate or sulphuric acid or scarification is at times necessary. Bone should gradually be deposited about the roots (Figs. 550, 551, and 552). P'ailure indicates some condition of sepsis; presumably the amputation has not included all septic root or the canal filling is defective. A still more radical method of surgical treatment involves the extraction and replantation of the root, if worth while. The mouth is sterilized and the tooth extracted, care being taken not to injure the enamel with the forceps. It is then placed in a 1 to 1000 solu- tion of mercuric chlorid at 120° F., or phenol sodique, 20 per cent. The apex of the alveolus is in the meantime sterilized with hydrogen dioxid plus mercuric chlorid and thoroughly curetted. Bleeding is checked with the same solution or phenol sodique, 20 per cent., and a tampon of cotton saturated with the latter is packed into the alveolus. The replantation may be deferred for a few days if the parts are badly infected. In such case granulation is permitted. Returning to the tooth, the apex is cut off slightly beyond the denuded area and smoothed; the pulp canal is well opened from the apex, all debris removed from it, and it is then well sterilized with sodium dioxid or 25 per cent, pyrozone, or both. The canal is then dried and filled entirely with gutta-percha, or partly with gutta- percha and the operation completed with gold, which is nicely smoothed. The tooth should be handled in an aseptic napkin or one wet with the antiseptic, and when ready should be returned to the sterilizing solution. All being ready, the tampon or granulations are removed, the tooth washed in sterile water and replaced in its socket, and a previously prepared retaining appliance cemented to place. This should remain from three to six weeks and be replaced should indications demand it. If the tooth be valueless for replanta- tion purposes, the operation of transplantation may be done either immediately after extraction of the offending tooth or a few days later. The possibility of resorption of the root after plantations should have careful consideration, though it is not prohibitory. The operation of transplantation may be done with a tooth 600 DISEASE OF PERICEMENTUM BEGINNING AT APEX recently extracted from another mouth or with a dried tooth, or, preferably, one kept in alcohol and glycerin, which many extracting specialists habitually retain to oblige applicants. If a suitable tooth be not obtainable, a root may have a crown mounted upon it in such manner as to have an open joint at a point to be placed beneath the gum line, and this joint should be filled with cohesive gold and polished. The tooth root is, of course, sterilized previous to and after the crown mounting, and its canal should have been thor- oughly filled with gutta-percha. Any of these may become firm if thoroughly splinted for a proper length of time. The alveolus should be made to fit the root snugly by means of a bone reamer. The operation of implantation differs from this only in the fact that it is done where a tooth alveolus has been obliterated by absorption and bone formation, as after extraction. If the tooth be not lost by resorption, it is probable that some resorption occurs — toleration then ensues and bony deposition in the bays of resorption and about the root occurs. Possibly a true ankylosis (which see) may occur. To select a proper tooth make a model and bite from an impression , taken before extraction or immediately thereafter, cut off the offend- ing tooth from the model, ream out a socket in the plaster; select tooth, and fit in place; attach with a little soft plaster, the model being thoroughly wet. Construct the retaining appliance, remove the tooth, sterilize, and fill the root. Then put the tooth in the sterilizing agent until needed. Mendel- Joseph and Dassonville^ have shown that in case of removal of a portion of the pericementum the lost portion may be regenerated. Several cases of fistulous openings into the antrum have been noted by canal exploration in which no history of discomfort from antral empyema could be obtained. It was assumed that the root ends approximated the floor of the antrum, and that the abscesses were of simple chronic type. Such cases were treated upon the common principle of canal antisepsis, flushing the abscess tract with hydrogen dioxid, and filling the canals, though -simple non- efferveseing solutions are better. The antral condition was explained to the patients, who were warned of possibilities, but such as yet have not been reported. A chronic abscess may discharge into the maxillary sinus for a long period before being discovered, unless the pus accumulation be extensive, when it escapes from the antrum into the cavity of the nose, discharging by one side. Smaller accumulations of pus find exit in the recumbent position, and attention is called to one antrum 1 Dental Cosmos, 190G. p. 1059. CHRONIC APICAL ABSCESS WITH FISTULA ()()1 Fig. 553 as the seat of affection by notinji; that in tlie niorniiifj ])us appears at but one nostril. The discharges from purulent nasal catarrh appear upon botlr sides. A more common history of antral empyema is the patient's com- plaint of (lull, heavy pains and uneasiness over one side of the face, and an offensive odor, which may not be evident to the operator. High transillumination of the tissues about the mouth and through the cheek, by means of the electric mouth lamp of 20 volts' capacity, the patient being in a dark room, may reveal an opacity on one or perhaps both sides, indicating the presence of fluid in the antrum. A clear pinkish transillumination is a sign of health. Tumors in the antrum entirely obstruct the light. Examination of the posterior teeth will show one of them to be pulpless, if the cause lie in apical abscess. If such a tooth be extracted a profuse flow of pus may follow, and a probe may be passed through an alveolus directly into the antrum. Although extraction is the usual surgical relief, dental conserva- tism rebels against the immediate condemnation of the offending tooth. Efforts at curing the antral condition through the pulp canal are well-nigh hopeless — the antrum is entered at some other point. The tooth is treated as any infecting root; is sterilized and filled. The most certain spot of entry to the antrum is about one-quarter inch above the buccal roots of the upper first molar or between the roots of the first and second molar. The part, or the patient, is anesthetized, and the soft tissues incised or a section removed by means of a tubular knife ; a drill or trephine at least one-eighth inch in diameter, driven rapidly, is passed upward, backward, and inward, piercing the thin shell of the antrum at this point. The opening is made of convenient size to admit of thorough exploration. The nozzle of an atomizer or syringe, filled with a mild antiseptic solution, is passed into the antrum and the cavity is freely sprayed. A probe or the finger is passed into the cavity and an exploration made to detect the presence of any dead bone or bony septi, which, if found, must be removed, the cavity of entrance being enlarged to permit their removal. The antrum is then packed with gauze impregnated with iodoform, etc. After a few days the cavity is Empyema of antrum due to abscess upon root of bicuspid tooth. (Radio- graph by Price.) 602 DISEASE OF PERICEMEXTUM BEGIXXING AT APEX sprayed about every other day with very dilute, warm Dobell's solution, Lugol's solution, or other mild sterile solution. (For further information see works on Oral Surgery.) The opening either heals of itself or may be made to do so by the use of caustics or stitching the parts. Unless necrosis of bone occur, cases of fistula opening upon the face or neck may be healed by the ordinary methods of canal treat- ment, carried out T\"ith extraordinary' care to accomplish the irriga- tion of the fistula, or at least sterilize the apical tissue. The scar formation is less than when extraction is practised for the removal of the cause. If the fistula be indolent, the granulations may be stimulated by means of an injection of 10 per cent, silver nitrate solution. If the fistula obstinately refuse to heal, the tooth should be extracted and necrosed bone, if any be present, surgically removed, though amputation of the root apex may^be tried. Fig. 554 Fig. 555 V^i^iri) Scar caused by alveolar abscess dis- charging on the face. (Black.) Operation for the remedy of scar on the face cau.sed by alveolar abscess. (Black.) Flagg^ suggested, as a means of lessening scar formation, that a seton be passed through the external fistula into the mouth, and that it be gradually drawn into the mouth as the external fistula heals, after which the tooth is to be extracted if otherwise incurable. In fistulse discharging upon the face the formation of scar tissue may bind the tissue of the cheek tight to the bone. When this occurs beneath the tip of the chin, the scar, after healing, usuall}^ resembles a dimple, and calls for no interference. The scar and 1 Lectures on Dental Therapsutics. CHRONIC APICAL ABSCESS WITH FISTULA ()03 binding down along the border of the inferior maxilla, or beneath the malar bone in the upper maxilla, may produce deformity calling for remedy (Figs. 554 and 555). Black's operation is to be performed to lessen the deformity, for its complete correction is not practicable. A finger placed in the mouth draws the cheek away from the alveolar wall, when the exact position of the cord of attachment is dis- covered. A tenotome knife is passed into the tissues, dividing the band of attachment; a long pin is passed through the most depressed portion of the scar, its centre, the long ends of the pin resting upon the face; strips of adhesive plaster laid upon the skin under the head and point of the pin will prevent the latter sinking into the soft tissues. The pin is retained for several days, until the cut in the mouth heals. The principle involved is the supplying of a new section of scar tissue which, while it shrinks, makes the total length of the cord greater, hence less binding. Systemic Complications. — The cachectic, debilitated, anemic, tuber- culous, and syphilitic are liable to extensive pus formation, which enlarges the cavity unduly and may involve the roots of other teeth or even cause devitalization of their pulps, which aids in the continuance of the abscess by adding a fresh cause. In such cases all the dead pulps should be removed after careful diagnosis, and the patient should be instructed in the use of a Sub. Q. syringe and a mild antiseptic, the object being to keep the dependent parts free of pus and allow granulations to form rather than be constantly broken down. In addition, such systemic medication or remedial measures as will raise the recuperative and resistant powers of the tissues should be employed. If very persistent, a vaccine may be employed, after the method of Wright, to raise the opsonic index. (See p. 57.) The direct results of infection, toxemic and septicemic, have already been considered. Chronic Blind Apical Abscess. — A true blind abscess is one with- out a point of discharge. It is a result of septic contamination from root canals, a condition in which bacteria in unfilled root apices or in the interspaces between a root filling and the canal wall find their way into the fluid entering such a space and produce putrefaction — a condition practically analogous to moist gangrene of the pulp. An apical abscess is formed and the apical tissue acts as a fibro- vascular envelope or sac. Under the pus pressure which is apt to be very slight, absorption of toxins and pus germs by way of the lymphatics occurs. The lymphatic glands may be involved; a low toxemia occurs. 604 DISEASE OF PERICEMENTUM BEGINNING AT APEX The dental symptoms may not be noticeable though the tooth may be slightly tender and there may be tenderness upon pressure over the apical region. The general conditions vary. There may be pain about the eyes in the back of the head or neck. The post- cervical glands may be enlarged. The joints may be affected as in arthritis. Eruptions may appear on the body. The patient suffers from lowered vitality due to the toxemia, and he may have slight fever or temperature below normal ; may lose weight, or offer other acute symptoms of malnutrition. The condition may produce more pain or so debilitate as to cause nervous breakdown. In one case of nervous breakdown of a prominent man who had many gold crowns, the condition was due to chronic abscesses at the apices of several teeth. It is to be remembered that antral empyema may occur from the influenza bacillus in the blood. It has been noted in connection with la grippe and may be secondary to empyema of the other sinuses. The .T-rays are valuable diagnostic means (Fig. 553). Also it must be remembered that if apices of teeth lie in or near the antrum the death of their pulps may be caused by the necrotic process. The shadow of the affected side is due to pus or even to thickened walls and increased vascularity. Skiagraphy either through the alveolar process or anteroposteriorly through the head exposes the various possible causes, the condition of the teeth, or, in the antero- posterior, a possible ethmoiditis or frontal sinusitis may be diag- nosticated as the primary cause, or as a condition secondary to a primary antral suppuration. In cases in which the teeth are suspected, radiographs should be made of teeth exhibiting any evidences of tenderness in the apical region, and if not due to conditions readily ameliorated by ordinary canal treatment or root amputation, extraction is warrantable as a means of cure of the general condition. In addition, if the germ infecting can be isolated vaccine therapy may be employed. BONE INFECTION ASSOCIATED WITH DENTAL LESIONS During the course of acute and chronic abscess the bone-marrow becomes inflamed by the pyogenic organisms and is broken down into pus. The condition may continue after extraction for apical abscess in the second stage. It may also occur from the bruising of the periosteal lining of the alveolus as the result of extraction of a hypercementosed root, or from a bruise induced by forcible use of forceps in the removal of deeply seated roots. BONE INFECTION ASSOCIATED WITH DENTAL LESIONS 60o The walls of the alveolus become infected by pyogenic organisms, among which the Diplococcus pneumonine figures prominently. The leaving of cotton tampons, placed as vehicles for pain-relieving agents, for an undue length of time also invites infection. If during extraction the alveolar margins be lacerated, and espe- cially if the bone be uncovered by clot, or the clot fail by solution, it also becomes infected and ulcerated, as shown by its suppurating and highly irritable surface; later the surface becomes insensitive, indicating superficial necrosis, which may become progressively deeper. Ragged gum margins may become gangrenous, although sometimes not. Symptoms. — The symptoms are those of local inflammation witli- out necessarily much swelling of contiguous tissues, such as occurs in acute abscess. Some circumscribed swelling may occur, indicating an abscess in association with it, or a diffuse swelling, indicating inflammation of contiguous tissue. The orifice may appear as though normal, but close examination demonstrates a sinus leading to ulcerated or necrosed bone. If due to an acute abscess in the second stage, the symptoms of that condition may continue. As a rule, the patient presents within a week of the date of extraction, complaining of pain. In the majority of cases the pain is of a deep, boring, continuous character. Reflex pains are also produced about the face. ]Much debility is caused by the wearing character of the pain, the loss of sleep and appetite, and probably also because of absorption of toxins. The gum margins are perhaps sloughing; the bone may be exposed and exquisitely painful to touch, or it may be necrotic and insensitive superficially. The case is one termed " dry socket." Cases of general septicemic or pyemic infection from this source have been recorded. Treatment. — The mouth and, in so far as possible, the inflamed part must be sterilized. Probably mercuric chlorid in hydrogen dioxid (1 to 1000) will answer best. If the solution be used hot, whether it be mercurialized or not, the pain is much relieved. iA.n injection of a 1 or 2 per cent, solution of cocain into the healthy tissue overlying the alveolus will assist in alleviating the acute pain and partly anesthetize the parts. All sloughing gum should be cut away. Exposed bone should be anesthetized by strong cocain solu- tions if painful to touch, or the patient should be anesthetized if necessary. Whether acutely inflamed or necrotic, the bone should be cut away with large sterile burs until healthy tissue is reached. After washing out the debris and further sterilization a clot is to be induced by curetting if necessary. The mouth is to be kept 606 DISEASE OF PERICEMENTUM BEGINNING AT APEX sterilized, and the patient is to be seen daily for a repetition of the curetting if the clot fail, or the alveolus may be gently packed with cotton saturated with balsam of Peru alone or with castor oil, equal parts, as a stimulant. In ordinary cases one or two local treatments will be effective, but the tonic, antiseptic, systemic medication recommended under the heading of acute apical abscess is advised. If the infection be of aggravated character, precautions in the form of suitable systemic medication should be taken against a possible septicemia. (See p. 580.) If the patient be not willing, or unable, to bear this operation at the first visit because of the demoralization produced by the pain, an alternative proceeding may be adopted. A pellet of cotton wet with campho-phenique should be rolled in powdered orthoform and introduced into the socket after sterilization with the mercuric chlorid solution, or a stiff mass made from orthoform, zinc oxid, and vaselin may be packed into the alveolus as an antiseptic and anes- thethic. (Jack.^) Trichloracetic acid in saturated solution may be used to cauterize the ulcerated surface before packing. The repeti- tion of this after five to eight hours will afford marked rehef . Later the radical operation may be performed if granulation does not set in. The introduction of cotton or gauze dressings into the alveoli for relief of pain immediately following extraction is to be done only with extreme care and for short periods, as such dressings are apt to be left in place by patients, and, becoming septic, act as causes of sepsis of the alveolar process. It is better to induce a clot if the removal of the cotton is not followed by hemorrhage. While alveoli will fill with granulations in the absence of a clot filling them, such a clot seems to be the best protection against sepsis. In some of these cases portions of bone may exfoliate. In one obstinate case the capsule of bone surrounding the apex of the alveolus came away, EXTENSIVE NECROSIS ASSOCIATED WITH CHRONIC ALVEOLODENTAL ABSCESS Every chronic alveolodental abscess carries with it the danger of bone complication. It has been shown that in bone infection the organisms are highly virulent. Fortunately in most cases the involve- ment is slight and the parts care for themselves when the cause is removed. In more aggravated cases, either caries or necrosis of the bone may follow. Pus is formed at the expense of the parts, and sometimes infiltrates the surrounding soft and the hard parts, 1 International Dental Journal, 1905. SEPTIC PERFORATIONS (i()7 causing the loosening of teeth. This may occur even though the causal tooth be extracted. In caries the pus escapes by se\eral fistulse, and examination leads to porous dead bone. In necrosis there is circumvallation of a portion or portions of bone, and finally one or more sequestra are loosened, and later, in part, liquefied. The remainder gradually works out of the fistula as one large or numerous small pieces. The patient may be much debilitated. In syphilitic or strumous cases an otherwise simple case may positively refuse to heal until the physical condition is improved by antisyphil- itic or tonic treatment. Surprising recoveries of extensively necrotic parts occur if the patient be brought into good physical condition, and the parts are antiseptically treated, the thorough loosening of the sequestra being awaited. By this means teeth have been retained in place and covered with new tissue, which operation would have exposed or removed. The determination of the point at which oper- ative interference is desirable must depend upon the particular case and the amount of deformity likely to result from the operation. In some marked cases with toxemia, drainage must be obtained surgically, even if extreme operation be necessary. Honl and Bukovsky are credited with the successful treatment of bad chronic suppurations by means of local applications of pyocyaneoprotein. Jesensky^ so treated a case of six months' standing, incurable by ordinary antiseptic and systemic treatment, and obtained remarkable results. Syphilitic intoxication or that of scarlet fever may cause a necrosis of alveolar bone, as may mercury. (See p. 222.) The extent to which the teeth or oral infection act as active exciting causes depends upon the condition present. SEPTIC APICAL PERICEMENTITIS COMPLICATED BY PERFORATION In the treatment of root canals the required mechanical work sometimes results in (1) the passage of the drill through the apical foramen, enlarging it; (2) through the side of the root, causing a perforation. In the first variety the complication chiefly concerns the root filling, which is to be conducted after sterilization upon the same plan as for filling an incomplete foramen. (See p. 530.) » Dental Cosmos, 1901. G08 DISEASE OF PERICEMENTUM BEGINNING AT APEX If a lateral perforation be made near the root apex, it may be filled after sterilization with a cone similarly applied, but made bevelled at the end, or a bit of aseptic sponge may be introduced against the tissue for a base and be covered by oxychlorid of zinc. The packing of a fairly stiff mass of zinc oxychlorid into the root and through the perforation into the fistula has caused the healing of several obstinate cases continually weeping pus or serum. The moisture, if slight, rather aids the adaptation of the cement. The same treatment used with greater care is useful in chronic abscesses without fistula. It is well to only fill the apical portions of canals in either case, so that any removal for another trial may not be too difficult; the later filling of the coronal portion of the canal is very simple. The use of a stiff paste of zinc oxid and eugenol or even oxyphosphate of copper in the same manner is useful. If possible-, Fig. 556 Fig. 557 Skiagraph of crowned curved root, with Showing the relations of an abscess upon perforation and protruding root filling near a temporary tooth, with the crown of a apical foramen. With septic conditions, would developing permanent tooth underlying it. require root amputation. (Price.') it is well to irrigate the fistula with water to remove any excess, though if left it usually works out of the fistula, which later heals or not, as the case may be. If septic conditions persist, the root end must be amputated, or the tooth extracted, prepared, and replanted. If made in the middle third of the root, the canal must be sought for and treated as usual beyond the perforation, which is then separately treated with a gutta-percha cone, or a plaque of gutta-percha may be laid over the perforation and antiseptic cements or copper amalgam used to secure it in position. Extraction and replantation may be resorted to, but amputation does not serve so well, as the root leverage is lost and the tooth may loosen. In a favorable case, after canal exploration, a tapering probe may be passed into the canal and copper amalgam gently tamped about it and against the perforation; the probe is then withdrawn, leaving 1 Items of Interest, 1901. APICAL PERICEMENTITIS IN TEMPORARY TEETH 609 a central canal, which is later treated. Girdwood has reported good results from the use of copper amalgam which, in this connection, the writer can confirm. In a few cases the fistula has been packed open and the perforation filled with amalgam through the sinus. The cases are mostly successful, but in one case healing did not occur until treatment after filling was suspended for several months. Chronic Septic Pericementitis in the Temporary Teeth. — Anj^ of the chronic septic conditions described may occur upon the temporary teeth. The presence of resorption and of the permanent crown usually confines the inflammation to a point lower in the alveolar process than in the case of permanent teeth. The loose character of the structure causes the ulceration to occupy a larger area, and the parts in chronic inflammation look more angry, but are fairly well tolerated. The treatment is practically the same for the curable cases; the others should be extracted. The root canals when treated should be filled with absorbable materials such as paraffin or wax combined with aristol. Buckley recommends, as a canal filling in these cases, the use of a stiff mixture of calcium phosphate and formocresol (formaHn, 1 part; cresol, 1 or 2 parts), to be packed into the pulp chamber and zinc phosphate quickly flowed over it; the cavity to be filled later. Johnson^ suggests that a eucalyptol solution of gutta-percha (see p. 526) be pumped into the canals and pressure exerted with tempo- rary stopping until the solution appears at the fistula. The temporary stopping that does not interfere with filling integrity should be left. Chronic Septic Apical Pericementitis (Non-purulent). — Continued inflammation of a low grade (interstitial gingivitis), or what may in reality be continued atonic hyperemia, may exist in the apical pericementum for long periods with or without pus formation. The actual state can only be determined by radiography. (See p. 565.) Cause and Pathology. — The cause consists of unremoved gan- grenous pulp tissue, septic serous collections in canal apices or about imperfect root fillings, or septic material in the root tubuli, all much the same in character. A very common cause is an other- wise good root filling which has failed to fill the apical portion of a curved fine or even well-opened root. While in skilful hands gutta- percha points and oxychlorid of zinc usually reach their apical destination, the editor has met unfilled apical canals after good operators as the most common of operative errors. An imperfectly iilled perforation may cause a similar condition, W'hich, however, the .r-rays should determine. 1 Dental Cosmos, 1899. 39 GIO DISEASE OF PERICEMENTUM BEGINNING AT APEX Albuminous fluid may enter the canal via the apical foramen, and, becoming infected, putrefaction ensues. The source of infection may possibly be via the blood, but leaking crown and root fillings Fig. 558 Fig. 559 Dentin from the root of an abscessed tooth, showing the penetration of cocci to a depth of about Yff mm. (550^ in.) ; the side o to 6 bordered upon the canal. X 1000. (Miller.) Sector of a cross-section from a diseased root: a, cementum; 6, stratum granulosum; c, very narrow and finely branched tubules; d, penetration of bacteria into tubules. X 150. (Miller.) more probably permit bacteria to enter from the mouth. The more or less constant result of filling roots with cotton permeated with evanescent materials only is evi- dence of this. The cotton absorbs fluid either from ^bout leaky fill- ings, too often placed in contact with it, or else from the apical tis- sues; infection readily occurs and a highly odorous cotton is removed because of the apical irritation. When the cotton is well placed and confined under tight-sealing materials to the apical half of the root canal, this result is long delayed in many cases. Portions APICAL PERICEMEXTITIS IN TEMPORARY TEETH Oil of gangrenous pulps remaining in canals may likewise become in- fected. Extra and untreated canals are frequently causes. Miller^ has shown that root tubules are infected only for a short distance at their canal ends, so that infection from the pericementum via the cementum and dentinal tubules is highly improbable (Fig. 559). The putrefaction produces gases, and these exuding slowly produce the irritation. If pyogenic organisms be present, apical abscess may at any time supervene. Mayrhofer- has shown that even formocresol fails to sterilize all tubuli, so that bacteria, especially streptococci, grow back into the canal. If the canal filling be imperfect it is obvious that apical infection may arise. Symptoms. — Subacute inflammation of apical tissue being present, the symptoms of this condition are tenderness upon decided pressure or upon percussion; the response may only be elicited by pressure or percussion in one direction. The tooth gives a dull note upon percussion, and is usually looser than its neighbors. The red line of the gum extends farther toward the gum margin than normal — quite to it in some cases. There is apt to be a response to heat. The patient is apt to avoid the tooth in mastication. In some cases acute reflex pains in other teeth may precede an outbreak of purulent pericementitis, a frequent sequel to this condition. There are also evidences of previous devitalization of the pulp in opacity, lack of response to tests for vitality, etc. At times a history of previous canal treatment may be obtained or the evidences of an attempt at canal filling may be seen upon opening the tooth. Diagnosis. — The condition requires careful differentiation from (1) non-septic apical pericementitis due to traumatism or malocclusion or to a perforation imperfectly filled; (2) pericemental abscess in the early stage; (3) abscess of the pulp in the later stages. In nearly all these cases the pulp may be vital. Being itself only subsequent to death of the pulp, tests for vitality are made. (See p. 538.) If pulp death be indicated by the tests, the pulp canal is explored, and, if found, treated, and filled; a septic condition about or beyond the same is looked for. There is great disadvantage in a large apical opening, particularly in the dressing and root-filling operation. Treatment. — The condition being analogous to that of moist gan- grene, or blind apical abscess, the treatment is the same. Before it can be applied the root canals should be opened, and to accomplish this all root filhngs involved require removal. If an extra canal be ' Dental Cosmos, 1899. 2 Items of Interest, March. 1910. 612 DISEASE OF PERICEMENTUM BEGINNING AT APEX found after apparently conscientious work has been done, this should receive attention before removing root fillings. The bulk of gutta-percha root fUHngs are best drilled out with Downie broaches revolved in the engine hand-piece or by hand, eucalyptol being used to soften or dissolve the gutta-percha. All cement fillings are removed by a drill so far as can be safely done, dryness being a great aid in locating the cement in the canal. When the danger of perforation arises, a stiff Swiss broach or a fine Downie broach may be rubbed down to a drill edge and used as a tamp drill. Sulphuric acid in 50 per cent, solution or aqua ammonia aid by dissolving the cement. The object sought for is an unfilled canal lumen, which, when found, is readily recognized by the ease of penetration with the broach and the absence of sensation until the apical tissue is reached. The fact that the. sides of the root canal can be felt is assurance of safety against perforation which may occur in any case. There can be no assurance of safety until the apical tissue can be explored, but perforation must be avoided. The fine Downie broach is useful in difficult cases, and, if necessary, a No. 1 Beutelrock drill may be used. When the apical foramen is open, or further work is impossible without the danger of perforation, the canal treatment is conducted upon the lines laid down for gangrenous pulp. (See p. 546.) A difficult class of cases sometimes presents in which the disease supervenes and where work which may be regarded as desperate has been done, or where pins have been inserted and are almost impossible of removal, as, for example, where a Logan crown, has been cemented to place. In such cases the idea of Watkins in apply- ing blue light directly by means of a funnel may be of great value in reducing inflammation, and mild applications of the ic-rays may be useful, but sometimes the work must be carefully dismantled to permit re-treatment. An a:-ray should always be first made as a guide. If the pericementitis have been of long standing, the thickening of the membrane will have caused protrusion of the tooth. The tooth should be ground off at its point of occlusion until it occludes with somewhat less force than its neighbors, the therapeutic principle in these cases being that of removing the source of irritation and procuring surgical rest. Indications of favorable results are found in the red gum line assuming its normal position, tenderness disap- pearing, and increased tightness of the tooth. This affection is extremely common about the roots of pulpless teeth, and always signifies more or less enforced disuse of the teeth, and, if uncorrected, their ultimate loss. SEPTIC PERICEMENTITIS AT BIFURCATIONS 013 This condition is sometimes associated with a ciiroiiic hhnd abscess. (See p. ()03.) Upon treatment, acute ai)ical abscess is apt to be Hghted up; therefore the steriUzation should l)e jjrolonged and thorough to avoid acute apical abscess. In one case of a cyst associated with a lower molar tooth which had a leaky gutta-percha crown and partial canal filling, extraction was a(h'ised for reasons other than canal treatment. The cyst then promptly developed as an acute abscess, which shifted its position toward the cheek and there discharged without production of scar. Septic Pericementitis at Bifurcations of Multi-rooted Teeth. — Teeth weakened by caries may fracture after filling in such a manner that the line of fracture exposes the pericementum at the bifurcation. The crack admits septic saliva, and a filling or fillings usually sink gingivally, wedging apart the two sections and admitting more or less food matter. If the canals of the sections have been previously treated and filled, it is usual to find a more or less general peri- cementitis due to the w^edging and septic irritation. It subsides upon sterilizing by means of a douche, while gentle broaching removes the accumulated debris. Formocresol, diluted with phenol camphor to a 5 or 10 per cent, formalin strength, is to be placed in the pulp cavity and covered wdth sandarached cotton, and a ligature of silk or wire is to be tied about the tooth to draw the parts together. A hollow metal crowai is to be constructed and before placement a little oxyphosphate of copper or oxychlorid of zinc cement is to be worked into the joint which is temporarily sprung open. The part may be joined by amalgam built into a dove-tail (Fig. 290), or a trephine may be driven into the face of the crown and a metal ring be cemented into it (Fig. 300). If the canals be septic, an apical abscess may complicate the condition and require treatment while the fracture is being handled. In some cases a metal staple may be placed in the canals of the two sections and so arranged as to spring the parts together when forced to place. The joint should have one of the cements worked into it before this staple is cemented to place. About the staple quick- setting amalgam should be packed, a copper band having been pre- viously adjusted to act as a matrix. Later, this band is to be removed and a porcelain-faced gold crown or a porcelain crown baked on a heavy w^ide platinum band and cap arranged to sustain it (Fig. 299). The staple may be utilized as a portion of a crown base of the Richmond or other variety, the bifurcation and crown cementing being deferred until the final operation. Irritation may arise in some of these cases, wdiich however, need not prevent the trial of the method as a last resort. CHAPTER XXI . NON-SEPTIC PERICEMENTITIS Various grades of pericemental irritation, ranging from a mild arterial hyperemia to actual inflammation, may be produced by non-septic causes. The most satisfactory evidence that inflammation may be so caused is furnished by Talbot's experiments with the mercurialization of dogs. Beginning with healthy pericementi, these were, after mercurialization of the animal, found to contain the round-celled infiltration characteristic of inflammation, and no bacteria could be found. Further evidence is given by the usual experimental study of inflammation with the mesentery of the frog. Simple irritation, even with antiseptic substances, produces the phenomena. Any of the causes which may produce inflammation may, if acting in more mild degree, produce arterial hyperemia. If the action of the cause be violent and then discontinued, as in the case of a blow, the inflam- mation resulting is acute, but may pass into a chronic form; but if the cause continue to act it produces a chronic inflammation. For purposes of description, non-septic pericementitis may be divided, according to its character, into traumatic and symptomatic, and, according to its location, into apical and general. TRAUMATIC PERICEMENTITIS By traumatic pericementitis is meant a profound irritation of the pericementum, the result of mechanical violence applied externally to the tooth, or of instrumentation or chemical irritation of the pericementum through the root canal. Causes. — Violence Externally Applied. — Excessive force deliv- ered directly upon the teeth, as in case of blows, falls, overmalleting in building fillings, the biting of nuts, thread, or other hard objects, or force indirectly delivered, as in case of blows received under the chin, bringing the teeth forcibly together, may all cause acute peri- cementitis. An excessive amount of filling on the occlusal surface of a tooth, a maloccluding crown or overfull fillings upon the proximal aspect. TRAUMATIC PERICEMENTITIS 615 maintaining a wedged condition, cause overocclusion upon the tooth and an irritation of its pericementum. The overstraining of the pericementum of a tooth as the result of overuse, as in cases where only a few teeth remain for mastication, or where pyorrhea or calculus has caused resorption of the alveolar process and looseness of the teeth, or where artificial dentures are clasped to remaining teeth, or where bridges are supported upon insufficient piers, are frequent causes of non-septic pericementitis of a degenerative character. The presence of a rough flaring or a too deeply placed crown band beneath the gum margins, portions of cement used in cementation of crowns, or excess of filling material beneath the gum, are all causes of marginal gingivitis, with which pericementitis may be associated. With these marginal cases septic causes usually have to be considered as complications. Too violent wedging is always followed by more or less peri- cementitis of the wedged teeth, and their neighbors, more marked when elastic-rubber wedges are used. In correcting irregularities of the teeth, if they be moved too rapidly, are not firmly directed during the operation, or, subse- quently, not firmly maintained in position, pericementitis of a high grade is frequentl}' excited. Violence Internally Applied. — If a wholly or partially vital pulp be torn from its apical connections, as in the use of pressure anesthesia, an apical traumatic pericementitis may be set up. This is usually transient. Secondary hemorrhage may occur and produce pericementitis. Excessive laceration of the apical tissue by means of barbed instruments, the inclusion of air or medicament under a root dress- ing or filling, the same exercising pressure upon the apical tissues; the mechanical irritation of a projecting root filling, pivot wire, broach, or drill, are all suflScient causes. The undue enlargement of the apex of the root canal or the passage of a reamer through the lateral aspect of a root may excite inflam- mation, and the perfect filling of the opening may be exceedingly difficult, so that if the tissues are not infected at the time, sepsis may later follow. Chemical Irritation. — The application of arsenic to a perfora- tion may excite inflammation and necrosis, which endangers the jaw. (See p. 504.) The use of arsenic as a pulp devitalizer may cause a hyperemia of the apical tissue, following the hyperemia of the pulp, and causing slight tooth extrusion, which is aggravated by the malocclusion. This is not dangerous. (See p. 497.) The undue use of escharotics, such as carbolic acid, sodium dioxid, 616 NON-SEPTIC PERICEMENTITIS zinc chlorid, sulphuric acid, or mercuric chlorid, in a pulp canal may excite an undesirable irritation. The limited irritation follow- ing their limited use is often more than offset by the advantages of the asepsis produced. Prophylaxis. — Many of these causes are avoidable, and operators mindful of possible irritations should avoid the mechanical irritation of apical tissues, neutralize powerful acids or alkalies, use escharotics with caution, wedge teeth gradually, and after wedging either pack gutta-percha between the teeth to permit them to rest for a few days or fix them immovably with wooden wedges or steel separators during malleting. During orthodontia teeth should be moved steadily, and after alignment is secured they should be firmly maintained in position until deposition of bone occurs. Patients should be warned against the evil effects of thread biting and biting hard substances. Pathology and Morbid Anatomy. — Chemical substances applied in excess cause a destruction of tissue dependent upon the quantity used. Inflammation tending to the resorption of the dead tissue occurs. The pericementitis presumably persists in some degree until the foreign (dead) material is removed by natural processes. In the case of protruding foreign bodies, such as root fillings, broaches, etc., there is a tendency of the inflammation to become subacute or chronic. The foreign body may to an extent become encysted, particularly in the case of a gutta-percha root filling. In other cases the continued vascular disturbance, if of mild degree, produces hypercementosis ; in more severe cases resorption of the root occurs. Cases due to perforation of the root and wounding of the peri- cementum, after the acute symptoms have passed, commonly assume an irritative and chronic type, the soft tissues included in the perforation being in a state of chronic inflammation. Many of these cases become infected owing to the difficulty of completely sterilizing the apical portion of the canal which lies beyond them. The pericementitis produced by pressure of included air, liquid, or plastic root filling upon the apical tissue is often severe. Upon removal of the root dressing or filling the engorgement is relieved b}" the gushing of blood through the root canal. The inflammation may, however, continue unless sedatives be applied to the apical tissue via the canal. In cases due to traumatism, such as violent wedging, rapid move- ment in regulating, overmalleting, blows, biting of thread, ice, nuts, etc., the condition is surgically one of bruise. TRAUMATIC PERICEMENTITIS 617 The phenomena of active inflammation make their ai)pearance to an extent governed l)y the degree of violence — exndation, swelling, redness, and pain; fibrinous and corpuscular exudations occur, and later a reorganization of tissue occurs, in some cases a degeneration, depending upon the completeness with which the indicated thera- peusis is applied and upon the vitality of the patient. Traumatic pericementitis in high degree in the young may be recovered from; but in the middle aged and aged it may give rise to a series of degenerative changes which only end with the loss of the tooth. In cases due to looseness of the teeth, of course, septic primary causes have to be considered, but the pericementitis may be quite as much mechanically as septically produced. In all cases the extrusion caused by the inflammation adds another exciting cause of apical pericementitis — /. e., malocclusion, which aggravates the condition. Symptoms and Diagnosis. — The amount of pericemental inflamma- tion present is evidenced by the soreness and extrusion of the tooth and the degree of redness in the overlying gum tissue. A history of violence may be obtained when it has occurred. Mal- occlusion may be detected by occlusion marks upon fillings or by means of carbon paper. The untoward results of canal operations may be inferred from a personal knowledge of the case or, perhaps, from the history. It is at times difficult to exclude septic, non- purulent, apical pericementitis as a cause, particularly if the case come from the hands of another practitioner. In doubtful cases the treatment for inferred traumatisms may be employed, and if followed by good results a post hoc diagnosis of traumatic peri- cementitis may be made. The a:'-rays afford a means of determining extruding root fillings, broaches, etc. Treatment. — Foreign bodies protruding from the root apex must be removed if persistent symptoms demand it. This may require an artificial opening for its performance, or root amputation. Per- forations should be carefully treated. If evidence of pericementitis persist, the end of the root including the perforation should be amputated, or if the tooth persistently extrude, the tooth may be extracted, the perforation and canal filled with gold or gutta-percha, and the tooth replanted under antiseptic precautions. In all cases due to violence the treatment is that adapted to injury; first, surgical rest of the pericementum. This may be accomplished in two ways: either by preventing the tooth striking its antagonists or holding it so rigidly that it cannot move if it does 618 NON-SEPTIC PERICEMENTITIS meet them. As a preliminary measure the tooth is gently but firmly lashed to its neighbors b}^ means of ligatures so that it is rigidly held. A swaged cap is either fitted to a neighboring tooth, or the antagonizing teeth are ground away until they fail to strike the injured tooth; the first method is to be preferred. In cases involving several teeth, such as all of the incisors, two metallic plates are quickly swaged to cover posterior teeth and raise the bite, and they are cemented in position to relieve the irritated teeth from occlusion. When the apical tissues have been irritated by way of the canal, sedatives, such as strong tincture of aconite or menthol in chloroform or phenol-camphor or eugenol or menthol-phenoP (menthol, 3 parts; carbolic acid, 1 part; melted together) or thymophen should be applied on cotton to the apical tissue by way of the root canal. All cases of traumatic pericementitis require the persistent use of counter- irritants, applied every other day to the overlying gum. (See p. 451.) Systemic derivation is also useful in the acute cases. In even mild cases not due to violence the guarding of the extruded tooth against malocclusion is of advantage. If the cause be some mechanical irritant at the gum margin, this should be removed and the case treated as above described. Recog- nizing the possible influence of septic causes, oral antiseptics are to be used. SYMPTOMATIC NON-SEPTIC PERICEMENTITIS By symptomatic non-septic pericementitis is meant an aseptic pericementitis occurring as the result of systemic conditions, or of the action of drugs taken internally. If mercury be administered to patients in large doses for long periods, or in one or more massive doses, or if the patient have an idiosyncrasy to the action of this agent, an irritation of the salivary glands is excited, followed by looseness and soreness of the teeth and swelling of the gums; that is, a general pericementitis and maxillary periostitis arise. The patient has a metallic coppery taste, coated tongue, and fetid breath; the gums are puffy and bleed easily. In advanced cases the tongue and cheeks are swollen. Potassium iodid administered in this condition relieves the maxillary periostitis and pericementitis; but the same drug administered in health, or for conditions other than mercurial poisoning, also causes irritation of the pericementum. Pilocarpin has a similar effect, though in much ' Dr. Morgan Howe. SYMPTOMATIC NON-SEPTIC PERICEMENTITIS 619 less degree. All of these drugs are partially eliminated by the gland- ular appendages of the mouth, and during elimination apparently act as local irritants. Lead poisoning may have a similar action. Patients who have a gouty heredity, or who are the subjects of active gout, frequently exhibit a tenderness of the entire pericemen- tum of one or more or sometimes all of the teeth. This pericemental disturbance may be the precursor of an acute outbreak of gout in the metatarsophalangeal joint. Scurvy — a very rare systemic disease — is attended by rapid degeneration of the pericementum of the teeth and of the alveolar tissues. Syphilis is also attended by pericemental irritation. This, of course, is of septic origin. Talbot's experiments on dogs show conclusively that a true peri- cementitis may be induced owing to the chemotactic properties of the mercury alone. (See Interstitial Gingivitis.) In auto-intoxication by intestinal toxins or by leukomains in diseases involving general malnutrition, the irritants are probably in part eliminated by the gums, which are in turn irritated. (See Gouty Pericementitis.) It has been shown by Loup that mercurial stomatitis may be cured by mercury used as an oral antiseptic; therefore, the logical conclusion is that oral organisms play a part in the production of the local effects of mercury; probably the mercury produces a local predisposition. This is further confirmed by the fact that if the teeth are attended to and oral prophylaxis be practised before the administration of mercury to syphilitics, they tolerate greater amounts of the drug before salivation or stomatitis. Treatment. — The drug should be discontinued, the disease, if present, should be antagonized, and the local complications, if any, should be appropriately treated, antisepsis being always advisable. If the pericementitis, gingivitis, and stomatitis be mercurial, the drug should be stopped and an antisialagogue used, such as atropin sulphate, y^-^ gr. each four to six hours, until relieved. Potassium chlorate as a mouth wash, or internally, is useful if the stomach is not irritable. EJ — Potassii chlorat gr. xlviij Tr. myrrh fSss Elixir calisayae q. s. ad fSiiJ — M. Sig. — Teaspoonful every five hours, or use as a mouth wash. (Hare.) Results of Chronic Non-septic Pericementitis. — If at any point of the irritated pericementum a constructive grade of irritation be maintained, the cemental tissue becomes hypertrophied (Fig. 560). 620 NON-SEPTIC PERICEMENTITIS If a more severe grade of irritation — i. e., low-grade inflammation — be present for a long time, the cementum and even the dentin of the root may be resorbed. Both of these results may go on concurrently at different points, or resorption may be followed by deposition of cementum if the conditions change. Chronic overuse or disuse of teeth result in degenerations of the pericementum. HYPERCEMENTOSIS (DENTAL EXOSTOSIS, EXCEMENTOSIS, HYPERPLASIA OF THE CEMENTUM) Definition. — By hypercementosis is meant a secondary deposit, or an increase of volume of the cementum of a tooth beyond the normal limit. It may be circumscribed or diffuse. Causes. ^ — A constructive degree of hyperemia or very mild inflam- mation is the proximate cause, which may be excited by numerous primary causes, such as a projecting root filling, a projecting edge of crown filling, deposits of salivary calculus, the overlapping of a cavity margin by the gum, malocclusion, non-occlusion, the biting of hard objects, such as nuts or thread, the overuse of certain teeth, the habitual tapping together of teeth, the habitual chewing of tooth- picks, the gradual pressure of gas from dead pulps. The pressure of a Fig. 560 tooth root against another root during eruption is a sufficient cause. (See Fig. 206.) The overcrowding of teeth in an arch has also caused this condition, as has also the impaction of a tooth (Fig. 239). Chronic alveolar abscess or pyorrhea alveolaris may cause it by inducing about itself at a distance an area of hyperemia. It also seems at times to be induced after pulp devitalization from any cause. Hypercementosis is a possibility in any case of chronic peri- cemental irritation; it represents a degree of irritation rather than any one specific cause. It has been discussed by some writers under the heading of Constructive or Condensing Pericementitis, and is fairly analogous to osteosclerosis. (See p. 137.) H YPERCEMENTOSIS 621 Situation. — Hypercementosis may be diffused over almost an entire root or several roots, or be localized as a distinct nodule at some lateral aspect, or exist as a circumscribed enlargement about the apex of a root, or at the neck of a root. It is always located where the cause (hyperemia) has been produced (Fig. 560). Fig. 561 Hypercementosis. (Skiagraph by Lodge.) Flagg noted that 75 per cent, of cases of hypercementosis were found upon posterior teeth, and that the teeth were usually of the character termed dense — i. e., the tissues of the individual were of recuperative type, tending to produce constructive changes. Fig. 562 m 'S/-^-., fi-~i\L< A .•'"■^Z / /l/f^//.s'jr,'/'7,.. L\\l\ ..vvM^I»(rt\t^tlilS Hypertroph\ of the cementum on the side of i root of a lower molar near the neck of the tooth of a man: o, dentin; 6, cementum; c, fibers of peridental membrane; from fc to c the cementum is normal and the incremental lines fairly regular, hut at d one of the lamellae is greatly thickened; at e this lamellae is seen to be about equal in thickness with the others. The next two lamellae are thin over the greatest prominence, but one is much thickened at q. and both at h. These latter seem to partially fill the valleys which were occasioned by the first irregular growth. From a lengthwise section. (Black.) Pathology and Morbid Anatomy. — For some time after eruption the cementum consists of but few lamellae of deposit. It, however, reaches a maximum normal development at which it normally rests, as in the case of the physiological pulp cavity. As age progresses 622 NON-SEPTIC PERICEMENTITIS it is apt to be more thickly deposited at the expense of the peri- cementum, which becomes more attenuated. Whether this is due to irritants floating in the blood stream, or to the various local irritants above mentioned, or to perfectly normal development, is not clear except for certain definite cases. Nodular and irregular forms arising from the general surface are clearly of abnormal type. Fig. 563 Apex of root of an upper bicuspid tooth with irregularly developed cementum: a, a, dentin; h, b, pulp canals. The lamellae of cementum are marked 1, 2, 3, etc.; d, d, d, absorption areas that have been refilled with cementum. It will be seen that the apices of the roots were originally separate, but became fused with the deposit of the second lamella of cementum, and that in this regular growth began and was most pronounced. It has continued through the sub.«equent lamellae but in less degree. It will also be noticed that the absorption areas, d, d, d, have pro- ceeded from certain lamellae. That between the roots has broken through the first lamella and penetrated the dentin, and has been filled with the deposit of a second lamella. Other of the absorptions have proceeded from lamellae which can be readily made out. The small points, e, seem to have been filled with the deposit of the last layer of the cementum, while others have one, two, or more layers covering them. (Black.) Successive lamellse are deposited; the pericementum recedes, causing resorption of the alveolar process. Union of the bone and cementum (ankylosis) very rarely occurs. A resorption of cementum and dentin may occur at some point owing to a different degree of irritation, and in the area a new deposition of cementum may occur (Fig. 563, d). In some cases distinct areas of hypercementosis and root resorption are seen in close proximity. Chronic apical abscess may produce a denudation of the root end, and a short distance H YPERCEMEN TOSIS 623 below an annular ridge of hypercementosis may occur. Areas of hypercementosis may be translucent or decidedly opaque, and sometimes the two are combined, a mottled appearance being produced. If the growth proximate another root, the pericementum may resorb at the point of contact and a deposition of cementum occur which firmly unites the roots in a union called concrescence. (See p. 251.) It has occurred that a root filling protruding through a perforation has caused a diffused exostosis of the alveolar process.^ The hyper- trophied process may be ivory-like in hardness. Symptoms and Diagnosis. — Many cases exist without active local symptoms. In no case is the color of the gum altered unless other disease than hyperemia be acting as a cause. In some cases there are symptoms of hyperemia expressed as a disposition to bite hard upon the particular tooth, or to grind upon it. A paroxysm of gnaw- ing pain lasting for some hours, and recurring at intervals, is also somewhat characteristic. Sympathetic hyperemia of the pulp with increased response to thermal changes may occur. The gum may have slightly receded. Neuralgia, functional blindness, functional deafness, chorea, epileptiform fits, paralysis, cardiac neuralgia, insanity, and other related conditions have been cured by the extraction of hyper- cementosed teeth. ^ The treatment of teeth presenting obstinate symptoms of peri- cementitis, apparently due to moist gangrene of the pulp, may at times be complicated by unsuspected hypercementosis. In such cases, if pulp or pericemental complication cannot be determined, suspicion should point to hypercementosis and an .r-ray examination be made, by which means the condition may be posi- tively determined. As entire dentures have been extracted, tooth by tooth, in a vain endeavor to cure a neuralgia about the head, this means of diagnosis should not be overlooked. Treatment. — The treatment for hypercementosis may first be a conservative one if only slight annoyance be produced by it. Counterirritation — correction of malocclusion, etc. — may be em- ployed. The symptoms may disappear. If they do not, or they are severe when the patient applies, the tooth should be completely extracted. The operation of amputation of the root end might be safely tried for apical hypercementosis, but there are no records of its 1 Garretson's Oral Clinic, 1884. 2 Brubaker: American System of Dentistry. 624 NON-SEPTIC PERICEMENTITIS employment as a means of cure. The bulbous condition of the root end may cause extraction to be difficult, and fracture of the root end may occur. Flagg recommended that in such a case a fissure drill be passed about the circumference of the root end to remove the bony obstruction to its passage out of the alveolus, after which it may be lifted away with tweezers. Cocain may be used as an obtundent. The use of alveolar forceps for the condition is little short of brutal, and only warranted by the impracticability of other means. Extraction for hypercementosis may cause considerable bruising of the walls of the alveolus, followed by excruciating pain lasting often for days. The alveolus may refuse to granulate, and a septic condition result. The pain has at times been relieved by the injec- tion of a 2 per cent, solution of cocain into the gum on either side of the alveolus, after which the surfaces of the alveolar walls should be sterilized and burred away until tissue capable of granulation is reached. The alveolus should then be irrigated and a clot invited by causing a slight hemorrhage. (See p. 604.) Fig. 564 m^ Vertical section of a human tooth ankylosed to the jaw: R, root; B, bone of jaw. The abso- lute continuity of the two hard tissues is strikingly shown. From the collection of the late Storer Bennett.' (Hopewell-Smith.) 1 Transactions of the Odontological Society of Great Britain. RESORPTION OF THE ROOTS OF PERMANENT TEETH 625 ANKYLOSIS (SYNOSTOSIS) By this is meant the union of bone and cementum, a condition analogous to ankylosis of bone. Hopewell-Smith' has described 5 cases, of which he offers the following explanation: (1) inflammation occurs and the membrane is changed into granulation tissue; (2) the cellular elements destroy portions of the bone and excavate the cementum; (3) the mass of granulation tissue is then ossified, joining the bone and cementum in a firm union. E. C. Rice^ has reported a case of a lady for whom an implantation of an upper bicuspid was done. In an effort made later to remove the tooth all attempts to loosen it in any degree with forceps failed. In my own practice an implanted tooth is firmly immovable in any degree, though several years in place. The union may not be osseous in these cases, though doubtless bone has entered areas of previous resorption. A remarkable case was shown the editor by Dr. J. Curry, of Philadelphia. Every pier tooth of four bridges was firmly ankylosed and immovable, yet large bays of resorption in each root necessitated extraction. This was not a plantation case. RESORPTION OF THE ROOTS OF PERMANENT TEETH By resorption of the roots of permanent teeth is meant the gradual removal of the cementum and dentin of permanent roots by phago- cytic cells existing in the adjacent soft tissue (osteoclasts). Causes. — ^The proximate cause is probably in all cases a degree of irritation greater than that required to produce h\'percementosis. Probably a mild non-septic inflammation exists. Talbot's demon- strations of interstitial gingivitis, a term meant to include interstitial pericementitis, show that it is a frequent cause of both root and alveolar resorption. (See Deeply-seated Gingivitis.) In other words, it is due mainly to an aseptic pericementitis. The disease has been discussed by other writers as "Rarefying Pericementitis," fairly analogous to osteoporosis. (See p. 137.) Chronic apical abscess seems to be a frequent cause. Although theoretically the alkaline pus formed should neutralize acid forma- tion, the fact of resorption remains, and is probably explainable ' Histology and Pathohistology of the Teeth. - Private communication. 40 626 NON-SEPTIC PERICEMENTITIS upon the ground that it is produced by the granulation tissue formed about the root apex during periods of lessened pus formation (Fig. 543). Fig 565 Fig. 566 Fig. 567 Fig. 665. — Apical abscess and resorption, produced by a protruding broach. Fig. 566. — Deciduous cuspid crowned, mistaken for permanent cuspid which lay in jaw and caused resorption of root of permanent lateral. (Skiagraph by Price.) • Fig. 567. — Resorption at cervical third in two replanted teeth, one broken in consequence. Editor's practice. (Skiagraph by Hagopian.) Fig. 568 Fig. 569 Case of extensive resorption about upper central. (Skiagraph by Lodge.) Resorption of roots. (Skiagraph by Lodge.) Protruding root filHngs or broaches are common causes (Fig. 565). Plantations are frequently followed by it. A peculiar resorption in the cervical third of two replanted incisors caused the fracture of one at the point of resorption and necessitated the removal of both teeth (Fig. 567). Plantations are usually f9llowed by peculiar resorptions over even the entire root. Looseness of a tooth with the resultant excess of movement excites deeply-seated gingivitis and resorption of bone and often of roots. Partial luxation as the result of a blow or fall produces the same result, the pericementum I RESORPTION OF THE ROOTS OF PERMANENT TEETH 627 becoming thickened, the tooth loosened and extruded, and mal- occlusion, which is also a cause, being induced. A toothpick broken off in the gum tissue has produced resorption at the neck of the root. The descent of a supernumerary or impacted tooth upon a per- manent root has caused resorption, exposing the pulp of the resorbed root, and producing pulp reactions. This may be quite extensive before violent symptoms occur (Fig. 5GG). In one case both the buccal roots of an upper molar were removed by a supernumerary tooth, the crown of which fitted the resorbed root ends. Fig. 570 Inflamed pericementum, osteoclasts in Howship's lacunae. (V. A. Latham.) Calculus beneath the gum margin has produced resorption through the production of gingivitis. In one case noted four lower incisors presented the characteristic bays at a point one-eighth inch below the gum line. Some of the cases exhibit no tangible cause; the root resorbs appar- ently as the result of a peculiar reaction upon the part of the tissues of the individual, who may lose many teeth by this process — i. e., a dyscrasia exists. The teeth may be non-carious and the pulps vital. In some of these cases neurasthenia or a uric acid diathesis seems to have some association with the condition (Fig. 570). 628 NON-SEPTIC PERICEMENTITIS Pathology and Morbid Anatomy. — Both resorption of cementum and its redeposition occur in deciduous teeth as physiological pro- cesses; at some aspect of the cementum the tissue becomes hollowed out, and later filled in by new cementum. Resorption of tissue throughout the body is accomplished by means of multinucleated cells (giant cells, osteoclasts). At some part to be physiologically resorbed these cells make their appearance in contact with the tissue to be removed, and it gradually disappears, the layer of multinu- cleated cells constantly occupying the excavated territory known as Howship's lacunae (Figs. 73 and 570). If a foreign (aseptic) body be introduced into living tissues, it becomes surrounded by these cells, which in some cases effect its removal; in others, failing to remove the foreign body, connective tissue forms about it and encysts it; encyst- FiG. 571 ment may occur after partial removal by giant cells. The resorption of a root may be of any extent, from a slight spicular roughness of the apex of the root to almost complete removal of the root. Perforation of the root from side to side Idiopathic resorption of may occur, of coursc, involving the pulp canal, permanent root. The bay ^ud, if thc pulp bc allvC, obsCUrC rCactloUS upon the side exposed the . ,-,-,. __^ , pulp and perforated the upon its part may occur (l^lg. 571). root as shown. Crater-like ^j^ aj-gg, of marked rcsorptiou may occur at resorption about apical • • i i i • i foramen. Pulp first devi- a pomt just bcueath the gum margm and taiized on account of per- ypQjj ^j^y aspcct of the tooth. In this situatiou sistent pain and the tooth . ... • c i i i i later extracted. it may Simulate a cavity or decay beneath the gum. It occurs upon either vital or devi- talized teeth, and may expose the pulp or the root-canal filling. The gum tissue is usually found within the cavity. It is probable that in plantations the root acts as an aseptic foreign body; mild inflainmation occurs, subsides, and giant multinucleated cells attack the tooth root and endeavor to remove it by solution; this they accomplish, in part, in spots; then a tolerance is estab- lished and connective tissue organizes about the roots; later, more complete regeneration is represented in the formation of bone; a condition of bony fixation is established, evidenced by the clear- ringing note elicited upon tapping the planted tooth. With reference to resorption after plantations. Miller^ records the 1 Independent Practitioner, 1887. RESORPTION OF THE ROOTS OF PERMANENT TEETH 629 toUowing results of his observations. The fixation of reimphuitefl or transpkmted teeth may be accomplished in three ways: 1. By simple encapsulation of the root. 2. By the bundles of connective tissue which fill up irregular absorption spaces, especially where the pericementum has not been present at that portion when the implantation was made (a pseudo- attachment). 3. By direct union of the surrounding tissues with the living pericementum. He inclines to think this the only j^ermanent attachment. He states that for the most part osteoclasts were few and that resorption was carried on by small round cells. Fig. 572 Resorption of distal root of a first molar. (Skiagraph by Custer.) Diagram of a cafe of root resorption after secondary dentin had formed: SD, secondary dentin; AR, area undergoing resorption; pecu- liar central spire of secondary dentin which has resisted the resorbent action. Specimen in possession of Dr. A. P. Fellows. The inflammatory reaction and resorption is least when replanta- tion is practised, but may at times be pronounced in even those cases. If the socket of a tooth extracted for resorption be examined, a mass of soft tissue will be found occupying the locations corre- sponding to the areas of resorption (Fig. 572). No acid reaction can be detected with litmus paper, but, nevertheless, it is probable that the cells producing resorption excrete an acid capable of dissolving the tissue. There is some evidence of this in cases of enamel resorption occur- ring upon the crowns of impacted teeth which have never been in relation with the oral fluids, and about which there is no e\iflence of caries in the areas of dentin resorption also present. In the fortunate specimens of these cases a superficial decalcification of the enamel surface may be seen which can only occur as the result of acid action. (See p. 296.) Symptoms and Diagnosis.- — The tooth may present symptoms of non-septic pericementitis, and may be loosened in advanced cases. In the early stages no looseness may be observed until a strain 630 NON-SEPTIC PERICEMENTITIS suddenly applied causes a luxation; thereafter the tooth progressively loosens. The condition may be discovered by accident; evidences of mild pericementitis appear, and the pulp canal is opened to search for a cause. The pulp may be found alive; if aHve, and it is killed, or if it is found dead, broaches pass suddenly into the mass of soft tissue underlying the root. The progressive loosening of the tooth, with its peculiar movement, is about the only constant symptom of the condition. In cases of live pulp this organ may be hyperemic, so that increased response to heat or cold is felt; this, taken in connection with the tenderness upon percussion which can usually be elicited, and with the peculiar loosening of the tooth, is a diagnostic guide. Flagg^ stated that reflex neuralgias occur in this condition, but that the most constant indication noted by him was a sense of dis- comfort about the jaws, vaguely associated with some one tooth. The patient is convinced that if the tooth were removed relief would follow. In the absence of the loosening, which may not occur until the root is nearly gone, the resorption is most commonly discovered by entering the pulp canal and finding its length much shortened. In some cases the resorption may be found near the gum margin and simulating a cavity of decay, from which it may readily be diagnos- ticated by its appearance when exposed by packing the gum away. Such cases appear to accompany a marginal gum resorption. The a:-rays should exhibit the condition with sufficient clearness to furnish an absolute diagnosis. If a treatment diagnosis can be made, the tooth should be extracted except in the cases near the gum margin alone, which may be filled with plastic fillings. DEGENERATION OF THE PERICEMENTUM Strictly speaking, the overuse, abuse, and disuse of the teeth are catises which produce a general hyperemia or inflammation of the pericementum (non-septic pericementitis) . If continued, the inflam- mation extends into the gum tissue and a deep-seated gingivitis is produced. The results of the causes are, therefore, classiflable under either non-septic pericementitis or interstitial gingivitis. Either of these conditions renders the tissues involved liable to the degenera- tions and resorptions which accompany continued inflammation, or acts as a predisposing cause to local infection by oral organisms, ' Lectures on Dental Therapeutics. I OVERUSE OF TEETH 031 beginning its action at the gum margin, and wliich sooner or later produces a purulent liquefaction of the gingival portion of the pericementum (pyorrhea alveolaris). In view of applied therapeutics it is well to consider these causes separately. OVERUSE OF TEETH By overuse of a tooth is meant such a variety of occlusion that the tooth receives a greater stress than its neighbors, or than it is designed to bear. The stress may be received in the normal direction, but be excessive in amount. The most prominent cause of this condition is the loss of one or more other teeth, permitting undue stress to fall upon the neighboring teeth, or, in some cases, on far-distant teeth. Too prominent artificial crowns, particularly those of the all-gold type, cause a general increase of stress upon the pericementum. Enormous overfull contour fillings may establish a similar condition. When but few isolated teeth remain in one denture and have antag- onists, the teeth are certain to be overworked. Isolated and other teeth to which are attached clasps of artificial dentures or too large pieces of bridge-work, are in the majority of cases being constantly overstrained. Pathology. — Like any other functional part which is overworked, the pericementum is first stimulated, causing the vessels to dilate. Soon evidences of overwork appear, and the condition passes into one of interstitial pericementitis; the tooth projects, and is loosened; the overlying gum deepens in color, and e\'idences of venous engorge- ment are common (interstitial gingivitis). The result of the con- dition is a softening and degeneration of the substance of the peri- cementum ; the alveolar wall is involved in the degeneration, and it melts down — is resorbed to a greater or less extent. At any stage of the disturbance infection may occur, and the degeneration and destruction of the pericementum be hastened by suppuration or other secondary degenerations, establishing pyorrhea alveolus. The symptoms, diagnosis, and clinical history are involved in the description. The prognosis is the inevitable loss of the tooth if the causes be not removed, in which event the prognosis is governed by the extent to which the degeneration has proceeded. (See Interstitial Gingivitis.) These cases are often seen at a time when it is difficult to say which came first, the pyorrhea or the overwork, but the con- ditions of evident overstrian, as when posterior occlusion is largely lost, and the usually prompt response to surgical rest lead to inference that overwork started the predisposition to pyorrhea. The teeth, if in overocclusion, should be dressed off until properly 632 NON-SEPTIC PERICEMENTITIS occluded. Prosthetic appliances should not be so attached by clasps as to unduly move the clasp teeth, expecially buccolingually. The U-clasp is worthy of consideration in this regard. The appliance should support the teeth laterally, if possible, and occasionally the enclosure of the teeth by the plate clasps, with the hooks facing each other or a buccal embracing wire stay, is required, as, for example, where four lower bicuspids only are retained for support to the plate, yet where they also require support (Fig. 583). Where incisors are loose yet teeth must be inserted on plates, the judicious shaping of the natural and artificial teeth as so to afford a restraint of the natural ones against the plate festoon is useful. In some cases the festoon causes gingivitis and tend to cause loosening. This may be due to an improper looseness of the clasps permitting a rise and fall of the plate or the inner edge of the festoon requires trimming. No attempt is made, however, to cause the artificial teeth to strike before the natural teeth, in the hope of giving surgical rest to these organs. Such attempts always result in failure, as they cause injuries to the tissues upon which the plate and teeth rest, which are more severe than the pericemental disturbance. Properly adjusted bridge-work frequently does good service in these cases, provided the overoccluding tooth or teeth be first dressed down short of occlusion and are given a period of rest until the pericementum recovers. The bridge, if carefully planned, may be made to direct and control the stress received by the injured teeth. In this connection what is termed the "overarch bar" is a valuable device. The wire crossing the palate from one bridge to another on the opposite side automatically throws some of the stress received by the diseased teeth upon teeth upon the other side of the arch, which naturally are forced in an opposite direction during mastica- tion or at least lend their support. Improperly occluding artificial crowns should have this fault corrected by removing the excess of material or by setting properly made crowns. All crowns should have full mesial and distal contact, as spaces permit a wedging of teeth and injury of the interdental gum septum, as well as allow movement to occur. Overfull fillings should be reduced to correct proportions and shape. Surgical rest is the only hope of saving the tooth. MALOCCLUSION OF THE TEETH Each tooth of a denture is not only designed to receive a definite amount of force, but to receive it in a particular direction or MALOCCLUSION OF THE TEETH 633 directions; any excess of this force, or alteration of its direction, is followed by abnormal stimulation of the pericementum and by its overstraining. The efi'ects following a general increase of stress have been considered under the previous heading. By malocclusion is here meant the constant reception of stress by the pericementum in directions to which it is quite unaccustomed, or are not in accordance with the anatomical design of the tooth. It is a peculiar form of overuse. Causes. — Original malpositions of the teeth may cause their faulty occlusion. The most prolific source of the condition is, however, altered occlusion due to those changes of position of the teeth which follow upon the loss of adjoining teeth. Artificial crowns, which do not occlude in correspondence with the other teeth, are a common cause. Improperly formed fillings are another cause. The shifting of positions of the teeth, in consequence of patho- logical changes occurring in or about the pericementum, causes the crowns of teeth to occlude improperly. Pathology. — The conditions established are those of overuse in a direction other than direct. A typical example of this condition is that of a lower second molar which has gradually tilted forward in consequence of the loss of the first molar; or a central incisor which has altered its position in consequence of secondary formations in or about the pericementum, a common precursor of phagedenic pericementitis. Some portion of the tooth, an edge, which before did not occlude with an antagonizing tooth, is brought into occlu- sion; if the occlusion be not unduly forcible, no immediate degenera- tive changes are evident. If the occlusion be excessive, the peri- cementum is not uniformly affected, but the greatest stress is brought to bear upon some lateral aspect of the structure. It responds in the degree of the overwork, and inflammation and degenerative changes occur, which, if the active causes be not removed, gradually spread to other portions of the pericementum, and the phenomena noted in connection with overuse occur, but are not so general in distribution. The tooth becomes more movable in one or more directions — i. e., is loosened; it may develop some degree of tender- ness upon percussion, and the gum color toward the affected side deepens, although it may remain normal in other parts. As in the previous cases, infection may — indeed, is likely to — occur. In some cases the pericementum may degenerate and be destroyed about one root of a multirooted tooth, and remain about the other. It is to be remembered that a less degree of irritation may produce hypercementosis. 634 NON-SEPTIC PERICEMENTITIS Pyorrhea alveolaris in any form is a localized suppurative peri- cemental inflammation, with which the pericementum in general or even the pulp sympathizes in a general hyperemia or even inflam- mation. Swelling occurs and the tooth is pushed up into malocclu- sion. Such teeth may sometimes be dressed off one thirty-second of an inch before the overocclusion is relieved. A direct result of the strain and compression brought to bear upon apical tissue is the production of non-septic pulpitis with reflex pain and response to heat and cold. Diagnosis and Treatment. — In all malposed teeth a careful examina- tion should be made of their mode of occlusion. If the tooth exhibit tenderness and looseness, malocclusion is almost a certainty; it only remains to determine its direction. The spots of faulty occlusion may be determined by placing a strip of carbon paper (articulating paper) over the tips of the antagonizing teeth and having the patient bite; the spots of contact should then be ground away until the tooth is slightly short of direct occlusion. Fresh strips of paper are used, and the jaws moved laterally, as in mastication, to note other points of contact; these should also be ground away. It suffices in some acute cases to place a rubber dam or metal cap guard upon a nearby tooth for a day or two to prevent occlusion upon the sore tooth, which regains its normal position in the alveolus as the inflammation subsides. The grinding and guarding may be combined, judgment being required. Prognosi&. — If the condition be not corrected every time occasion requires, the degeneration progresses until the tooth is lost. If marginal infection have occurred, purulent or non-purulent marginal pericemental liquefaction (pyorrhea alveolaris) may have to be considered. DISUSE OF TEETH Definition. — By disuse of teeth is meant a degree of usage less than the amount, the forms, and structure of the teeth and contiguous parts fit them for. The disuse may be absolute or relative; teeth may not occlude at all, owing to the loss of antagonists or to extremely irregular positions. Partial Disuse. — Causes and Pathology. — If soft food be used instead of that requiring vigorous mastication, or if one tooth of a side be diseased so that that side of the mouth is unused in mastica- tion, or if one of the antagonists of a tooth be lost, the pericementi of the teeth involved do not receive their proper amount of exercise, and a degree of atony ensues. DISUSE OF TEETH 635 This partial disuse has a more distinct relation to the health of the gum margin, which does not receive a normal amount of friction from mastication, and if this be not offset, in part, by prophylaxis, marginal gingivitis ensues. Infection and the formation of calculus increase the irritation to a marginal gum inflammation, which is liable to run into a pyorrhea alveolaris. This is the real significance of disuse as a cause. Diagnosis and Prognosis. — A diagnosis of disuse (relative) is usually made out by inquiring as to the food habit of individuals. It is excessively common in civilized communities, particularly among the well-to-do, and is of almost constant occurrence in gourmands. Treatment. — Patients should have pointed out to them the results of insufficient mastication, together with the evils of faulty oral hygiene. Every effort should be made, by the use of constant pro- phylactic measures, to forestall the occurrence of pyorrhea alveolaris. This and similar conditions are particularly to be feared in the degenerative periods of early and late middle age. It is between the ages of thirty and fifty years that ill-consequences are most to be feared from acquired debility of the pericementum. Absolute Disuse. — Teeth which perform no work directly in mastication, or indirectly by serving as abutments for a bridge-piece, may be said to be in a condition of absolute disuse. Results. — A tooth or root whose pericementum receives no stimulus becomes relatively a foreign body to the organism. It is a useless part, and the body attempts to cast it out. Perhaps these phrases are insufficiently exact; however, a disused tooth is lost through a series of pathological changes. Teeth which perform no work may be retained in the mouths of young adults for long periods without marked changes occurring in their vital connections, but during the degenerative period of life they are usually lost with a degree of rapidity differing in individuals. The pericementum is irritated and sw^ells slightly, extruding the tooth. This is a fairly rapid process, and occurs often after the trimming of teeth for bridge-work so as to interfere with the planned occlusion, unless the bridge be rapidly made. If unopposed, it extends progressively, the neck being usually exposed, though some- times the alveolar process becomes developed and lies on a lower level as though it had followed the tooth down. Usually the bifur- cation of a molar becomes exposed, calculi form, and the extrusion becomes hastened by marginal gingivitis. The tooth may be firm, even though half its root length be exposed, though often it becomes looser than normal. Sometimes it strikes other teeth with a glancing motion. If the teeth in Fig. 574 were closer this would occur, and 636 NON-SEPTIC PERICEMENTITIS such a process (malocclusion) hastens the loosening. The opposite gum may be injured by such a tooth. Another effect is the wedging of food between the teeth owing to a favoring entrance, the laterally unsupported tooth wedging apart and then closing upon the food. This injures the gum septum. Finally the loosening or the annoyance compels the removal of the tooth. The danger of marginal infection is always great in these cases. Some degree of infection, no doubt, exists in all of them, which serves to explain the increased rapidity of the degenerations. Prognosis. — If teeth can be directly or indirectly brought into use, so that their pericementi receive exercise, the cases may recover, provided the atrophic changes are not very pronounced; in which event the atrophy proceeds, although more slowly. Teeth crowned Fig. 574 Absolute disuse and elongation of an upper and a lower molar; partial disuse of bicuspid; small abscess ca\'ity in the bone about a root. (Philadelphia Dental College Museum.) or made abutments for bridges, after degenerative changes have become established — i. e., when the normal pericementum has been replaced by a thickened mass of partially organized connective tissue — usually become progressively looser; the alveolar atrophy proceeds until all attachment is lost. If this principle be utilized early, the teeth may be saved. The results are better if the teeth or roots be utilized before the age of thirty than at later ages. Treatment. — The treatment, as might be inferred from the fore- going statements, consists in bringing the teeth into use, if the degeneration have not proceeded too far. In crowning for a bridge FIBROID DEGENERATION OF THE PERICEMENTUM 637 pier it is customary to shorten the crown to the general occlusal level, though even if a little longer and not in direct occlusion the tooth is brought into a sort of mastication which is useful if it does not introduce an element of malocclusion, i. c, if the distal or repelling strain upon its mesial slope is compensated for by the mesial strain upon a pier or piers more mesial to it or upon a pontic tooth, for example, upon the cuspid of Fig. 574, or pontic bicuspid occluding with the mesial slope of the lower first molar. In such a case as this grinding both the upper and lower molar occlusally and the intro- duction of an upper bridge is indicated. Later, extraction is inevit- able. The operation, when determined upon, should not be delayed, for not only are bacterial growths invited about the loosened tooth, but the soft tissues are frequently increased in volume, and if extrac- tion be delayed until complete local atrophy of the alveolar walls has taken place, a soft and spongy mass remains, which interferes with the comfortable wearing of prosthetic appliances in the future. FIBROID DEGENERATION OF THE PERICEMENTUM Fibroid degeneration of the pericementum is a senile atrophic change occurring in teeth, the pericementi of which have run a healthy life course, but finally have become subject to senile marantic constitutional changes of not clear nature. The condition thus first defined by Hopewell-Smith^ is further described as found in that class of teeth of the aged which have resorbed alveolar margins and exposed cementum, but not necessarily subject to pyorrhea alveo- laris; though traumatic pericementitis may be present. In some cases the teeth may be firm. Pathohistology. — The chief characteristics are an increase in size of the fibers of the pericementum, the loss of their nuclei, their generally structureless character, and their arrangement in promi- nent bundles about large spaces (areolae). (See Fig. 575.) The fibers are firmly implanted in both bone and cementum. The cementum does not become hyperplastic (hypercementosed), but the bone becomes osteoporous and the Haversian canals contain a shrunken fibroid tissue resembling that in the pericementum (Fig. 576). The gum tissue in the vicinity also undergoes retrogressive changes in sympathy, becomes less vascular and more fibroid. The condition may persist without inflammatory or suppurative ' Dental Cosmos, 1904. FiQ. 575 Fibroid degeneration of the pericementum: C, cementum; A, alveolus; F, fibers with decrepit nuclei. Transverse section. (Hopewell-Smith.) Fig. 576 A — M Fibroid degeneration of the pericementum: C, cementum; M, degenerated pericementum; A, alveolus; H, enlarged (osteoporous) Haversian canals. Transverse^section. (Hopewell-Smith.) ACCIDENTS TO TEETH 639 changes, though it may act as a cause of obscure neuralgia or as a predisposing cause to pyorrhea alveolaris. Hopewell-Smith points out that the areolar spaces ma^' admit microorganisms to deep parts, thus predisposing to antral disease or, possibly, osteomyelitis. ACCIDENTS TO TEETH Apart from fracture of the teeth by accident, several interesting accidental conditions invoh'ing therapeutics require consideration. Teeth Driven into Alveolar Process. — Blows, falls, etc., have occasionally caused teeth to be driven forcibly into the jaw. The condition may be complicated by fracture, in which case the judg- ment of the operator must be exercised. If the tooth be not frac- tured it may be drawn down with forceps and ligated in place until firm. The use of zinc phosphate upon the ligatures, if possible to use it, renders them more rigid. If evidence of pulp death be noted by subsequent test, or apical pericemental inflammation ,^the pulp should be removed. Luxation or Partial Dislocation by Accident. — Teeth may be par- tially knocked out and driven either lingually or buccally. The pulp connections will be ruptured, as a rule, but after asepsis of the parts by means of antiseptic sprays the teeth may be pressed into place, and if ligated or splinted may again become firm by deposition of bone about them. The pulps nearly always give evidence of death so that they should be later replaced by canal fillings. Mendel Joseph and Dassonville^ record experiments on dogs showing a vital attachment of the pulp of an immediately replanted tooth. They used strictly aseptic precautions. Occasionally evidences of reattachment of pulp have been recorded, - even after total displacement. If the accident result in elongation of the tooth with production of a chronically spongy pericementum, the operation of replantation should be performed. Total Dislocation of Teeth by Accident. — If the accident result in total displacement from the mouth, the tooth or teeth may be prepared as for replantation (see p. 599), and under aseptic pre- cautions replanted in their alveoli. If held by ligatures or splints they w^ill usually become firm. Attachment of Teeth. — Two or more teeth may be attached by the intervening alveolar process, fracture of which may cause both teeth 1 L'Odontologie. See Dental Cosmos, 1906, p. 1060. - Kirk and W. Trueman. 640 NON-SEPTIC PERICEMENTITIS to be removed in extraction. In a few cases of loose deciduous teeth the gum has been sufficient attachment to cause the removal of two teeth at once. In some cases the tough, fibrous nature of the pericementum causes the alveolar bone fractured by the leverage upon it to remain attached to the tooth, and Fig. 199 illustrates teeth attached by union of pericementum only. Attachment of the Alveolar Process. — Slight fractures of the alveolar plate are of little consequence, as a rule. In some cases one plate may be fractured, and unless removed with the tooth, may usually be pressed back into place. Reunion may be looked for if asepsis be maintained. Fractures of the alveolar process from blows, kicks, etc., upon the jaw may become septic and sequestra may form, necessitating removal of both bone and teeth. Such fractures should have immediate attention. Fractures of the max- illae should, of course, be immediately reduced. Hemorrhage following Extraction. — Even in the absence of hemophilia postextraction hemorrhage may be somewhat severe, and is well controlled by a little tannic acid or powdered alum and thymol upon a pellet of cotton, or nosophen gauze wet with phenolsodique. If necessary a linen compress should be placed over it and a Barton or Garretson bandage applied. The internal use of calcium chlorid or other hemostatic is indicated if the bleeding be continued. (See p. 115.) Lacerations. — The tongue, floor of the mouth, etc., may be lacer- ated by the careless use of forceps, and the lacerated parts should be irrigated with antiseptics and the mouth kept under astringent antiseptics while the parts are healing. Postextraction Alveolitis. — This has been already discussed. (See p. 604.) For ordinary transient pain, phenol-camphor with or without mentho added or equal parts of phenol-sodique and laudanum are useful. ' SECTION VI rERlCPLMENTAL DISEASES BEGINNING AT THE GUM MARGIN CHAPTER XXII GINGIVITIS The diseases which begin at the gum margin are all inflammatory, and are due to mechanical, chemical, and infective local irritants, and probably may be due to overexcitation of the gum tissues by leukomains or other toxic products which are formed intrinsically within the body in malnutritional processes, also to overexcitation by certain drugs, both of which the gum is endeavoring to eliminate. The inflammation resulting is termed gingivitis. ]\Iany mechanical or septic causes which produce pericementitis, such as overuse or apical abscess, finally induce an inflammation in the alveolar bone (osteitis), and later an inflammation of the gingival tissue. In reverse order, inflammations beginning in the gum, reach the bone, and later the pericementum. It is plain then that pericementitis and gingivitis are often associated, and at the gum margin are almost inseparable. If at any stage of a gingivitis, whether of mechanical or chemical primary causation, infection enter the inflammation becomes septic, and if pyogenic bacteria are the infective agents, pus is formed. At this juncture there is a pus flow from beneath the gum margin, usually from a pocket extending into the substance of the perice- mentum or the location previously occupied by it in the alveolus, and from this fact it is called pyorrhea alveolaris. Some writers treat of all cases of gingivitis as cases of pyorrhea, advanced or incipient, andin view of the fact that a simple gingivitis may become a pyorrhea there is some justification from a preventive standpoint; nevertheless, there are so many phases of gingivitis that for purposes of discussion and applied therapeutics it is advisable to specify the various forms that may exist. 41 642 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN If confined to the gum margin it is properly designated marginal gingivitis; if the inflammatory elements (leukocytes and exudates) have infiltrated the deeper tissues, they are usually in the connective tissues of the part, and hence may be called deeply seated gingivitis or interstitial gingivitis. If a pus flow from the alveolus accompany the deeply seated gingivitis the condition of pyorrhea alveolaris is established. With any of these conditions an hypertrophy or an atrophy may be associated, which, on the one hand, may result in hypercementosis or exostosis or thickening of gum, or on the other in resorption of gum or bone. MARGINAL GINGIVITIS Definition. — By marginal gingivitis is meant an inflammation con- fined to the margins of the gums about the necks of the teeth. Causes.^ — The causes of marginal gingivitis are local and general, which may be subdivided into predisposing and exciting. Both local and general causes may be in action at the same time. Local Causes. — Marginal gingivitis may be excited by the pres- ence of food masses or unremoved collections about the necks of teeth, their fermentation liberating chemical products more or less irritating. Miller^ has shown that the materies alba about the necks of teeth may have either an alkaline or acid reaction, and the gums be inflamed. Bacterial plaques not unlike those producing dental caries have been shown by Miller^ to be formed upon many surfaces of the teeth even when no ill results are notable. In practice staining the teeth with tincture of iodin will readily demonstrate the presence of such bacterial films. Under favoring circumstances these no doubt pro- duce marginal gum irritation, a fact proved by the relief of such a condition by prophylaxis of the teeth — i. e., the removal of the plaques. Talbot^ has demonstrated that a deep pocket may normally exist at the gum margin favoring the retention of food and other debris. Mechanical causes produce direct irritation; these are deposits of salivary calculus resting upon the gum or beneath the gum margin; fillings projecting beyond cavity margin; gum overlying cavity margins; bruising of the gum margin by food crowded between teeth and removed by toothpicks; the fermentation of such crowded food (see p. 323); the mechanical action of toothpicks or floss silk improperly crowded upon the gum margin; projecting edges of 1 Dental Cosmos, 1894. 8 Ibid., 1902. ' Interstitial Gingivitis. f MARGINAL GINGIVITIS Mo artificial crowns or bits of eemeiit used in their cementation; tooth- brush bristles; fragments of toothpicks, bones, or oyster-shells, etc.; rings of rubber or of torn rubber dam or ligatures left in position; the crowding back of a gum by ligation which produces ischemia for hours; improper contact of the edges of prosthetic plates or appli- ances about the necks of teeth; injuries inflicted by rubber dam clamps, wedges, ligatures, etc. ; the eruption of teeth through the gums. An interesting case of recurrent epileptic attacks was proved due to a toothbrush bristle forced into the gum.' The action of any of these causes may be complicated through the infection of the mechanically irritated part by oral bacteria. An excellent example occurred in the editor's practice. A perfect gum margin was irritated by the margins of a gutta-percha cap used as a remedy for hyperemia of the pulp. Pyogenic organisms produced a marginal suppuration which subsided upon removal of the cap. Excessive smoking and the use of alcoholic liquors produce local irritative effects, resulting in catarrhal stomatitis and gingivitis. Lack of exercise or brushing of the gums produces an atonic condition of the gum margin, predisposing to gingivitis of infective character. Too persistent brushing with stiff brushes may be equally injurious by causing marginal irritation. A ^'ariety of marginal gingivitis exists under the name of stomatitis ulcerosa; the cause is clearly infective, but the exact bacterium has not yet been recognized. It tends to rapidly penetrate the peri- cemental tissue. The gum margin has a pasty, sloughing appearance. The ulceration is rapidly cured by a wash consisting of mercuric chlorid in hydrogen dioxid (1 to 2000). Syphilitic chancre may begin at the gum margin and there is no reason why aphthae should not be so located though usually elsewhere. A form of phagedenic pericementitis causing very rapid destruc- tion of the pericementum and loss of the teeth without loss of alveolar wall has occasionally been noted. In one notable case two upper incisors came away three weeks after an ulceration appeared about their gum margins. The patient wore the teeth for several weeks in sifu, and could remove and reinsert them at will. The alveolar walls were bare, but intact. There was but little pain. The sockets healed after ^emo^'al of the teeth and the freshening of the bone. The clinical features of this case were entirely distinct from those of the phagedenic condition recognized as phagedenic pericementitis, and were more probably caused by the so-called stomatitis ulcerosa. Cook has shown that stimulant and astringent washes, if used 1 Dental Cosmos, 1910, p. 594. 644 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN to excess, have a degenerative influence upon the gum margin. (See p. 79.) A too powerful formaldehyd wash has the same effect. The production of deeply seated gingivitis by causes of systemic or drug origin involves a marginal gingivitis, but marginal gingivitis is not always produced by local causes of interstitial gingivitis; at least, not at first. Systemic Causes. — These are the same as for Deeply Seated Gingivitis, which see. Pathology. — The pathology of marginal gingivitis is that of an inflammation located in a peculiar situation — i. e., in the marginal gum tissue — and tending to spread into the deeper interstitial tissues. (See Pathology of Deeply Seated Gingivitis.) As shown above when pyogenic bacteria enter, a pus flow or pyorrhea is established. Symptoms. — The symptoms of marginal gingivits depend upon the cause and degree of inflammatory action. When mechanical causes are acting the gum presents an inflamed appearance; it is swollen, of a bright red or purplish color, very sensitive to touch, and bleeds readily. If a calculus rest against the gum, the latter may present a raw, chronically inflamed surface in contact with it. A ragged, red, split margin of gum is often associated with calculus upon the labial surfaces of lower incisors, cuspids, and bicuspids, and upper cuspids and bicuspids. At times the lingual surfaces of the lower incisors present such an appearance. If subgingival calculus be present, the gum margin, if markedly afi^ected, appears loosened, and is of a flabby appearance and purplish in color. In some cases the gum margin appears thickened or hypertrophied. A bloodshot appearance — i. e., enlargement of terminal vessels — is often seen in gingivitis. In cases due to unhygienic conditions — i. e., food collections or vitiated secretions about the necks of teeth — a raw, red, outer surface of the gum margin is noted, particularly in young persons. In stomatitis ulcerosa a yellow, pasty ulceration of the gum mar- gins may occur. It is rodent in character, very painful, and may cause rapid loss of the pericementum and of the tooth. In gingivitis due to oral infection by the coccus of gonorrhea an intense gingival inflammation, with looseness of the teeth, pyorrhea alveolaris, and profuse salivation, may occur.^ Talbot^ describes a greenish gray glazed surface of ulcerated ■ Vines: British Journal of Dental Sciences, 1903, and Dental Cosmos, 1903. 2 Dental Cosmos, 1905. MARGINAL GINGIVITIS 645 raw gum in two cases of profuse interstitial gingivitis due to the gonococcus. The classification of the gingi\'itis depends upon the cause and progress of the disease. Prognosis. — If the case has run an acute course and is due to the action of mechanical causes plus infection, recovery is usuallj^ prompt upon the removal of the cause and sterilization of the injured part. In the chronic cases due to the more slowly acting mechanical and infective causes combined — e. g., salivary calculus plus infection — much deeply seated gingivitis may have occurred accompanied by pericemental and alveolar resorption. This usually constitutes a permanent loss. If the gum margin is in a state of atony or inflam- mation as the result of collections of bacteria, etc., upon the crevices of the teeth, their condition may be improved by frequent cleansings of the teeth. The idea of systemic infection from the mouth is gaining such headway that it deserves increased prominence. Even should its influence be overestimated, it will serve as a strong argument in presenting the subject of oral prophylaxis to patients who unfor- tunately often require the education imparted by bitter experience in order to fully grasp its importance. Treatment. — The treatment of the condition consists in removing the source of irritation and restoring the normal circulation in the parts. If the source of the disorder be in some underlying constitu- tional condition, the symptoms may be ameliorated, although not entirely cured, by the correction of the general disorder. Cases due to mechanical irritation are commonl}^ confined to one or several teeth, rarely to an entire denture, except cases continued in consequence of deposits of scaly calculi beneath the gum margin or under plates. Foreign bodies, such as bristles and fragments of bone, should be removed. Projecting fillings or overhanging crown margins should be made flush with the general tooth surface. Salivary calculi should be removed. When food crowds upon gum margins between teeth, lateral or mesiodistal contacts should be established either by contouring filling, introducing a bridge which establishes such proximal contact, or in some cases by wedging at some con- venient point so as to crowd several teeth together, then intro- ducing a contour filhng or inlay. In some cases a small bit of iridio- platinum w'ire may be embedded in one filling and cantilevered upon another. Following this, perfect cleansing of all teeth is indicated, this to be maintained by monthly prophylaxis, at least until the case is cured. 646 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN Antiseptic mouth washes should be employed frequently, no matter what the cause. If the gum tissue be soft and spongy, showing signs of venous hyperemia, antiseptic astringent mouth washes should be freely used: I^ — Zinc, chlorid gr. x Aq. menth. pip f§j — M. Increase as desired. The above preparation, used in spray from an atomizer or if diluted as a wash several times a day, is an excellent local application, meeting both indications. Prescriptions containing eucalyptus and benzoic acid are excellent: I^ — Acid, benzoic 3 parts Tinct. eucalypti 15 parts 01. menth. pip 1 part Alcohol 100 parts Saccharin 2 parts — M. (Miller.) The above formula diluted one-half is agreeable and efficient. An alkaline 1 per cent, salicylic acid wash is useful, not only for the gingivitis, but any attendant fetor of breath: I^ — Sodii boratis 3iss Acidi salicylici gr. xv Aquae menthse pip f§iij — M. The following is astringent and antiseptic : I^ — Bo>oglycerini, Tinct. kramerise, Tinct. calendulse, Alcoholis aa f5j — M. Sig. — One or two tea.spoonfuls to a small glass of water. Truman advises the use of hydronaphthol in an astringent vehicle as an effective germicide for use by a patient : I^ — Hydronaphthol gr. x Glycerol f5j Alcohol ■. . fSj Aquae destil f5j — M Sig. — Use as a wash several times a day. (Pierce.) Talbot recommends for gingivitis the following: I^ — Zinc iodid 15 grams. lodin 25 grams Glycerin 50 grams Water 10 grams — M. (Talbot.i) 1 Dental Cosmos, 1905, p. 1312. MARGINAL GINGIVITIS 647 Apply on cotton wound on an orange-wood stick or metal appli- cator freely to all gum surfaces, and dry each after painting. The following is a 5 per cent, formaldehyd solution which, diluted, can be used as a mouth wash, having astringent and antiseptic qualities. It is also useful in various strengths as a germicide for root canals. A formula for quantity is given, which may be reduced in prescriptions: No. 1 H— Thymol 3iss Menthol 3ss Oil of eucalyptus, Oil of gaultheria, Oil of cassia, Oil of cloves aa fSiss Alcohol f?)ij— M. No. 2 Formaldehyd, 40 per cent, sol Oj Boric acid. Sodium biborate aa 5 iij Water Oij~M. No. 3 Water to ga . j. Make up No. 1 first and shake well. Place No. 2 in a gallon demi- john and shake well; add No. 1 and shake again; add No. 3 and shake well. For dispensing this may be filtered; for ordinary use this is not necessary. For mouth use one-half teaspoonful is to be diluted in two ounces of water, making a 1 to 600 formaldehyd solution. Equal parts of Listerine and ordinary distillate of hamamelis is a useful combination. Glycothymolin is a very popular proprietary mouth wash. Phenol-sodique, 1 to 7 of water, is quite useful. P'or mercurial gingivitis and stomatitis the following has been rationally recommended :^ I^ — Tinct. myrrhse fSiiJ Potassii chloratis 5ss Sodii chloridi 3ij Aquae dist q. s. ad f5viij — M. Sig. — Use as mouth wash. Repeat every two hours. All mouth washes require an application of about two minutes' duration at least twice a day after cleansing the teeth in order to produce the best effects. As this is somewhat fatiguing to the oral muscles, several applications may be made, one after the other, until the total is attained. For the restoration of gum tissue between molars and bicuspids ' Medical Press, via Dental Cosmos. 648 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN L. Ashley Faught^ has recommended a few applications of 10 per cent, trichloracetic acid on an orange-wood stick every day or two until the case is cured. DEEPLY SEATED GINGIVITIS^ (INTERSTITIAL GINGIVITIS, TALBOT) Definition. — This may be defined as an inflammation characterized by the presence in the deep connective-tissue elements of the peri- cementum and gum tissue of an excessive number of leukocytes, attracted thither by a general or local irritation of the tissue mentioned. Local Causes. — Any of the local causes producing marginal gin- givitis, if acting deeply, may produce a deepl}^ seated gingivitis. In addition to these, the eruption of teeth, the wedging of them, or their movement in orthodontia, the overuse, malocclusion, or dis- use, in short, any of the causes of pericementitis, septic or non- septic, if producing inflammation extending beyond the confines of the pericementum, are causes of deeply seated gingivitis. Pyorrhea alveolaris is a suppurative deeply seated gingivitis and pericemen- titis combined. Necrosis and ulceration following extraction cause gingivitis. Systemic Causes. — Systemic causes act to produce a deeply seated gingivitis. Drug or metal poisoning, or auto-intoxication, whether gastro-intestinal or by leukomains, and acute infectious diseases, are systemic causes. A case of spontaneous loss of all but one of the upper teeth, with subsequent complete alveolar atrophy as the result of trophic disturbance from peripheral neuritis in a tabetic woman, has been reported by Gaucher and Dobrovici,^ the diagnosis being confirmed by trophic disturbance in the foot followed by plantar perforation. It seems quite certain that in conditions of general faulty metab- olism substances are generated in the system or are retained by reason of faulty elimination, and which, floating about in the blood stream, act as irritants to the pericementi and gum margins about the teeth. Moreover, the pericemental glands seem to be eliminating organs which may become overstimulated and thus diseased. 1 Dental Cosmos, 1905. 2 The writer has introduced the term to replace interstitial gingivitis, not to multiply terms, but because it indicates fairly the anatomical situation (See p. 641.) Strictly speaking, all inflam- mations are interstitial. 3 Ibid., p. 1505. DEEPLY SEATED GINGIVITIS 649 In all general nutritional disorders parts peripheral to the circu- lation are most affected, become debilitated, and tend to a degener- ative metamorphosis of cells. Khein found, after repeated examinations of hospital patients, that "marginal gingivitis was an accompaniment of typhoid fever, tuber- culosis, malarial disorders, acute rheumatism, pleurisy, pericarditis, and syphilis, among the acute diseases. Of chronic nutritional dis- eases, it was commonly observed in cases of gout, diabetes, chronic rheumatism, several forms of nephritis, scurvy, chlorosis, anemia, leukemia, and pregnancy. Also in disorders of the central nervous system and following the administration of mercury, lead, and iodin." Rhein states that the gingivitis produced by any of these diseases has distinctive features which may even serve as diagnostic signs of the nature of the general malady. Talbot's experiments in the mercurialization of dogs (see p. 614) demonstrate that efforts upon the part of the pericementum to elimi- nate the bichlorid of mercury result in a non-septic pericementitis, exhibiting in its morbid anatomy the characteristic round-celled infiltration of inflammation. Black^ has shown that a gingivitis produced by the systemic administration of potassium iodid may be proved to be caused by its elimination by the pericemental glands by test of the gingival secretion for the iodin reaction. It is quite reasonable to suppose that irritative substances origin- ating in the body and floating in the blood stream may act in like manner. This has been termed auto-intoxication. Irritation resulting from the administration of mercury, lead, and iodin, or from toxic substances absorbed from the intestines, is, of course, extrinsic intoxication, but acts in the same manner. It has been claimed by Hunter, Herschell, Goadby, W. B. Keyes, D. D. Smith, and others, that the toxins formed by oral fermenta- tions and the septic infection of the stomach, intestines, etc., arising from the mouth are competent to excite a train of systemic dis- turbances ending in a general malnutrition. Certain accomplished cures of such states by constant oral pro- phylaxis lend plausibility if not certain proof to this argument. Still, the malnutrition, whatever its cause, oral or otherwise, may become a predisposition by lessening the resistance of the soft parts about the teeth to local irritants or add the irritation due to auto- intoxication. Talbot claims that interstitial gingivitis is largely due to auto- ' American System of Dentistry. 650 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN intoxication due to intestinal fermentation with production of by- products, notably indol, which, when absorbed, may or may not be eliminated through the eliminating organs — liver, kidneys, skin, and lungs — and that if these be insufficient to the task, retention occurs and even further disease of the organs themselves, especially the kidneys. Constipation aggravates the condition if not producing it by retention of fecal matter, with which the poisons should be eliminated. The overstrain of the kidney in the endeavor to take up the work of the liver (when that is diseased) in elimination, pro- duces renal inflammation and impairment of eliminative function. The blood is surcharged with accumulated poisons, the heart and arteries degenerate, and cardiac hypertrophy and arteriosclerosis are produced. Blood pressure is increased and end artery and nerve degeneration occur, in the brain, eye, alveolar process, pulp, etc., being noticeable first in the gums. He draws attention to the transi- tory nature of the alveolar process], and the inability of the arteries to expand, as in soft tissues, and that poisonous products settle in the end arteries, and points out that gingivitis is a natural result of these conditions. The demonstration of infarction in the pulp due to systemic conditions, even in the young, has been made by Hopewell-Smith, and also indicates end-artery strain. Talbot regards indican, the product of indol, which is found in the urine, as the excitant of gingivitis in intestinal fermentation (auto- intoxication), and the general acidosis, as indicated either by an excess of acidity in the urine or a deficiency therein, as excitant in various conditions of malnutrition. The excess of acidity above 40° in the urine indicates excessively imperfect oxidation, while defective acidity (below 30°) indicates insufficiency of renal elimination. In both cases systemic acidosis is the condition. (See p. 484.) Diagnosis of Systemic Causes. ^ — The diagnosis of systemic cause by malnutritional conditions involves almost the entire range of medical diagnosis, a subject obviously beyond the scope of this work. If local causes do not explain the oral pathological condi- tion it is well to refer the patient to a competent medical diagnos- tician for examination and treatment. Urinalysis or salivary analysis may, however, be made by either the dentist or a specialist in that work, and together with symptoms some information may be gained. Talbot directs that twenty-four-hour urine should be obtained and the following points looked for.^ (See also page 618.) Amount. — This should be about forty ounces. ■ Interstitial Gingivitis due to Auto-intoxication, Journal American Medical Association and Dental Digest, 1900. DEEPLY SEATED CI NO IV IT IS 651 Specific Gravity. — If high, it indicates an increased proportion of solids per ounce. Degree of Acidity. — If above 40° it indicates acidosis by imperfect oxidation; if below 30° it indicates renal insufficiency and retention n blood of acid products. Indican. — If present, it always indicates intestinal fermentation. Albumin. — Not of certain origin. Hyalin Casts. — If bloody, they indicate renal inflammation. Compound Hyalin and Coarsely Granular Casts and Waxy and Amyloid Casts. — Indicate changes in structure of kidney. Symptoms. — Headache, loss of appetite, loss of memory, irrita- bility, biliousness, fatigue, muscle soreness, hypochondriasis, in- somnia, vertigo, muddy complexion, tinnitus aurium, general ner- vousness, cold extremities, impotence, leg cramps, twitching of muscles, neurasthenia, pruritus, acne, urticaria, arteriosclerosis, gout, rheumatism, Bright's disease, diabetes, uric acid diathesis, nervous disorders, asthma, anemia, lethargy, stupor, insanity, etc., are symptoms which, in part, may develop from the auto-intoxication by the toxins and acidosis. (See General Malnutrition.) Unnatural odor of the breath, armpits, and thighs indicate an effort of the lungs and skin at elimination.^ FiG.'_577j Fig. 578 Fig. 579 Resorption of alveolar process due to interstitial gingiviti.s, cau.sed by marginal irritation from excessive filling material. (Radiographs by Price.) Pathology and Morbid Anatomy. — The local or systemic causes produce direct inflammation; the bloodvessels become overfull, and waste products collected in the end arteries produce local degener- ation, diapedesis of leukocytes into the interstitial submucous gum tissue occurs, and the spaces are filled with inflammatory exudate. The papillee become enlarged and the epithelial layer undergoes an increase in formation of cells (hyperplasia). The gum in consequence of these changes becomes swollen, its color deepened, and it bleeds readilv. 1 Talbot. 652 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN If the process be advanced the alveolar process is involved. After a time the effects of continued low-grade inflammation are expressed in resorption of bone or cementum, or both, or hyper- trophy of bone or cementum, or both, as the two processes may be in evidence at the same time. Fig. 580 /^^^"'' •«"'ll •■ -"i^ f'M t jto. ' :-.fi»iiivniiiJi^ ^ VBHP^ Marginal gingivitis located in septal tissue between upper second and third molar (see text). Also shows anterior drifting of second molar, due to extraction of first molar early in life. Talbot describes several forms of bone resorption occurring in interstitial gingivitis : (a) Lacunar resorption carried on by the osteoclasts normally lying upon the surface of the bone. Under irritation they increase in number and excavate irregular bays in the bone (Howship's lacunae). These are then deepened and widened, destroying areas of bone. (See p. 138.) (b) Perforating canal resorption beginning in the small canals normally perforating the trabeculse of bone in various directions and transmitting the bloodvessels from one medullary space or Haver- sian canal to another (Volkmann's canals). The osteoclasts widen these, necessarily reducing the substance of the trabeculse (Fig. 71). (c) Halisteresis ossium, beginning with a decalcification of masses of the bone, the organic matrix being for a time undisturbed, but is later removed. This is a local expression of what may occur in other bones of the body in the condition known as osteomalacia (Fig. 74). According to Talbot premature resorption of the alveolar margins, either local or general, is due to this process, called by him alveolar osteomalacia, and occurs in pregnancy or senility, as a rule. He states that the decalcified bones may be recalcified after con- finement in pregnancy, but is never restored in senility. A lesser degree of irritation may set the osteoblasts at work and cause the building up of the alveolar process, either as a restoration DEEPLY SEATED GINGIVITIS 653 of resorbed bone or as an hypertrophy of either the alveolar process or the cementum of the root (hypercementosis). Endarteritis obliterans is a thickening of the intima of an artery or capillary, due to chronic irritation, and causing a lessening of the lumen of the vessel, even to the point of obliteration of the capillaries. The blood flow is impeded and nutrition of cells impaired. Any cause of deeply seated inflammation may produce it. In all cases of chronic deeply seated gingivitis the bloodvessels are so diseased (Figs. 581 and 582). If at any time pyogenic infection occur at the gum margin, the purulent phenomenon of pyorrhea alveolaris is produced. It is to be understood that deeply seated gingivitis presents many of the features of pyorrhea alveolaris and that the latter is a gingivitis. The conditions are, however, pathologically separable. The following is a good example: A lady presented an upper first molar which had had a pyorrhea which had been cured by treatment of gum margins and the mesiobuccal root amputated. There was no longer any appreciable pus pocket, but the tooth overoccluded one-sixteenth inch and had tipped forward. It was not supported mesially or distally by adjoining teeth. It was loos- ened. The overocclusion was removed by grinding, the tooth was wedged against its mesial neighbor, and a distal amalgam filling contoured out to its distal neighbor, thus affording support in the direction of its movement in mastication. It became much firmer. The writer considers this case as presented for diagnosis one of deeply seated gingivitis due to malocclusion and non-support, and not a case of pyorrhea. In like manner each case should be considered on its own symptoms. When food enters the interproximal space it crushes the gum septum and later depresses it. The inflammation causes its absorp- tion as well as that of the bone septum, so as to leave the buccal and lingual portion higher. This may also be inflamed and further de- pressed. The pericementi of both teeth suffer necrosis to the gum level. The pocket generally finally suppurates and a lateral abscess may result from this cause. While this may be classified with pyorrhea alveolaris it seems to the writer rather a distinct form of deeply seated gingivitis, at least until the pus flow is established. The writer has seen another form of this condition in which caries at the linguocervical aspect of two molars premitted food to pack laterally (not from the occlusal), under tongue pressure. The decay proceeded up the sides of the lingual and buccal root adjoining, and a large pocket formed, the gum being stripped away. The wedging out of the gum, touching 654 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN with silver nitrate after cavity preparation, filling with amalgam, and polishing reduced the pocket to a simple one. The gum grew in as far as it could, and the part remains relatively healthy, without pyorrhetic symptoms. In another part of the same mouth pus was found exuding from beneath the ulcerated flap of gum overlying a lower third molar. Otherwise the patient's teeth exhibited no pyorrhea. Such cases might be considered pyorrhetic if pyorrhea is to include all pus flows from the alveolus, but then we must consider apical abscess such. The writer believes it better to differentiate the conditions. Fig. 581 Fig. 582 Fig. 581. — Longitudinal section of gingival border, showing round-cell inflammation, due to mercury, and extending to the inner coat of the bloodvessel, and also plasma mast cells. From a dog. (Talbot.) Fig. 582. — Endarteritis obliterans: A, adventitial E, elastic tissue between middle coat and intima; M, muscular coat: J, thickened intima. fTalbot, after Kaufmann.) In another phase of this condition in the writer's ,own mouth the extraction of a lower third molar allowed the distal cusp of the lower second molar to wedge between the upper second and third molars, so that the third molar was pushed distally, and shredded food packed in simultaneously causing extreme and annoying gingi- vitis. In such a case if grinding the cusps of the molars does not relieve, only extraction or firm attachment of the third and second molar will give relief (Fig. 580). Local Treatment. — The treatment must be directed to the removal of the underlying cause. All local causes must be removed and the teeth put into physiological use as far as possible. This includes DEEPLY SEATED GINGIVITIS 655 the rein()>al of causes of inalocclusion or overuse of the crowding of food between teeth, the removal of local mechanical irritants and infective agents. The local treatment in general rs that emj)Ioyed for marginal gingivitis or for pyorrhea alveolaris. (See p. 045; also Pyorrhea Alveolaris.) Systemic Treatment. — This, of course, depends upon the systemic condition and its causes, but if due to torpid biliary function or defective elimination with consequent retention of body products, the restoration of the eliminative function should be aimed at. In intestinal auto-intoxication impacted fecal matter should be removed by repeated injections, if necessary, of warm water, and the bow^els be kept clear by flushing with soap and water once or twice a week. The massage of the abdomen restores the tonicity of the bowels. The bile function should be restored, and the bile be increased in flow by calomel and soda, yV ^o \ gr., every hour until 1 grain is taken; to be followed by a saline laxative (as Seidlitz powder); or podophyllin, y\^ to \ gr., up to ^ gr., may be given instead of calomel. Talbot^ also uses: IJ — Aloin i gr. Strychnin sulphate So Sr. Extract belladonna i gr. Pulv. ipecac Yij gr. — M. Take at bedtime and follow w^ith a saline cathartic next morning. If the stools remain unhealthy, administer each two to four hours 2 to 5 gr. of compound lime, soda and zinc carbolate until the stools are healthy. To continue the stimulation of the liver administer bilin y ^ to \ gr. four or five times a day. The urine should be examined for evidence of established disease, and if this be found the patient referred to a general practitioner. (See General Malnutrition.) If found only symptomatic of hepatic or renal insufficiency and nutritional disorder, the amount of urine should be increased to 40 ounces by the drinking of 3 pints of water (including table beverages) per day, which will aid bow'el and renal elimination and flush tissues of accumulations, including retained acids. If the urine be abnormally acid (above 40°) administer 3-gr. tablet of lithia, sodium bicarbonate, or sodium chlorid in a glass of water four times a day. Hot or Turkish baths keep the skin free for eliminative function. Well-apportioned rest and exercise and moderate eating of proper nutritious food are indicated. (See pp. 91 and 99.) When organic disease it present the treatment should be relegated to the .medical practitioner. 1 Therapeutics and Treatment of Interstitial Ciingivitis, Dental Digest, I'JOO. 656 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN MARGINAL ATROPHY OF THE GUMS In advanced age there exists often a tendency of the gums to shrink evenly away from the enamel, exposing the cementum. Hopewell- Smith describes this as accompanied by fibroid degeneration of the pericementum (which see), and regards the latter as a purely senile change. It may be noted upon the buccal side only of a denture, and be due to vigorous brushing. It is also seen localized at cervices next to a space from which a tooth has been extracted. In one case the editor saw a slightly hypertrophied gum distinctly overlapping a cavity margin drawn back one-eight inch within a month a§ the result of extraction of the adjoining root. Fig. 583 Recession of gum in senility; beginning decalcification of cementum; alveolar resorption after extraction. (Philadelphia Dental College Museum.)' Apart from senile changes, and possibly even including them, these effects seem to be the result of an overstimulation of the gums resulting in atrophy. It may be that collections upon the teeth are in some degree responsible. The gums have, for the most part, a healthy look, but are in a condition predisposed to pyorrhea alveolaris. Treatment. — If localized and the restoration of the gum be desir- able, Harlan's method may be tried.^ (1) Cleanse the exposed tooth 1 Dental Cosmos, 1906, p. 927, and 1907, p. 598. MARGINAL ATROPHY OF THE GUMS 657 surface and slightly roughen it near the gum margin. (2) Dissect away the gum from the root to about one-quarter inch in depth, wiping the blood away carefully with mouth open until hemorrhage ceases spontaneously, or check with adrenalin solution. (3) Make three incisions into and through the gum tissue. (4) When bleeding has almost ceased fill the cuts with dried zinc iodid, allowing the blood to liquefy it so that it may be carried around the gum margin. This creates a profound irritation, which should not be disturbed. (5) The patient should use a mild antacid antiseptic wash, as of sodium bicarbonate or milk of magnesia. (6) Repeat three or four times at intervals of three or four weeks, with cuts in a new location. (7) Use silk or pure silver ligatures around the teeth under the gum for further irritation. (8) To allay overirritation paint with 1 part adrenalin and 3 parts compound tincture of iodin once in three days. Harlan states that a long time may be required in some cases. It should not be attempted over a gold filling, but an unglazed porcelain may be covered, though no attachment will exist. The principle involved is that of coaxing the gum into adherence with the roughened root, and the filling in of the cut with scar tissue. As a wash use : ^ — Hydronaphthol gr. xx Oil eucalyptus TH, x Oil cassia TTl x Alcohol fSiij Distilled water fSxiij — M. Sig. — Use freely five or six times daily, diluted, if necesary, with more water. The gums should not be brushed for several days after operating. x\void insoluble dentifrices. If this treatment be considered inad- visable the appearance in a given case may be improved by the use of a pink porcelain inlay. For general recession due to osteomalacia the general acidosis may be treated. 42 CHAPTER XXIII SALIVARY AND SERUMAL CALCULUS Calculi are more or less hard concretions found in varying situa- tions and composed of inorganic and organic matter combined in an unknown manner. As related to the teeth, calculi arise from the following recognized sources: 1. Obviously from the saliva, and deposited in situations which clearly indicate its source, salivary calculus (or ptyalogenic calculus — Peirce) . 2. From the serum of the blood deposited at some point along the side of the root between the gum margin and the apex of the root, and called serumal calculus (Black), or sanguinary calculus (Ingersoll). Of this there are several varieties: (a) That associated with a probable fermentation and an altered secretion from the gum margin, and known as subgingival calculus. (6) That occurring in situations in which a chronic pus flow is found, whether apical or subgingival, and which may be called pyogenic calculus. (c) That found upon the roots of teeth at a point to which saliva has no access and over which pus does not flow, and which is there- fore deposited by the lymph derived from the blood, and to which the appellation hematogenic calculus (Peirce) is applicable. •In this class Kirk found two varieties resulting from pericemental inflammation: (1) Subpericemental deposits, and (2) intraperice- mental deposits.^ These several names will be adhered to in further descriptions as having definite significance. SALIVARY CALCULUS Definition. — Salivary or ptyalogenic calculi are hard formations composed of salts of the saliva which have been deposited or precipitated and combined in an unknown manner with organic substances, probably mucin or globulin. 1 Dental Cosmos, 1905. HA LI VA R Y CA LC VL US 659 Fig. 584 ()ccukkp:nce. — They are found upon tlie surfaces of the teeth, notably in situations opposite the mouths of the saUvary glands, in the ducts of the muciparous saHvary ghmds (subhngual and sul)- maxillary), and upon artificial dentures. A photograph of a plate^ containing an enormous mass of calculus, the result of seven years' accumulation, is shown in Fig. 584. The teeth are occasionally buried in it. The editor extracted three lower incisors which had been wired together, and were absolutely covered from the neck to the apex l)y calculus. Varieties. — Clinically two distinct varieties of salivary calculus are recognizable: (1) The soft, friable, whitish yellow deposits found chiefly upon the buccal surfaces of the upper molars and upon the lingual surfaces of the lower anterior teeth; (2) dark-colored and hard deposits found more frequently in the latter situation, less frequently in the former. Origin of Salivary Calculus. — The origin of salivary calculus may be studied from several standpoints: (1) The formation of calculi in other parts of the body; (2) an analysis of saliva and salivary calculi; (3) extra- oral experiments upon saliva with a view to the formation of salivary calculus extra-orally; (4) the changes observed clinically in salivary calculus during its deposition. Ziegler- states that all free concretions have an organic basis or nucleus (inspissated feces, vegetable material, epithelial scales, mucus, etc.). As to cholesterin gallstones, he states that if the cholesterin be dissolved out by ether, a yellowish organic matrix remains which retains the form of the stone and presents upon examination radiating spaces formerly occupied by the crystals. He describes the forma- tion of the gallstone as an infiltration or incrustation of degenerated organic matter (epithelial scales, etc.) with cholesterin, bile pigment, etc., to which, after a nucleus is formed, other portions are added in like manner. Salivary raleulus attached to a lower par- tial plate worn seven years without removal. Shows form of sublingual space. Practice of Dr. Ford, Toulouse, France. (Specimen in possession of Philadelphia Academ.y of Stoma- tology.) ■ In posse.ssion of Academy of Stomatology of Philadelphia. ' General Patholog.v. 660 SALIVARY AND SERUMAL CALCULUS Of urinary calculi he states that Ebstein has shown an organic substance albuminous in nature to be left after dissolving out the various salts. In stratified calculi this stroma also shows stratification. Such a stroma may be seen after decalcification of a bit of salivary calculus. Analysis of salivary calculus shows it to be composed of about 22 per cent, of water and organic matter as the portion removable by burning the calculus, and about 78 per cent, inorganic matter as the portion removable by decalcification with acids. Following are the analyses of salivary calculus by Stevenson and Schehevetskey, respectively •} Soft tartar Hard tartar on on molars. lower incisors. Water and organic matter . 21.48 17.51 Magnesium phosphate 1.31 1.31 Calcium phosphate with a little carbonate and trace of fluorid 77.21 81.18 100.00 100.00 Water and organic matter 22 . 07 Magnesium phosphate 1.07 Calcium phosphate ; . 67 . 18 Clacium carbonate 8.13 Clacium fluorid 1 . 55 100.00 These observers are practically agreed upon the substances present in calculus as mainly calcium phosphate with some calcium carbonate, calcium fluorid, and magnesium phosphate combined with organic matter. Talbot furnishes the following analysis of serumal calculus by J. H. Salisbury r^ Water and organic matter 32.24 -Magnesium phosphate 0.98 Calcium phosphate 63 . 08 Calcium carbonate 3.70 100.00 To these Kirk^ adds ammoniomagnesium phosphate as a product of putrefaction. According to Mitscherlich,^ parotid saliva contains globulin, but no mucin, and contains calcium carbonate; calcium phosphate being present in but minute amount. The submaxillary saliva contains a large amount of mucin, which gives to mixed saliva its viscid nature. 'Talbot: Interstitial Gingivitis. * Ibid. 3 Dental Cosmos, 1905, p. 752. ♦ Halliburton: Physiological and Pathological Chemistry. SALIVARY CALCULUS 661 Analyses of submaxillary saliva and mixed saliva by Bidder and Schmidt gave the following results: Submaxillary Saliva Water 991.45 Organic matter 2.89 Inorganic matter • Calcium clilorid \ 4.50 Sodium chlorid J Calcium carbonate Calcium phosphate \ 1.16 Magnesium phosphate 1000.00 Mixed Saliva Water 995.16 „ . ^^ / Epithelium 1.62 Organic matter ^ „ , ui • ** t oa [ Soluble organic matter 1.J4 Potassium sulphocyanid 0.06 Inorganic matter ^ Sodium, calcium, and magnesium phosphate . . . 0.98 Sodium and potassium chlorid 0.84 1000.00 That an error of experiment or estimation exists in these analyses is shown by the fact that calcium carbonate is not mentioned as existing in mixed saliva, while it exists in submaxillary saliva; this is a physical impossibility. It is presumptive, however, that calcium carbonate has not been specially estimated. If a bit of calculus be dried and then burned at a red heat, the organic matter present will burn out, the calculus retaining its form. If a similar bit be subjected to dilute acid (1 per cent, nitric) the inorganic matter will be removed, the calculus will float to the top of the liquid, and, after a time, remain as a light stroma of nearly the original form of the piece. If a bit of calculus be transversely ground, it is seen under a low- power lens to present a laminated appearance — i. e., it has been deposited in layers representing periods of activity. The under surface of the calculus shows a concentric formation. Beneath the mass a nidus of darker calculus may be found, and if section of extensive calculi be made the greenish deposits may be seen scattered through the mass. Black has noted the presence of urates in nearly all specimens examined by the murexid test. Foreign bodies are sometimes entangled in the mass. Peirce recorded a case in which a small clasp plate was securely fastened to the teeth, and the patient denied possession of such a substitute. In some cases extensive salivary deposits are found associated with highly offensive odors — i. e., putrefaction of the organic matter 662 SALIVARY AND SERUMAL CALCULUS occurs as a part of the process — indeed, bacteria are constantly associated with the mass and may furnish their quota of the organic matter. Extraneous matters, such as tobacco smoke or other pig- ments, cause discoloration of the mass. With data relative to the physical and chemical analysis of calculi, the mode of calculus forma- tion may be studied. It will be noted that the necessary elements of calculus formation are supplied by the saliva and food debris — i. e., an organic basis is furnished in which calcium salts may be entangled, precipitated, or chemically combined. If a test-tube be filled with saliva and allowed to remain at rest for several days, a flocculent, light yellow precipitate will be noted at the bottom of the tube. If the supernatant fluid be drawn off with a pipette and the precipitate be allowed to dry, it will be found possessed of the chief characteristics of calculus — hardness, friability, a light yellow color, tenacity of adherence to objects with which it is in contact, and capability of ^"^- ^^^ analysis into organic matter and inorganic salts. The blood contains about 0.8 per cent, of inorganic salts, includ- ing those found in salivary calculi, and a certain percentage of them is also found in the blood corpus- cles. They probably, therefore, exist in body cells in some pro- portion. The salts are also taken into the body in the form of food. Their appearance in the various excretions and secretions of the body is to be regarded as in all probability an effort upon the part of the system to eliminate a superabundance of inorganic material from the body. The ingestion of quantities of animal or vegetable food rich in phosphates, or the excessive liberation of the phosphoric acid in mal- nutrition, may produce an excessive elimination of these in the excre- tions and cause a tendency to the production of calculi about thebody. This condition, known as phosphaturia, is observed in certain nervous diseases, rachitis, osteomalacia, leukemia, gout, and rheumatism,^ in which the phosphaturia is symptomatic of an excessive katabolism; also in intestinal disturbance resulting in imperfect assimilation of food. (See p. 104.) Whether taken in as food or liberated during metabolism it is probable, as pointed out by Talbot, that if one excretory organ fail A, nidus; B, calculus. 1 Thompson: Practical Medicine. SALIVARY CALCULUS 663 to perform its office in full degree another must take up its work. For this reason, in any bodily condition affecting elimination a super- abundance of inorganic salts may appear in the blood and hence in the saliva, and, probably, in even the secretions from the gingival margins. That the deposit of calculus may have some dependence upon the superabundance of calcium salts in the saliva is evidenced by the fact that in young children but little calculus is deposited upon the teeth, though the oral fermentation is not lacking. The salts are needed in bone formation. The Organic Factor of Calculus Formation. — Black^ has argued from experiment that the organic basis is probably a colloidal agglutin- ating substance precipitated from saliva in the form of small oval or cylindrical globules, made up of a mulberry mass of fine globules. This substance he has called "agglutinin." This lodges upon solid objects and the minute particles of inorganic salts are precipitated into this. This substance is coagulated (white) at 200° F., but as freshly deposited is transparent, and has a soft, greasy, sticky feel. Micro- organisms multiply in it after a time, but at first it is free from them. Black has shown that this deposit precedes the infiltration by the salts Black regards this substance as some product of faulty metab- olism, and as the determining factor in calculus formation rather than the presence of more or less calcium salts, and believes this to account for fluctuation in deposit. He found that the use once of Epsom salt as a cathartic would stop the accumulation of calculus for from a few days to several weeks, according to the condition of the patient. He regards the condition as not due to constipation, but rather due to the formation of a larger quantity of chyle than can be readily assimilated. In his own case he was able to limit calculus formation by reducing the intake of food and thorough mastication, and to bring it on at will by partaking heartily of rich foods.- Exposure of the roots of teeth, especially the lower anterior ones favors the deposition of calculus, owing to the difficulty of brushing the surfaces. ^ Items of Interest, June, 1911. 2 It is known that about one-third of calcium and other salts are eliminated in the intestinal secretion. It is therefore not certain from Black's experiments with Epsom salt whether the salts necessary for calculus formation are not so eliminated because of the stimulation of secretion from the surface of the swept and stimulated intestine. The fact that the quantity of the chyle remained the same during the several weeks of lessened calculus formation seems rather to prove that retention of some organic or inorganic factor is of more importance than the quantity of chyle formed, .\gain, a lessened ration may reduce the quantity of the factors. 664 SALIVARY AND SERUM AL CALCULUS That rest or relative quiescence of the saliva is favorable for the formation of calculus is shown by the fact that it occurs at points which are ordinarily not subjected to agitation — i. e., buccal surfaces of upper molars, lingual and labial surfaces of lower incisors. Adhesive precipitations of newly formed and very soft calculus form in these latter situations in the course of twenty-four hours. If not removed by brushing they harden and thicken. An unused side of a denture often accumulates calculus in greater degree than the side used for mastication. This does not occur, however, if the brush be used properly and equally vigorously upon both sides. Fig. 586 Fig. 587 Unclean necks of teeth, salivary calculas, and green stain. (Philadelphia Dental College Museum.) A, maxillary sinus; B, duct of Steno; C, parotid calculus; E, submaxillary gland. Burchard pointed out that irritations of various natures about the teeth and gums may by reflex action cause secretions of fluid, abnormal in quantity and quality, from both the salivary glands and the buccal parietes (glands and gum margins). It is more probable, however, that the systemic condition and uncleanliness, together with tooth form, is largely responsible. The editor has a patient who is abstemious, eats moderately, exercises indefatigably in the open air, and drinks water freely. During the golf season, when per- SALIVARY CALCULUS 665 spiration is free, he has somewhat less calculus, but always has some at uncleansed spots. This appears within two weeks of prophylaxis. An increase of oral fermentation is commonly associated with an excess of calculus formation, but conditions of oral fermentation may be seen in which but little deposit occurs. The mouths of many children are examples of this. S.L.S.L C, calculus; S. L. C, sublingual ca^^ty; S. L. GL., sublingual gland. Fig. 589 Right side, abrasion from overuse; left side, deposits due to stagnation. Calculi harden with age. It is commonly noted that soft calculus may be readily removed with a brush. Calculus deposited upon lower teeth within a week or two after a thorough cleansing may be scraped awaj' as a cheesy mass; after a much longer time it comes 666 SALIVARY AND SERUMAL CALCULUS away as a hard scale. In very old deposits it may be exceedingly hard and quite firmly attached to the teeth. These clinical observations confirm the deduction that an infiltra- tion of calcium salts occurs in the organic stroma of the calculus analogous to that occurring in dead or degenerative tissue throughout the body (calcareous infiltration or degeneration). Another theory is possible — i. e., that a firmer chemical combination of the organic and inorganic elements of the calculus occurs, density being thereby increased. The organic basis is evidently a precipitation of a col- loidal material, probably mucinous in character, upon the teeth, and into this the salts are precipitated. In the analyses furnished by Stevenson (p. 660) it will be seen that hardness is, in part at least, due to an increased proportion of inorganic elements. Fig. 590 Fig. 591 Section of a lower incisor, with a large deposit of salivary calculus impinging upon and causing inflammation of the gum. (Black.) Section of an upper molar with deposit of calculus on its buccal surface, causing inflam- mation and absorption of the gum and lower border of the peridental membrane and alveo- lar wall. (Black.) Theoretically, subgingival calculi, pyogenic calculi, and hemato- genic calculi formed within the unbroken pericementum may derive their organic agglutinating material from the secretions or necrotic tissue of the part, and their inorganic material (largely phosphate of calcium, carbonate of calcium, and sodium biurate) from the serum of the blood (serumal calculus). In the case of simple subgingival calculus the saliva may play a part by furnishing the necessary calcium salts, as claimed by Peirce, but this does not seem to be absolutely proved, nor would it seem to be necessary; indeed, in certain cases of pyorrhea pockets located about lower incisors in SALIVARY CALCULUS 667 which saHvary calculus might readily be deposited, and from which both salivary and serumal calculus has been thoroughly removed, the serumal calculus has again collected in (juantity, while the sali- vary calculus has not l)cen redej)()sited. Pathological Effects of Salivary Calculus. — In contact with the mucous membrane a salivary calculus excites first marginal gingivitis, and later deeply seated gingivitis and its effects. There is sometimes in this stage the wavy, gnawing, uneasy sensation, associated with mild inflammation, and the pulp being reflexly irritated the teeth respond more readily to thermal stimuli. The gum margin is inflamed, and occasionally pyogenic organisms cause pus formation. The gum margin recedes and coincidently a resorption of the alveolar process is produced. More calculus is deposited and the process proceeds until much of the alveolar support is lost. Microorganisms no doubt aid in the process. Fig. 592 Fig. S93 Sectional illustration of a heavy deposit of salivary calculus on a lower incisor, with partial destruction of the alveolus of the tooth. (Black.) Sectional illustration of lower incisor, with deposit of salivary calculus less heavy than that shown in Fig. 590, but with greater destruction of the alveolus. (Black.) The tooth is thus progressively loosened, first by inflammation, later by loss of alveolar process, moves about, and a resultant mechanical interstitial inflammation of the remaining pericementum occurs; as a result the membrane is thickened and the alveolar process partially resorbed (Fig. 590). Increased looseness occurs until the tooth drops out, unless mechanically held in place. As soon as the alveolar loss is considerable, infection usually occurs and suppuration may be grafted upon the results of mechanical irritation. The entire process may occupy but a few years; in other cases the atrophy of the alveolar walls is very slow. I have recently seen 668 SALIVARY AND SERUMAL CALCULUS a case like that shown in Fig. 592 on about eight lower teeth. The patient had not consulted a dentist for thirty years. Fig. 595 George H. Cushing's scalers. The forms and general character of these scalers are well shown. All the instruments except No. 6 are intended to be used with the push stroke. Nos. 1 and 2 are specially intended for application to the posterior surfaces of lower incisors; they are also admirably adapted for removing calculus deposits below the gum between molars and bicuspids, and from the posterior surfaces of the last molars. No. 2 can be passed quite to the extremity of most roots with less disturb- ance to the soft tissues than a thicker or more rigid instrument would cause. Nos. 3 and 4 are for removing deposits at and below the gum between the teeth, particularly the lower front teeth. They can also be easily used upon the sides of the roots of many teeth, being passed toward the apex of the root in a line nearly or quite parallel with that of the axes. No. 5 is intended to be passed between the lower front teeth at or near the gum and then directly upward, to remove the deposits on the proximal sur- faces. No. 6 is a hoe, and is intended to be passed quite to the apex of the roots, where a hoe is desired. Prognosis. — The prognosis of this condition depends upon the extent of alveolar atrophy. If the loss of support be not so extensive as to cause marked loosening of the tooth or teeth, the teeth may be retained for an indefinite period if they be so attached to neighboring teeth as to render them firm. If left unsupported, the pericementum is certain to degenerate, owing to the increased mobility. The alveolar atrophy will continue, and probably infection of the degenerated perice- mentum occur. Redeposit is almost certain unless all morbid conditions are removed and extraor- dinary precautions be taken as regards cleanliness, which precautions are difficult to carry out with- out the aid of a dentist. Treatment. — The treatment may be divided un- der three heads: removal of deposits, correction of the effects of their presence, and prevention of their recurrence. The sole means of removing salivary calculi should be instrumental. Flat scaler I 1 i SALIVARY CALCULUS Fig. 596 669 Fig. 597 -T^^ E. C. Kirk's scalers with dentate ends, designed to cut into calculus as well as maintain the course of the scaler upon the root side. Fig. 598 Fig. 599 No. 3 Scaler. No. 11 Darby- Perry scaler. Fig. 601 Fig. 602 Fig. 600 5 6 Pyorrhea scalers Nos. 5 and 6, revised set. S. S. White Dental Mfg. Co.'s Catalogue. Intended for use between teeth as well as for pyorrhea. i I No. 9 Darby-Perry No. 35 Darby-Perry scaler. excavator Burton Lee Thorp's scalers. 670 SALIVARY AND SERUMAL CALCULUS It is frequently recommended that mineral or some of the organic acids be used to soften the deposits or facilitate their removal. Anyone having seen a case in which a solution of sulphuric acid has been used for this purpose needs no further warning against the application Acid solutions will certainly soften the deposits, but at the same time inevitably cause a roughening of the enamel of the teeth by a solution of the calcium salts. To be sure, the acid does affect the calculus more than it affects the enamel, but the roughened surfaces of the latter not only invite widespread Fig. 603 Smith scalers. deposits of fermentable material, but render certain the more extensive accumulations of calculi in the future. After oral steri- lization the gross deposits may be removed by means of large, sickle-shaped scalers, nearly all used with a draw cut. The instru- ments should have sharp edges and be introduced beneath the deposits, so that the gum be not unnecessarily wounded. The scaling should be continued until every surface which can be cleansed by these instruments is perfectly smooth. For the approximal surfaces of the lower anterior teeth the flat- bladed instruments should be used with the push cut, or that in SALIVARY CALCULUS 671 Fig. 595 with the draw cut. Younger's pyorrhea scalers are very useful (Fig. G15). For the removal of associated subgingival calculus not too deeply placed beneath the gum a No. 35 Darby-Perry excavator is of almost universal utility. It is used with the draw cut for the most part. A l)air of them may be employed and made safe-sided by rounding one edge if desired to avoid injury of the gum margin. The back of the instrument may be sharpened to an edge for a push cut. Smith's file scalers (Fig. G03) are useful for rubbing off calculus that can not be scaled off as a flake. All of the calculi visible, and all that can be detected by their roughness, are thoroughly detached and scraped away instruments. The surfaces of the teeth are next cleansed with pumice made into a paste with glycerin to prevent spattering, and with a few drops of hydrogen dioxid for anti- sepsis; flavoring matter or cologne may be added. The paste is applied to the surfaces of the teeth with rubber cups, or Abbott's or Robinson's brush wheels, which are used to cleanse the labial, Moose-hide wheels. buccal, and such lingual faces of the teeth as they will reach (Figs. 605 to 609). The gum should not be injured. When using brush wheels it is well to apply the brush to a point away from the gum and spread the bristles against the tooth as it is carried tow'ard the gum. The second brush in Fig. 605 is the best for the labial sur- face and lingual of bicuspids and molars, and the third one for the lingual of lowTr incisors. The lingual surfaces of upper and lower incisors are cleansed wdth moose-hide wheels and wheel brushes; a finishing bur^ is useful in the removal of thinly distributed hard calculi on lingual and occlusal surfaces, especially in the mouths of smokers. The approximal surfaces of the teeth are cleansed wdth fine linen tape or flat floss silk charged with the pumice paste. More inac- cessible parts require the use of an orange-wood point mounted in a Jack porte-polisher (Fig. 610). It is advisable to repeat the polishing with precipitated chalk and the same carriers. ' Guilford Lectures. 672 SALIVARY AND SERUMAL CALCULUS After cleansing, the associated gingivitis should be reduced and the parts kept sterilized while healing by means of an antiseptic astringent mouth wash. (See Gingivitis.) If desired, the operation may be divided, the gross deposits and subgingival calculus being removed at the first sitting. After a few days' use of the mouth wash the stains and bacterial plaques upon the teeth and any overlooked deposits may be removed. Tincture Fig. 605 of iodin painted over the teeth brings the deeper stains of the collection into prominence, as does also a solution of potassium permanganate. Register states that a forcible spray of 1 per cent, hydrogen dioxid used after the application of tincture of iodin will soften the stains and render them more readily removable. The iodin is also rather germicidal. Prophylaxis. — The smoother the surfaces of the teeth are made, the longer the redeposition of calculi will be delayed. Black sug- gests the use of the syringe and plain water, a forcible stream being accurately used to wash away the agglutinin. As a means of calculus prevention it should be valuable. It is a wise measure to cleanse the teeth before any long series of operations is undertaken, and as a prophylactic measure in the SUBGINGIVAL CALCULUS 673 combat with caries and pyorrhea alveolaris the operation should be frequently performed. Indeed, the teeth should be cleansed fre- FiG. 608 Fig. 609 Fig. 610 quently, so that it may not be necessary to remove actual salivary calculus, except in those cases in which it collects with abnormal rapidity. A stick in a metal handle for self-prophylaxis is useful if the patient will use it. (See Prophylaxis of Caries and of Pyorrhea Alveolaris.) In cases of very rapid recurrence of salivary de- posits, evidence of an associated systemic condition should be sought. In this direction sialosemeiology and urinalysis may develop data worthy of attention. The systemic condition, if recognizable, should receive appropriate treatment. If not recognizable, the method suggested by Black of reducing the quantity of food and the thorough mastication of such as is taken, may be conjoined with the occasional use of Epsom salt, if further needed, asal so suggested. SUBGINGIVAL CALCULUS L By subgingival calculus is meant that form of deposit which occurs beneath the free gum margin and between it and the tooth. The jack porte-poiisher. 43 G74 SALIVARY AND SERUMAL CALCULUS deposits consist of small scales or granules, usually quite smooth and much darker (olive green) than salivary calculi (Fig. 611) Fig. 611 Fig. 612 A, subgingival calculus; B, receding peri- cementum. (Black.) Resorption of the septum of bone and re- cession of the gum between the central and lateral incisors, caused by deposits of serumal calculus under the gingivae. (Black.) Composition. — They consist mainly of calcium phosphate combined with undetermined organic substances. (See pp. 660 and 668.) Fig. 613 The alveoli irreparably destroyed by calcic inflammation. (Black.) Cause and Pathology. — It is probable that some degree of marginal gum irritation first occurs, though many cases of an apparently healthy gum with a scale of calculus beneath it are seen. Whether the irritation arises through fermentations about the unclean necks of the teeth or as the result of an effort upon the part of the gum margin to eliminate waste products from the system is not absolutely certain. The theory most tenable is that uncleanliness exists; fermentation of the mixed marginal collection and altered gum secretion contain- ing agglutinin, occurs, the gum secretion containing also calcium salts; these are precipitated into the agglutinic organic matter, forming a calculus. Fig. 282 shows a calculus on unerupted tooth root showing SUBGINGIVAL CALCULUS 675 that the blood contains the elements necessary for its formation under localized irritation. Talbot has shown that a natural pocket may exist at some aspect of the gingival space which is capable of harboring collections of foreign material. The normal gum margin closely approximates the tooth and has an apparent protective influence over the portion it covers. For some reason, such as a lack of normal friction or the presence of microbic plaques just above it, the gum may lose its normal tone and the calculus deposition be favored. Its secretion is also probably altered in quality. Effects and Symptoms. — The direct effects are exerted upon the gum margin. The mechanical irritation may cause the gum and alveolar process to undergo resorption, the calculus being exposed. At times this resorption is accompanied by evident marginal inflammation, at others the gum margin has a normal color, but the resorbing portion is sharply defined by a fine line (or crease) from the normal gum tissue, especially at the interdental septum. In a more advanced stage this demarked portion appears sunken or atrophied, and may have a sort of semihyalin redness characteristic of the inflammation. At times the gum margin appears everted (Fig. 612 a). If the deposit occur on only one side of a root the gum resorption may be confined to that side. The lingual root of an upper molar is often exposed for a con- siderable portion of its length by successive deposits of calculi. The same is true in other situations, notably upon the labial surface of a lower incisor. This might be called a form of phagedenic gingivitis. If the deposit be generally distributed about the neck of the tooth the resorption is more equalized. In some cases the bifurcation of roots may be exposed and calculi deposit in that situation. In some cases the gum margin becomes simply atonic or passively congested and is pushed away from the teeth by large masses of the calculus, which undergo lateral accretion. It appears as a flabby, thickened, loosened gum margin, which readily draws about the necks of the teeth if the calculus be removed. I have noted this in cases of suboxidation with bluish lips, and in renal insufficiency. Finally, pyogenic infection may occur about the calculus and the symptoms or pyorrhea alveolaris be implanted. When this is estab- lished, calculi may be deposited farther up the side of the root. This pathology often precedes the condition of pyorrhea ah'eolaris which may supervene if pyogenic organisms enter the area. Treatment.— The calculus should be removed by means of delicate scalers used with either the push or draw cut, as most convenient, G76 SALIVARY AND SERUMAL CALCULUS after which astringent antiseptic mouth washes should be prescribed. The subsequent frequency of removal and oral prophylaxis are of great importance. Figs. 614, 615, and 616 show convenient forms Fig. 614 5 6 9 10 II IZ 13 14 15 Younger's new set of pyorrhea instruments. (Revised by Dr. Robert Good.) Fig. 616 Tompkins' pyorrhea scalers. also useful for the deeper pyorrhea pockets. In most cases healing is spontaneous even without medication, but often the washes are of advantage. If pyorrhea be present on any tooth it is to be con- sidered separately. HEMATOGENIC CALCULUS G7' PYOGENIC CALCULUS Pyogenic calculus is that form of serumal calculus which is deposited at parts of the tooth root over which pus more or less continually flows. Talbot has shown that pus is rich in calcium phosphate. In chronic apical abscess the root end may become encrusted with it, and in those cases in which apical abscess discharges along the pericemental tract it is common to find over the area fine granular deposits which vary in color from a light yellow to a reddish brown. The same is true of active pyorrhea pockets. This calculus prevents the healthy apposition of the gum tissue to the roots, probably because of its irritant and infective nature (Figs. 537 and 617). Treatment. — All such calculi should be removed by whatever means possible, w^hich may necessitate scraping the root end or its side, or even the amputation of the apical end of the root. In some cases 25 per cent, sulphuric acid or Tartasol may dissolve it. (See pp. 597 and 702.) HEMATOGENIC CALCULUS (Syn. SANGUINARY CALCULUS) This form of serumal calculus occurs in the so-called gouty peri- cementitis, a form of pericemental abscess. It may occur in the absence of apical abscess or a primary pyorrhea alveolaris, and, therefore, at points not acted upon by saliva or pus; hence it must be deposited by the blood through the lymph. Miller^ has offered satisfactory evidence of this in a description of a case of impacted cuspid well embedded in the bone, and not in any way exposed to either saliva or pus influence except that at a point over the cusp the gum underwent suppuration for a short time. The crown had undergone resorption, showing local irritation, and an olive-green calculus had formed upon the middle third of the root. Cases of pericemental abscess have been noted opening upon the gum face and presenting dark green calculi upon the root in that situation (Fig. 282). (See Pericemental Abscess.) Peirce found in such deposits a proportion of sodium urate as shown by the murexid test and the cases associated with goutiness of the patient. While such deposits may not cause immediate irritation, they may in time excite inflammation and necrosis of tissue, resulting in a discharge of glairy material representative of the condition. This form of dental disease will be further discussed. > Dental Cosmos, 1901. CHAPTER XXIV PYORRHEA ALVEOLARIS General Considerations. — ^The term pyorrhea alveolaris means a flow of pus from a pus pocket located between the root of the tooth and the alveolar wall at the lateral aspect of the root. Apical and lateral abscess from gangrenous pulp or perforation are excluded. The latter may be more or less intact and either be exposed and necrotic or, as more generally the case, be still covered with its internal periosteum, which is the remains of the pericementum. In some cases the bone has disappeared and the gum tissue forms the outer covering. Pyorrhea alveolaris always involves the consider- ation of marginal and deeply seated gingivitis, but these need not necessarily be pyorrhea. It is therefore somewhat difficult to differ- entiate from gingivitis proper, as any form of gingivitis may later assume the characteristics of pyorrhea owing to infection. In a general way pyorrhea alveolaris may be diagnosticated when there is a progressive gum pocket formed at the expense of the lateral portion of the pericementum and the tooth becomes pro- gressively loosened. Usuallj' calculi and a pus flow are found, but in some cases neither are much in evidence. The disease ceases spontaneously with the loss of the teeth, though the alveolar process is further resorbed as after any extraction. Causes. — It seems that anything which may induce a gingivitis may initiate the process when infection is added of a character that will destroy the pericementum and produce the pocket at its expense. Therefore the causes of gingivitis are the primary causes of pyorrhea alveolaris. The gingivitis itself is the proximate predisposing cause and the specific infection is the proximate exciting cause. It is obvious that these are difficult of exact differentiation, i. e., it is difficult to say when gingivitis ceases to be such and becomes a pyorrhea, but when the pocket is established the case may practically be called a pyor- rhea, and is treated as such. From a prophylactic standpoint it is wise to remove all causes of gingivitis as it is apt to lead to a pyorrhea. ■ The causes of marginal gingivitis are mostly obvious and have been discussed. (See p. 642.) The causes of deeply seated gingivitis apart from pyorrhea are more obscure, but, as stated in the dis- GENERAL CONSIDERATIONS 679 cussion (p. 648), are either the more deeply acting causes of marginal gingivitis or are due to local or systemic causes which produce a more or less profound pericementitis or gingivitis apart from the alveolar pockets, and which have a tendency to cause inflammatory degeneration of the soft tissues and to produce a resorption of the bony tissue, thus predisposing the soft tissues to the local action of bacteria, or in other words, lessening their resistance to bacteria. Aside from inflammatory conditions actually produced by sys- temic conditions, the pericementum may be influenced by a lack of proper nutrition, as in anemia or neurasthenia or some form of systemic drain, as peripheral nutrition is evidently lessened in such states, and tissues seem more subject to infection. The opsonic index is probably lowered. (See p. 57.) Investigations as to cause have proved negative in so far as the determination of a specific bacterium is concerned. Galippe and Malassez, Miller, Black, Talbot, Goadby, Younger, Cook, and others have all failed to definitely isolate such a specific bacterium. The closest approach to a demonstration yet made was the determination by Kirk of the presence of a pure culture of the Diplococcus pneumoniae in a few cases of freshly opened pericemental abscesses (which see). The investigations of Goadby, however, do not confirm this as a cause of pyorrhea alveolaris in general, but rather point to the prob- ability that the cause may be found among other oral bacteria, possibly thread forms or some of the blastomycetes. Talbot believes the ordinary pyogenic cocci to be the cause of the pus production. Curtis^ believes obstinate cases of the disease to be either caused by or aggravated by tertiary syphilis. He bases his belief upon observations of fresh blood which, he states, upon the authority of Dr. Robert L. Watkins (New York City), contains syphilitic spores. "Egg-skin" eschar is the oral pathognomonic sign. According to Curtis, the local infection in nearly all cases is of so mixed a type as to render it at present uncertain whether the liquefaction of the peridental membrane, etc., is due directly to the pyogenic organisms present in the pus formed or to other oral bacteria of uncultivable type which may initiate the process, after which pyogenic organisms may enter and form pus. The fact that pyorrhea alveolaris is seldom found fully established before thirty years of age, but is common after that period, and that it occa- sionally occurs in youth or even in childhood associated with some pronounced systemic state or disease, strongly indicates a systemic factor in the more pronounced forms of the disease. I Dental Cosmos, 1901. 680 PYORRHEA ALV SOLARIS The type of teeth affected is usually that of the narrow-necked variety in which the angle formed by the gum and tooth is less accessible to the brush and friction of mastication. This leads both to formations of calculus and to the retention of infective material. In brief, it may be stated that the infectious nature of pyorrhea alveolaris is becoming more established, though not yet fully scien- tifically proved, and that the causes rec^uire a local predisposition for their action. This local predisposition may be the outcome of local sources of irritation and degeneration alone or be produced by waste products floating in the blood stream, etc., or by a lack of nutrition due to general causes. Clinically, fully established cases of pyorrhea alveolaris may be divided into three classes: (1) Cases associated with a primary gin- givitis and with the formation of hard, scaly, dark, annular calculi beneath the gum margin (subgingival calculus), the pockets not usually extending far beyond the deposits; (2) cases beginning with a marginal gingivitis and apparently not dependent upon the associa- tion with calculus, though frequently complicated by it; (3) cases having an apparent origin at some point between the gingival margin and the apical tissue, the gingival margin at first being apparently intact. It is probable that the infecting agents in these types differ in their nature, or that in the event that they may be proved to have a similar origin the tissues react differently to them, either partially resisting them, forming calculus as a result of the irritation, or rapidly giving way to them, permitting a deep action. In the absence of known causes the conditions may be divided according to their clinical expressions. In the consideration a pus flow due to apical abscess, lateral abscess upon a perforation, or that due to obvious salivary calculus (for these, see under proper headings), also simple gingivitis or deeply seated gingivitis, not resulting in the clinical feature of pyorrhea as defined, are excluded. PYORRHEA ALVEOLARIS BEGINNING AS A MARGINAL GINGI- VITIS AND ASSOCIATED WITH SUBGINGIVAL CALCULUS Causes. — The causes of this condition are those predisposing and exciting causes of marginal gingivitis which have been described. (See p. 642.) Several local factors have to be considered in this connection: (1) The marginal infection; (2) the irritative effects of any calculus that may be formed; (3) the deep infection by pyogenic PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS OSl organisms; (4) the modification of the progress of the disease by the attendant loosening of the teeth and deatli of the ]nilp. Clinical History, Pathology, and Symptoms. — There is usually an unclean condition of the teeth; infection exists either in tenacious films of bacteria attached to the necks of the teeth and requiring reasonably close observation for their detection, or in masses of detritus readily noticeable. Subgingival calculus is obviously pres- ent (Fig. G21). Fig. 617 Seriimal calculus, showing stalactite-like formations. (Talbot.) The gum margin may be atrophied or be inflamed ; or it may have a fairly normal appearance. When the gum margin is pressed upon, pus may be squeezed out in variable quantity. It is assumed that the local infection brings about the deposit of agglutinin (see p. 663) at a point beneath the gum margin, and that formation of subgingival calculus occurs, followed by pyogenic infection and pus formation. The gum may now be resorbed either with apparently normal bulk or the margin may be everted and thickened into a cord-like margin which is either of normal color or inflamed; the shrinkage of the gum causes the exposure of the calculus (Fig. 611). In this manner the bifurcations of the roots may be uncovered and calculi be deposited in that situation. The resorption may only be con- 682 PYORRHEA ALV SOLARIS Fig. 618 fined to one side of a root and be the result of several successive depositions which may remain when the gum recedes, or which may be removed and again be deposited. In this way the side of the root may be exposed nearly to, and in some cases quite to, the apex. The destruction of the tissues may assume several forms. In certain mouths, especially in neurasthenic and anemic patients, a viscous material may accumulate upon the necks of teeth or exposed roots; and the peri- cementum, bone, and gum may rapidly inflame and disappear, leav- ing the roots exposed to collect more of the material. The resorption may occur as shown in Fig. 619, or the gum may be split and the destruction follow the length of the root on one side only until even the apex is reached (Fig. 618). The tooth may be loose or firmly attached by the remainder of the pericementum. This is especially true of those teeth having very narrow necks, in which the roots describe a prominent curve just above the cervix. Fig. 619 Destruction of pericementum, bone, and gum over buccal root of a molar. Resorption of gum over palatal root of an upper molar, associated with but trifling deposit of calculus, but the root is covered with a viscid deposit. Age thirty-two years. Patient neuras- thenic Ejnd of tuberculous diathesis. Condition in 1904. Tooth lost in 1907. In 1912 several other teeth were lost. Fig. 619 is a model of the lingual side of the right upper teeth undergoing the former process. The left upper posterior teeth and the lower incisors have also been lingually affected. There is but little calculus, but the viscous material is quite abundant, black stain is present, and dental caries is rife. The patient has been anemic and neurasthenic for years, and one lower molar has been removed for resorption of the apices of the roots associated with looseness. PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS G83 In such cases the pus pockets may not be deep and the pus formed may readily be washed away. Such cases present some resemblance to simple gingivitis and might be so classed if there be no pus flow. Instead of this the pericementum may be progressively destroyed by suppuration and the gum margin remain practically intact. In these cases the pus flow is more abundant, a deep pocket is formed, extending a third or even two-thirds or more of the length of the root (Fig. 621). It is common to find beads of calculus deposited along the side of the root and presumably of serumal origin. (See p. 658.) The cementum being deprived of nutrition, its minute nutri- tional openings or openings containing fibers may harbor bacteria. These inflammatory disturbances necessarily involve deeply seated gingivitis or infiltration of leukocytes into the interstitial connective tissue of the gum. As pointed out by Talbot, resorption of various kinds and at times constructive changes accompany such an inflammation. (See Deeply Seated Gingivitis.) Endarteritis is also noted. These results are noted in connection with this variety of pyorrhea alveolaris. In the early stages of the disease the probe usually fails to discover uncovered alveolar bone, although it may do so. If not uncovered its loss is due to resorption; if, how^ever, necrotic and bare alveolar bone be found, it is undergoing a molecular necrosis under the influence of the pyogenic organisms. In some cases the pericementum may be destroyed at the cervical third of the root, the alveolar process may be resorbed on its inner surface, and an accompanying constructive irritation may cause the deposition of bone upon the outer aspect of the alveolar process; the gum margin is also thickened by cell proliferation. The condition imparts the appearance of hypertrophy of the gum and gum margin (Fig. 621). The inflammation of the pericementum may become general and the attendant swelling forces the tooth into malocclusion wdth its antagonist. The mechanical factor is now introduced and the extrusion increases gradually or even rapidly. Sometimes such teeth can be ground one-eighth inch before removing the excess occlusion. Such constant pounding is deadly. When about one-half or more of the root has been stripped of pericementum and deprived of alveolar support, loosensss and extrusion of the tooth become marked. The advance of the disease now becomes more rapid; the undue mobility and malocclusion of the tooth excite an inflammatory reaction beyond the directly infected part, so that soreness and looseness are further increased. Extraction at the later stages reveals a thickened apical pericementum as the sole attachment to the bone. After the looseness of the tooth becomes marked, the pulp 684 PYORRHEA ALVEOLARIS \ of the tooth undergoes hyperemic changes, reacts to thermal stimuli, and is often killed by strangulation of its vascular supply. Pulp nodules often are formed before its death. Reflex symptoms may occur at this stage when the pus pocket approaches the apex. (See Fig. 620 Fig. 621 Pyorrhea pockets. Mesial root of molar largely denuded. Treated by amputation. (Price.) Section of an upper incisor, showing at a, a, a deposit of serumal calculus within the free margin of the gum. (Black.) Pulpitis.) Infection of the dead or partially dead pulp readily occurs, and septic apical pericementitis arises. The symptoms of the latter condition are modified, according to the facility with which Fig. 622 Fig. 623 Section of an upper incisor, showing de- struction of the peridental membrane and eversion of the alveolar wall, with thick- ening of its border: a, serumal calculus; b, thickened border of the alveolar wall; c, pus cavity. (Black.) Section of an upper molar with its alveolus, etc., showing deposit of serumal calculus under the gingival borders: a, a, serumal calculus. (Black.) the pus finds vent along the pyorrhea pocket. In some cases an abscess becomes associated. The disease proceeds until the affected tooth or teeth are cast out, the alveolar walls having been largely absorbed, and the pericementum largely destroyed. The remainder PYORRHEA A LV SOLARIS AS A MARGINAL GINGIVITIS 685 of it is usually swollen. The disease ceases with the loss of the affected teeth, leaving a flattened or absent alveolar ridge covered by a mass of more or less spong}' gum tissue. The duration of this disease may be months or years, and a number of teeth may be affected at once. A general subcatarrhal condition of the mouth usually attends the disease. The presence of pus often imparts to the breath a peculiar, sweetishly fetid odor which may, however, be masked by an odor of putrefaction (pigstye or sewer-gas odor) . Fig. 624 n I^JP^H ^^^^K^v'^^^l i^feiki. ^^^^^^^1^ H ^^^^Rk^; VH^JHb ^ iKL ■IK ^KttH^P^;^. -jmS IHS m^jfti Inflammation of pericementum, endarteritis obliterans, Talbot's case. (Latham.) It is often the case that the shifting of pyorrhetic teeth permits the other teeth to move into a position in which they malocclude. This brings in a mechanical cause of interstitial gingivitis, which, with the existing infection, brings other teeth into the pyorrhetic state. Associated Abscess. — In a number of cases of deep pyorrhea pockets an infection of the alveolar structure, or, at least, of the tissue remaining over the deepest portion of the pocket, may occur, and an abscess form which discharges by a fistula through the labial or 686 PYORRHEA ALV SOLARIS lingual aspect of the gum. It is to be regarded as an abscess secondary to a primary pyorrhea alveolaris. The passage of a silver probe through the two sinuses at once will reveal this (Fig. 625). In a tooth treated for apical abscess such a pyorrhea pocket existed, and doubt arose as to the cause. The fact that it was near the gum margin and the probe could not be passed into a sinus leading to a root-end was considered evidence of abscess secondary to pyorrhea. Evacuation and antisepsis were sufficient to effect a cure. In one case of pyorrhea alveolaris of the variety under considera- tion the pocket existed upon the mesiobuccal aspect of a right lower third molar. The second and first molars were absent. The pus dissected away the periosteum of the bone and formed a large abscess over the entire area of bone between the third molar and second bicuspid. After evacuation of the abscess, the probe was passed Fig. 625 Fig. 626 Gingival abscess secondary to pyorrhea alveolaris: C, calculus in pyorrhea pocket; F, fistula leading to pocket PP; B, bone on lingual side Diagram of abscess secondary to pyorrhea alveo- laris (see text): PP, pyorrhea pocket; AC, cavity of secondary abscess: B, bone. through it to the pyorrhea pocket (Fig. 626). Another expression occasionally occurs. The infection travels via the natural channels in the pericementum from the pyorrhea pocket to a deeper point in the pericementum (for example, to a point one-quarter inch or more below) producing what is called a pericemental abscess. The tissue between may seem unbroken and the fistula may seem like that associated with chronic apical abscess. Fig. 627 will illustrate the manner in which this may occur. In a recent case of a pyorrhea pocket on a lower lateral, transillumination showed a bright red spot at a point a quarter-inch below the pocket, and to the side of the root. The pain was intense, and only relieved by opening at this point with a lancet. In another recent case a fistula appeared on the buccal gum about one-third inch above the margin and about between the buccal roots of an upper molar. The crown was tapped PYORRHEA A LV SOLARIS AS A MARGINAL GINGIVITIS 687 by a student for dead pulp, but exposure of the pulp demonstrated its vitality. Exploration showed a distolingual pyorrhea pocket leading into the bifurcation between the distobuccal and lingual roots. From thence the pericemental abscess discharged buccally between the buccal roots. Fig. 627 Pericemental abscess associated with a pyorrhea pocket. (V. A. Latham.) While dental caries may occur with pyorrhea alveolaris, it is usual to find the teeth of the most highly organized structure. The pulp tissue is usually increased in density, and there is a tendency to the constructive changes, secondary dentin, nodules, etc., and the inevitable degenerative changes following these diseases. It has been contended that these pulps are responsible in a measure for the pyorrhetic condition, and it is possible that they may, by reflex action, influence the tissue nutrition of the pericementum and gum margin, though the contrary process is more than probable, 688 PYORRHEA ALV SOLARIS as pyorrhea frequently causes a pulp hyperemia which subsides with the cure of the pocket. If the pulps be degenerated, which is likely in very loose teeth or deep pockets, their removal aids the cure of the disease by diverting the blood they receive into the pericemental bloodvessels. This probably counterbalances the effects of the end- arteritis obliterans. (See Deeply Seated Gingivitis.) It is also true that calculus does not seem to form as readily upon a devitalized tooth as upon one containing a vital pulp; it does form at times, however. Diagnosis. — The diagnosis is easily made when the disease is established by observance of the phenomena just described. In difficult cases with pocket approaching the apex or bifurcation, a skiagraph may be necessary for accurate determination of the extent of the disease (Fig. 620). A persistent gingivitis with an exaggera- tion of the space between the tooth and gum margins means, as a rule, a future pyorrhea. The same is true of a receding gum margin constantly associated with an uncleanly tooth cervix. The causes of the condition are to be removed and the patient cautioned to seek frequent dental attention as a prophylactic measure. Prophylaxis. — As outlined above, the prevention of pyorrhea alveolaris of the first class involves the removal of the local and, if possible, the systemic causes of the gingivitis, if any exists, and the systematic cleansing of the teeth at short intervals. The daily use of the tooth-brush and antiseptic powders and washes by the patient is also important. D. D. Smith advises, for this class of cases, a thorough cleansing once a month, or at first even oftener. The cleansing is to be done with an orange-wood point, grasped in a Jack porte-polisher and charged with pumice paste, best made with hydrogen dioxid. The local sources of gum infection are thus continually removed and the gums stimulated by the mechanical irritation with the wood point. Bridges require careful cleansing. (See pp. 415 and 701 for further ideas of prophylaxis.) Treatment. — The treatment of well-established pyorrhea alveolaris of the first class is to be considered under three headings: (1) The removal of pus, calculus, and bacterial films; (2) the prevention of extreme mobility; (3) the medicinal treatment and the prophylaxis, or prevention of a relapse into the diseased condition. The Removal of the Causes. — Calculus being an obvious irri- tant, it should be removed from crowns and all parts of the roots. To prevent infection of surrounding tissues and to remove the pus present the pockets are to be flushed out with hydrogen dioxid, which may be done by means of a syringe with fine nozzle or an PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 689 atomizer operated by compressed air. The forcible spray lifts away the gum margin and cleanses the pockets mechanically as well as chemically. The mouth is reasonably sterilized at the same time. If large quantities of supragingival calculus exist, it is well to next remove the gross deposits and permit the patient to use an astrin- gent, antiseptic mouth wash for a few days, or the operation may be proceeded with. Fig. 628 Showing the manner of holding an instrument for detaching calcareous deposits when using the pushing motion. The third finger rests on the edges of the teeth, allowing freedom of the hand to make rapid and effectual movements in dislodging the calculi. Following this, cotton containing 10 per cent, trichloracetic acid is to be packed into the gum pockets in order to superficially con- stringe the gum tissue, lessen the hemorrhage, and render more facile the removal of the subgingival calculi. The latter is accom- plished with scalers of any suitable form, working either with a push or pull cut as best suits the case. 44 690 PYORRHEA ALV SOLARIS Fig. 626 illustrates the method of guarding against unnecessarily wounding the soft tissues. If the calculi be extraordinarily inacces- sible the pockets may be enlarged by packing for ten or fifteen min- utes with cotton tampons saturated with the 10 per cent, trichlor- acetic acid, which also softens the calculi, or salicylized cotton may be left in the pocket for a day. (Black.) In some cases cocain injec- tions or applications of powdered cocain carried into the pocket on the working instruments must be made to prevent excessive pain. After removal of the bulk of calculus with scalers any fine granules or gummy collections should be well rubbed off with Rhein's approx- imal trimmers, or Smith's pyorrhea instruments. After this medi- cinal applications are made (see later) . The scaling of each tooth is to be completed at one sitting, though more than one may generally be done, as repeated scalings interfere with the regenerative process, and the pocket is most accessible at that time. Hartzell claims that if the cemented surface be scraped away to the depth of the attach- ment of the peridental fibers a source of infection lying in these minute openings will be removed, to the great benefit of the tooth.^ This does not necessitate much removal of cementum. Fig. 629 Fig. 630 • f I Illustration of the position and form of incision through the gum for exposing the root of the tooth Scalers (three times natural size). and injured alveolar process: a, incision. (Black.) The gum margins are not to be unnecessarily wounded, but very redundant granulations may be cut away. In case the pockets are so deep or have such form that the alveolar margins cannot be well trimmed without overstretching or injuring the gingival edges, Black advises that gum flaps be raised, exposing the alveolar margins (Fig. 630). A semicircular incision is made and turned back, and bleeding checked. By means of sharp chisels the alveolar borders are freely scraped, the pockets are flushed with hydrogen dioxid, 1 Dental Cosmos, 1908. PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS G91 and the flap secured by a couple of stitches. Cocain anesthesia should precede this operation. The same writer advises, in cases where eversion of the alveolar margin has occurred, that the process be exposed by cuts and broken down by three cuts made with a sharp chisel and mallet; the loosened segment of bone to be pressed firmly against the root. It is desired next that the entire pocket will fill with granulation tissue, and organization of the granulations take place, furnishing reattachment. That this occurs in some cases is undoubted. A reproduction of alveolar margins also occurs in some cases. The hope of good results lies in keeping the parts aseptic after all foreign deposits and dead material have been removed. In cases of excessive loss of the pericementum of one root it is well to devitahze the pulp, as, in all probability, that organ will have been overstimulated and will be in a degenerative condition, and sometimes is actually infected. An abnormal response to thermal changes (ordinary cold) may occur (hyperemia or inflammation), or the pulp may fail to respond to extraordinary cold (ethyl chlorid), indicating degeneration. If the condition be marked and persistent after pocket treatment the pulp should be removed and it is well to resort to its removal at once when the pocket approaches the apex of the root as the pulp is apt to be hopelessly affected. It has been claimed by Rhein, Smith, and others that the nutrition received by it will be diverted into the pericementum, to the benefit of the latter. Clinical experience seems to confirm this statement. The method also permits the use of pins placed in the root canal as part of an appliance fixing the teeth in position. An exposed pocket in the bifurcation may be treated by scraping and filling the same with oxyphosphate of copper cement. If the pulp be devital- ized, the bifurcation may be opened for the purpose of successfully placing gutta-percha, which is known to be well tolerated by the soft tissues (Figs. 631 and 632). Oxyphosphate of copper cement is more readily placed by flowing it in. It is also antiseptic. In case of hopeless involvement of one root of a multirooted tooth the root may be amputated if the remaining roots will endure the strain put upon them. Indeed, the other roots are apt to be firmer if the adjoining inflammation is thus removed. The canals of the roots must have been previously carefully filled. Rhein^ calls attention to the fact that collections are apt to occur about the surfaces left by the amputation, and that postextraction resorption of the alveolar process occurs. To obviate this he suggests the use of a porcelain root to replace the lost root, and about which ■ Dental Cosmos, September, 1900, and September, 1902. 692 PYORRHEA ALVEOLARIS the tissues contract firmly and remain in a healthy condition. This operation Rhein terms " heteroplasty following the amputation of natural roots." Fig. 631 Fig. 632 Pyorrhea pocket in bifurcation. The same treated by scraping and filling with gutta-percha or oxyphosphate of copper. (Radio- graphs by Price.) Fig. 633 Heteroplasty following the amputation of natural roots. (Rhein.) Briefly outlined the process is as follows : 1. Prepare and fill the root canals as far as the pulp chamber; fill this with temporary stopping. 2. Amputate the necrosed root by means of a fissure drill, and remove. 3. Coat the root with a film of paraffin to allow for shrinkage of the porcelain. 4. Take an impression of one-half of the root (longitudinally) by embedding in plaster; make articulating grooves and pour plaster I PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS f)93 for an impression of the other half; separate and remove the root from the plaster. 5. Burnish matrix platinum into each half of the impression, stiflFen with porcelain, and reburnish. Complete one side with porcelain as in inlay work, in the other fuse a platinum box formed over a square platinum pin (this pin should be left in the box until the packing of the porcelain about the box is complete). 6. Flatten the proximating sides of the halves; paint with thin, fresh body; press together and fuse. 7. Strip off all platinum and dress off all protruding points, coat the entire porcelain with a thin film of body, place in furnace in an upright position, and heat almost but not quite to a glaze. 8. Wash out socket of natural root with antiseptics and remove temporary stopping from the crown cavity; try porcelain root in place, and if right dry everA'thing; fill the box with cement, return the root to place, and pass the pin through crown cavity and into the root box. Adjust root, leaving a slight space for an amalgam joint. 9. Pack the crown cavity and the joint with amalgam, and at a later sitting finish the same (Fig. 633). The Prevention of Excessive Motion. — The excessive move- ment of loosened teeth but increases the deeply seated gingivitis in the remaining tissues. These demand rest. Any excessive occlusion due to the swelling of pericemental tissue may be compensated for by grinding the occluding surfaces. Such excessive occlusion and motion are readily detected during the' act of occluding the teeth or by means of carbon paper. The fixation of teeth is a matter of mechanics, and the device used depends upon the case. Slightly loosened teeth may be temporarily splintered with ligatures of wire or floss silk. To prevent the slipping of these toward the gum margin it has been suggested^ that small buttons of Harvard or other adhesive zinc phosphate should be placed upon the labial faces while under the rubber dam (Fig. 634). The floss silk may be saturated with a solution of chemically pure celluloid in acetone (155 to 500 gr.-) to render it impermeable and more lasting. The preparation after application is allowed to dry under the dam to a coagulum and then dismissed for twenty-four hours, when it may be polished. It lasts for several months. The wire should ordinarily be of brass, as it is less likely to permit caries, and may be applied as a single strand being woven in figure-of-eight fashion, or a single loop may be made about all the teeth to be included and smaller loops about the wire at the interspaces, and these twisted tight to effect a tightness of the first wire. The fault in ligatures is that some 1 Reitz. s Kowarska'a paste. 694 PYORRHEA ALVEOLARIS mobility is always present. They may slip toward the gum, in which case a loop or two may be carried over the occluso-interproximal embrasure. For certain cases Dr. Hugh Mitchell has suggested a bar of iridioplatinum wire adapted to the lingual surface of the teeth to be splinted, and soldered to simple gold bands to be attached with cement to two of the teeth adjoining the loose teeth. The other teeth are braced to the splint with fine wire, gold or platinum being preferred for anterior teeth. Fig. 634 Fig. 635 Temporary splint of silk floss or silver wire 30-guage (one turn only shown). Buttons of zinc phosphate. (Rhein.) Such a splint may be quickly made and is very effective, all slipping of ligatures being prevented; moreover, the wire may be kept away from the necks of the teeth and the gums. After a reason- able period of immobility the attachment secured by treatment may be tested (Figs. 636 and 637). Very loose teeth which have lost much of their supporting alveolar process must be secured by per- manent splints. The simplest of these is a series of rings soldered together, or its equivalent, shown in Fig. 635. The teeth are firmly ligated at their necks with floss silk. A wire measure is taken of the entire circumference of the teeth to be included, allowance being duly made for burnishing. A piece of thin platinum or 22 k. gold, No. 34 gauge and one-eighth inch wide, is cut to measure and a lap joint made and soldered. The ring is placed upon the teeth and moulded to their surfaces and to their interspaces. The thinnest separating saw is used to cut almost through the splint on both sides at one interspace. In this groove a straight piece of the plate is placed and the whole withdrawn from the teeth and the joints soldered. The process is repeated at another interspace and so on until the piece is complete. If the teeth are very tender, a plaster impression of the tips of the teeth may be taken and the work done on a fusible metal model. If space be necessary, the teeth may be slightly disked upon their proximal sides. If such spacing be not PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 695 desirable, the necessary room can usually be obtained at the median interspace, but one platinum septum is placed and the piece is to be somewhat stiffened with solder at the indentations representing the Fig. 636 Fig. 637 Diagram showing labial view of Mitchell's splint, with two bands and wiring. Diagram showing view of Mitchell's splint with two bands and bar. interspaces. To render the appliance less conspicuous the entire lingual side may be stiffened with solder and solder be placed liber- FiG. 638 Fig 6.39 Fig. 640 Five rings and included artificial Two rings and included artificial Method of making tooth. (Evans.) tooth. (Evans.) rings as in Fig. 538. ally at the junction of band and septum on the labial side. Nearly all the labial portions of the bands except the end ones may be cut Fig. 641 Labial view of a splint (see text). Lingual \-iew of splint shown at A. c. onnnno Occhiaal view of the splint. away, leaving T-buttons at the labial portions of the septa (Fig. 641). The teeth may loosen in this more readily than in that shown in Fig. 635. 696 PYORRHEA ALVEOLARIS Evans' method is readily comprehended by reference to Figs. 638, 639, and 640. These spHnts are to be cemented with adhesive zinc phosphate so manipulated as to set quickly. Ames' cements are excellent. The foregoing splints are too conspicuous for use in some cases. A simple device introduced by Dr. L. C. Bryan^ consists of a pure gold band about one-eighth inch wide, nicely bevelled at its edges, and adapted about the necks of the lower incisor teeth to be splinted in somewhat the same manner that the splint illustrated in Fig. 631 is adapted. Particular attention is paid to the interspaces in the endeavor to bring the labial and lingual sections together as nearly as possible at that point. When ready the piece is sprung off, the rubber dam is applied, zinc phosphate is placed within the band and upon the necks of the teeth at all points, and the band is put in place and burnished. Before the cement has set gold wire is to be passed around the interdental portions, tightly twisted, and the twisted end cut off nearly to the band, and the remainder bent back into the indentation in the band. Dr. Bryan recommended gold clamps in the place of wire, but these are difficult of adaptation. Such a piece is to be placed only on those lower incisors about which salivary calculus promptly collects, and should be avoided in the mouths of patients who will not present frequently for pro- phylactic service. Confined to such cases they do good service, and the cement does not readily wash away; indeed, a slight coating of calculus seems to protect the surface of it from solution. If the calculus be kept from the gum this remnant does no harm. Several devices have been offered which require the devitalization of the pulps and filling of the root canals of the several teeth to be splinted. D. D. Smith^ suggests reduction of the lingual surfaces of the teeth and the fitting to them of thin metal backings, which, after adaptation to the teeth, are perforated and pins are thrust through for the root canals. After soldering each pin to its plate, readapting the latter and stiffening with solder, an impression is taken and the plates are united. The whole piece is cemented to place with oxy- phosphate. A modification for vital teeth would be to drill three safe pits for pins for each plate instead of the one central pin for the canal, or to drill one hole through the incisal portion above the pulp for each plate. With this device one or more artificial teeth may be included to replace lost incisors (Figs. 642 to 644). The incisal edges, if broad, could have individual inlay casts on two safely placed pins (Fig. 277) and these soldered together. 1 International Dental Journal, 1899. 2 Dental Digest, 1902, Fig. G42 Fia. 643 Splint for securing previously treated lower Upper teeth prepared for splint. (Ames.) anterior teeth. (Ames, after Smith.) Fig. C44 Splint for use in the case shown in Fig. 643. Fig. 646 Same as Fig. 643. Splint in position. Fig. 647 Fig. 648 Fig, 645 Root with cap fitted. (Ames.) Fig. 649 Tooth with Richmond cap. (Ames.) Splint for lower incisors. (See text.) (Ames.) 698 PYORRHEA ALV SOLARIS Ames^ suggests that in certain cases of lower incisors the teeth be devitalized and amputation be performed at the neck of each. Each root is then trimmed and fitted with a gold Richmond cap without pin (Fig. 645). Each natural crown is slightly trimmed and fitted with a gold Richmond cap with a pin (Fig. 647). These two caps are united with wax, carried to the mouth, and adjusted in position (Fig. 648) . Each Fig. 650 Splint for lower incisors. (See text.) (Ames.) Fig. 651 Splint and double saddle bridge combined. Front view. (Ames.) is then carefully removed, the natural crown laid aside (in water), and the gold sections invested and soldered together. The individual parts are readjusted in the mouth, an impression taken, an invest- ment made, and all soldered together. The natural crowns are then fastened in their prepared sockets with cement, and the piece 1 Dental Cosmos, 1903. PYORRHEA A LV SOLARIS AS A MARGINAL GINGIVITIS 699 is cemented to place. Pins may be placed in the roots if desired (Fig. 649). If desired the piece may be further attached to the adjoining teeth by means of the Ungual plate and pin (Fig. 650). The Ames device would be useful in cases in which approximal cervical caries exists. It may be stated that three or four teeth fairly loose individually when united together may, as a whole, be quite firm. Ames further suggests that in case the pericemental attachment is hopelessly lost, such teeth may be extracted, the roots amputated, and prepared as for replantation, and then adjusted in the gold bridge, otherwise made as above described. These roots are to go in their own sockets, and, being firmly fixed in position, the tissues settle about them. Ames claims that the extension bridge shown in Figs. 651, 652, and 653 lasted for years and was in as good condition then as at the beginning. Fig. 651 gives the anterior view. Fig. 652 that of the right side, and Fig. 653 that of the left side. Fig. 652 Fig. 653 Right side of extension bridge shown in Fig. 647. Left side of extension bridge shown in Fig. 647. Rhein offers the following: After pulp removal and root filling a transverse groove is cut in the lingual side of the central or loose teeth and a half-groove upon the mesiolingual aspect of the pier teeth. A staple is formed of triangular iridioplatinum wire to fit into the root canals of the pier teeth. To this is soldered a pin for each of the central teeth. The face of the wire should approximately fit the bottom of the groove (Fig. 654). Rhein suggests the following method of attachment: (1) Fill the root with a paper point, place cement over that, and fill the cervical margin of the cavity and its floor with gold ; (2) drill through the gold to the paper point, remove it, and refit the retaining appliance; when ready set with zinc 700 PYORRHEA ALVEOLARIS phosphate, avoiding excess; (3) when this is set cut away to the gold and complete the gold fillings. A less elegant but still practical method would be to cover the pins with a good, color-keeping amalgam pressed into the excess of cement before it has set. The margins are then to be freed of cement and the operation completed with amalgam, which later should be polished. Smith's, Rhein's, and Ames' devices permit the use of an artificial tooth if necessary. The same may be said for the device which consists of a series of gold rings (Evans'). For the molars and bicuspids Rhein's device is transferred to the occlusal surface (Fig. 655). Short metal caps made for the incisal tips of lower incisor teeth adjoining a space will successfully hold a bridge tooth. The device is, however, rather conspicuous. Gold inlays joined by solder or cast together or a staple in two or more roots of different teeth about which staple fillings are later built may be useful. Carmichael attachments will serve for some teeth. For the molar and bicuspid teeth it seems good practice to adapt short crowns to the teeth trimmed only to the fullest point of con- tour, and unite these with solder. A sort of bridge is thus made which causes the teeth to be firm even if all are originally loose. It is mainly this factor which renders bridge-work useful in pyor- rhea alveolaris upon isolated teeth. If the necks of such teeth are hypersensitive, silver nitrate may be used (Fig. 656). The use of united barrel crowns reaching the gum margins is at times useful, but the configuration of exposed roots may render this impossible in some cases. By the use of pure gold crowns, which may be stiffened occlusally with solder to gain strength, better adaptation at cervical portions may be obtained by hand burnishing after cementation of the piece. All appliances cemented to the teeth and having a free margin are subject in some degree to a solution of the cement.. These cases should be seen frequently in any event for prophylactic purposes, when the condition of the appliance may be noted. Extraction and bridge-work may be at once resorted to in some of the aggravated cases, though if the appliance be mechanically con- structed teeth which may be extracted with the fingers may be firmly held in splints for years. While this is a fact, good judgment may demand the early removal of such teeth before an appliance is constructed. E. Ewing Roach^ has suggested that in case of loose incisors drill 1 Dental Cosmois, 1908, p. 65. PYORRHEA ALVEOLARIS AS A MARGINAL ClINGIVITLS 701 holes may be made from mesial to distal or the reverse, and a plati- num wire, 18 or 20 gauge, be cemented through the several teeth. The cases must, of course, be selected. If desired the bridge may be made so as to mount the natural teeth after their extraction, by constructing sockets of gold for the recep- FiG. 656 Permanent splint for cases of pyorrhea alveo laris on molars and bicuspids. Permanent splint for cases of pyorrhea alveo- laris in upper or lower incisors. (Rhein.) Fig. 655 tion of the necks of the teeth somewhat after the manner em- ployed in the Ames method. The sockets are then soldered to each other and to the bridge piers, after which the teeth are attached. These sockets are to be made deep at first, and it is well to at- tach the teeth with gutta-percha in order that the row of sockets or a new row may be lowered to fit the gum if desirable. This will require the raising of the teeth to the occlusal level. Occasionally the use of the overarch bar is demanded to prevent the overuse of the teeth acting as piers for bridge-work. The lateral support of teeth by plates is occasionally of use in pyorrhea, but the question requires careful consideration. (See p. 632.) The prevention of mobility in advanced cases may be at times an impossibility. In such case extraction, and the use of artificial teeth, is probably better judg- ment than the retention of the teeth until extracted one by one. The Medicinal Treatment and Prophylaxis. — Simple cases often heal spontaneously after thorough work and antisepsis. If aseptic a clot drawn after the irrigation of the pocket with hydrogen dioxid is often useful. In a few days the inflammation subsides. In order to control the patient and watch the case, any pocket existing after a week should be washed out with hydrogen dioxid and then filled with balsam of Peru which can be kept ready at hand in a Safety Sub. 2 syringe. This substance is a mild antiseptic stimulant of a viscidity sufficient to fill the pockets even though wet if the needle is inserted to the bottom. Thereafter it should be used once or twice a week. 702 PYORRHEA ALVEOLARIS If the case refuse to heal there may be calculus overlooked upon the roots. An acid is used to soften this if not removable by instru- ments. Head recommends the use in the pockets on each fourth day of ammonium bifluorid^ as a solvent of calculus and tissue stimulant. It does not dissolve enamel or cementum. The tissues are to be protected against burns from any overflow which must be removed. It produces no harm "s\dthin two minutes. It is to be injected with a rubber syringe with a platinum point (Dunn syringe) . Lactic acid full strength (Younger), trichloracetic acid, 25 per cent, strength (Kirk) ; sulphuric acid, 25 per cent, strength (Triunan) are all solvent for tartar and stimulant germicides if infection con- tinues the ulceration. As an astringent antiseptic zinc chlorid deliquesced, or sulpho- carbolate of zinc in 10 per cent, solution, or ziric iodid in 10 per cent, solution, or copper sulphate, 10 per cent, are all useful. As an astringent lotion, zinc chlorid, gr. x to each fluidounce of aquae rosse, aquae gaultheriae, aquae menthi piperitae, etc., may be applied by the patient daily on a cotton swab made by rolling cotton on the end of a tooth pick. It may be diluted to an agreeable astringence for a mouth wash (or two-minute bath), or tincture of iodin may be applied every other day, or iodoglycerol (see p. 646) may be painted upon the gums. Gentle massage of the gums by means of the finger-tips stimulates the tissues and squeezes out secretions. If common table salt be used in conjunction the stimulant antiseptic effect is obtained. Powdered sulphur is recommended by Gordon White instead. The use of a strong stream of water from a syringe is recommended by Black to wash away the agglutinin collected. Dr. A. B. Harrower has suggested the following formula for a powder which has in his own and my hands given good results as an astringent antiseptic: 3 — Magnesium carbonate . lb. j Cream of tartar lb. iss Red cinchona bark gij Calcined alum §j Oil peppermint f3v Oil cinnamon fSiiJ Oil rose geranium f3j All ingredients to be finely powdered. The oils are to be added to the magnesium before thorough mixing of the powders. The whole is to be sifted through silk. Saccharin may be added to the above as a sweetening agent. The powder when wet is almost neutral, and should do no harm in its limited use as a therapeutic agent. ■ "Tartar Solvent," or " Tartasol," is made by neutralizing hydrofluoric acid with ammonium carbonate, filtering, evaporating to half the bulk, adding again an equal bulk of hydrofluoric acid, and again evaporating to one-half bulk (at 90° to 105° F.). (Items of Interest, 1909, p. 175.) PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 703 Black has recommended the use of the 1—2—3 mixture, or phenol- camphor, to be put into the pockets every three days, and a few drops to be used on the tooth brush. 3 — Oil of cinnamon 1 part Carbolic acid 2 parta Oil of gaultheria 3 parts. I{ — Gum camphor, Crystal carbolic acid aa q. s. Mix in a mortar to an oily fluid. Regeneration in the pockets should not be disturbed, so that unless the pus flow be active one should wait until sufficient time has been afforded (about a week or ten days) for granulations to form. If pus be then detected the pocket should be again treated thoroughly. Good results are obtained from the use of an astringent antiseptic wash used in forcible spray from an atomizer or introduced by means of a syringe. This should be done daily by the patient. Stagnant fluids in the pockets are washed out and replaced by the antiseptic, thus inhibiting the bacterial growth in the pockets and the mouth. The teeth should be cleansed after meals to prevent media for infection lodging about the interstices, after which the antiseptic spray will aid in inhibiting bacteria. If the case still refuse to heal Beck's bismuth paste may be used. 3 — Bismuth subnitrate 30 parts White wax 5 parts Paraffin 5 parts Vaselin 60 parts Mix while boiling. It is injected from a syringe kept for the purpose. Good results from the application of the .r-rays and high-frequency currents have been claimed by Parker,^ Price, Guy, Satterlee, Tousey, and others. The local treatment outlined must first be given and the a:-rays and high-frequency currents used as an adjunct. Tousey recommends an .r-ray tube made of lead glass except for a single window of ordinary glass, through which the rays pass in one direction only, and thus both patient and operator are protected from the unintentional action of the rays. Applications of a minute or two have beneficial effect. The high- frequency currents are applied by small vacuum tubes or electrodes directly to the gums. They contain and emit violet and ultra-violet rays, which not only stimulate the part through the electricity, but ' Dental Cosmos, December, 1903. 704 PYORRHEA ALV SOLARIS also produce ozone upon the gum surface and carry it in and also produce ozone in the tissue by electrolysis. Good results have been obtained in some cases by extraction and replantation, after root preparation and sterilization of the tooth and alveolus. The alveolus may have to be deepened. An effort has been made to utilize the opsonic index in the diagnosis of pyorrhea alveolaris and its treatment by means of vaccines prepared from the variety of germ found to be the probable infection. It may be stated that the effort is to raise the opsonic index, or, in other words, the property of the blood serum which assists or promotes phago- cytosis, so that the infection may be killed out. That is, the resistive force of the patient to the particular infection is raised. (See p. 59.) If the interstitial gingivitis underlying the case be of systemic origin — i. e., due to auto-intoxication from any disease, the alimen- tary canal, the pyorrhea itself, or to drug action — these should have attention. The systemic disease should, if possible, be cured by correct medical attention. Pyorrhea patients are of the hyperacid type (Michaels), and treatment should be directed toward elimina- tion of waste products and the reduction of hyperacidity by the use of alkaline remedies. The bowels should be kept active and the skin pores open. Brisk exercise in the open air, if not specifically contra- indicated by organic disease, is valuable in both directions. Warm baths followed by cold douches and vigorous rubbing stimulate the skin. Turkish baths followed by massage directed to stimulation of the eliminating organs are valuable unless contraindicated. Free drinking of pure water is necessary to the successful elimination of the waste products of the body. The water entering the blood increases the blood pressure and flushes the tissues and the kidneys, dissolving waste products. Water should be freely taken between or before meals in order that digestion be not interfered with, and if medicated with salts of lithium the alkalinizing effect and solvent action of lithium upon urates are obtained. Patients exhibiting an aversion to water drinking are more apt to take it when medicated than as a physiological necessity. (See also pp. 99 and 655.) The prophylaxis of pyorrhea alveolaris is all important, especially in the cases of systemic origin in which chronic disease or mal- nutrition may not be readily overcome owing to confirmed habit of life or advanced stage of disease. The local conditions existing even after a cure of pyorrhea are such as to invite reinfection, and the establishment of microbic plaques, which frequent cleansing of the teeth will remove. The system of monthly or, if necessary, more frequent cleansing abvocated by D. D. Smith should be practised. Its good results are particularly manifest in this class of cases. Also SYSTEMIC EFFECTS OF PYORRHEA ALVEOLARIS 70o the use of the prophylactic stick by the patient twice a week and the careful and proper use of floss is very beneficial. The patient performs these manipulations with difficulty, and is apt to backslide. (See p. 419.) Recurrence of the condition is probable if the oral prophylaxis or systemic treatment be neglected. The simpler cases yield quite readily; the advanced ones, in which much of the alveolar process is lost, and especially when the gums are flabby and admit food to the pockets, tax the patience of operator and patient alike, and are apt to end, sooner or later, in loss of the teeth affected. This fact, however, should not prevent the retention of these teeth by every means at command during the period for which they may be made useful. If, however, any tooth prove an incurable source of pus formation, or from the first be likely so to do, it should be removed, otherwise the remaining teeth are continuously infected. SYSTEMIC EFFECTS OF PYORRHEA ALVEOLARIS It has been abundantly shown by Hunter and others that the pus of pyorrhea and other intense oral sepsis is a source of systemic infection, producing effects ranging from gastritis to actual septic infection. The importance of this fact is not to be lost sight of, and patients are to be informed of the dangers of constant pus formation, as well as of the presence of other forms of sepsis about the mouth and teeth. R. D. Watkins, M.D., has examined the blood of pyorrhetic patients, and has found a mild condition of septic blood similar to but less than found in puerperal fever and advanced carcinoma and in other infective conditions.^ Goadby^ reports the cure of a case of profound muscular weakness, mental depression, and insomnia after unavailing general medical treatment for neurasthenia, as following the extraction of teeth aft'ected by pyorrhea. VaneP cites a case of chronic septicemia with symptoms of pallor and asthenia, and ecchymotic patches (see p. 113) on the legs, associated with pus formation about the roots of teeth. The symptoms disappeared in a few wrecks after the oral treatment. Hunter and Leith* have described cases of subacute and chronic catarrh of the stomach and phlegmonous gastritis due to the ' Items of Interest, 1904. 2 International Dental Journal, July, 1902. ' Dental Cosmos, 1908, p. 192. * Transactions Odontological Society of Great Britain, International Dental Journal, 1899. 45 706 PYORRHEA ALV SOLARIS ordinary pyogenic cocci, such as are found in the mouth, and which the gastric juice of the stomach of the particular individual at least was not competent to kill. Considering the fact that an oral subacute catarrhal condition is established in pyorrhea, the local transfer of the infection is not surprising. Park^ believes many cases of appen- dicitis to be due to oral infection. Kirk adds to this list pernicious anemia, bronchopneumonia, malignant endocarditis, pyemic lymphadenitis, etc., as possibilities of secondary infection or extension by natural contiguous channels. HartzelP claims that three deaths from septic endocarditis were traceable to violent pyorrhea. D. D. Smith^ claims to have cured cases of confirmed nervous dyspepsia, nervous prostration, and other local and systemic con- ditions simply through constant dental prophylaxis. The thorough removal of causes and treatment of the systemic condition consequent upon them is the indication. PYORRHEA ALVEOLARIS NOT DEPENDENT UPON CALCULUS FORMATION A form of pyorrhea occurs in which calculus does not seem to be the exciting or contributory cause. It seems rather to be due to infection localized in soft bacterial collections in localities protected from ordinary friction. Sometimes no perceptible calculus can be found upon the roots, but a soft gummy collection may be noted. The forms of the necks of the teeth readily permit bacterial collections and the infection causes a bright red marginal gingivitis. A pocket forms and the infection becomes deep. The gum tissue is sometimes destroyed between two teeth. There is often evidence of infection of other gum margins with the bright red color. In another form the gum margins are separated from the teeth. Pockets are formed which collect food. There is not much pus apparent, but there is a pig- stye odor of putrefaction. The marginal bone is lost. In another form a deep pocket forms and necrotic bone may be found. The advance of the disease is sometimes rapid and sometimes not. Sometimes a lateral abscess is associated with it. The diagnosis is that of pyorrhea alveolaris of aggravated type, and probably special infection, and its progress, symptoms, and treatment are practically the same as in the first class. 1 Surgery by American Authors. 2 Dental Cosmos, 1908, p. 340, s Proceedings Philadelphia County Medical Society, 1903. PYORRHEA ALV SOLARIS 1{)1 The advance of the case may be very slow and limited to the teeth originally involved. The following is an example: ]\Iiss H., aged twenty-five years, presented with well-established pockets, extending one-half inch toward the apex, upon the mesial aspect of the root of the right upper central incisor and distal and distobuccal aspect of the right upper lateral incisor. There was a history of traumatism due to violent and persistent wedging with rubber at about the age of sixteen. The case was then of several years' standing, and the two teeth elongated about one-eighth inch beyond their fellows (Fig. 657). There was no subgingival calculus. The pockets were treated with some benefit, and the teeth shortened for the cosmetic effect, but the patient left the city suddenly before Pyorrhea alveolaris without calculus. Pockets as shown. Teeth were one-sixteenth inch longer, but have been shortened. Practically no calculus and but slight flow of thick, creamy pus. Gum prominent over affected teeth. Condition in 1904. recovery, and was not seen again for three years. At this second visit it was found that the pockets were nearly the same as at first, and no other teeth had become involved. Xor had the teeth further elongated. During the four years from 1904 to 1908 elongation and grinding reduced nearly all the crown of the lateral, which had one-quarter inch of its root cervix exposed. Coincidently with the exfoliation the pockets have disappeared as though by a drawing up of the bottom, but the teeth are doomed and only retained because of the obstinacy of the patient (only the central remains in 1912). The consideration of this form of pyorrhea should be that it is specially virulent. CHAPTER XXV PERICEMENTAL ABSCESS In comparatively rare cases there begins in the lateral aspect of a pericementum a swelling which finally discharges its contents either at the gum margin or directly through the gum tissue. The pulp of the tooth may be perfectly vital and the attachment at the gum margin at first at least practically unbroken. A deposit of calculus may or may not be formed in the area, and the discharge may consist of a glairy mucus or of purulent matter. Cases of this disease have been noted and described by Darby (1874), W. E. Walker (1895), Talbot^ (1896), D. D. Smith (1897), and Kirk (1898). Black claims that he has never found such a condition without local injury. Forms of Pericemental Abscess. — There are four forms of perice- mental abscess as described and seen: 1. An ordinary pyorrhea begins at the gum margin and extends into the alveolus at the expense of the pericementum. The bacteria find their way to the bottom of the pocket or into the tissue at its side. They develop in the said location and the pus burrows into the lateral gingival tissue, causes swelling and pointing, and dis- charges at the lateral gingival aspect or analogous situation. (See p. 685.) This is not always opposite the gum orifice of the pocket. (See Figs. 625 and 626.) In one case a fistula was found at the buccal aspect of the gum opposite a point midway between the buccal roots of an upper molar at the middle third of the roots. The pulp was exposed and vital, having been drilled to on the supposition of its death. A gum pocket was found at the distolingual aspect of the lingual root and the pus had burrowed into the bifurcation between the lingual and distobuccal root, and discharged as stated, remaining as a chronic abscess. 2. There is a pyorrhetic condition at the gum margin; later an abscess develops on the lateral aspect at a point a little higher up toward the apex, usually at the gingival third. There may be no detectable connection between the two, but probably a deeper infection has occurred, the avenue being along the connective tissue 1 International Dental Journal, 1896. PERICEMENTAL ABSCESS 709 spaces, the bloodvessels or the glands of Black. In one case of this sort the fistula was formed over the highest point of the middle third of the root of a cuspid retained for plate work. The gum margin was flabby, but not markedly pyorrhetic. There was firm tissue at the bottom of the pocket on all sides. The pulp was vital. Examination showed a small calculus on the root surface below the fistula. The abscess tract was limited. Sometimes it is of greater extent. 3. An acute swelling occurs over a root, the gum margin is un- broken, a discharge of glairy or purulent material occurs, and a calculus or none may be found. In this connection Fig. 282 shows that a calculus may exist as a primary cause of the pericemental abscess. As calculi of gouty (sodium bi-urate) or other origin occur in other parts of the body and in the pulp, there is no valid reason why one should not occur in the pericementum or upon the root under it if some sluggish condition of the circulation renders the tissues into a degenerative state favoring it. (See p. 82.) The peri- cementum contains white fibrous tissue which is particularly prone to such deposits. Whether such a deposit occurred primarily in the case of the cuspid described under Class 2 and infection followed, or whether the infec- tion and pus came first and the calculus followed is not quite clear. In two distinct cases, with healthy gum margins, the editor has seen an acute circumscribed swelling which was not yet open as a fistula and which was perforated by an explorer, disclosing a loss of alveolar bone and a small cavity filled with clear liquid in the tissues. The explorer reached the root without obstruction, and no calculus was present. After discharge and curettement the cavities healed. These two swellings looked like blisters or simple cystic swellings near the gum margin. If they had discharged at the gum margin they might have produced a gum pocket simulating pyorrhea. 4. In some cases of apical abscess the infection may travel along the pericementum and develop a secondary abscess at some point in the pericementum (as, for example, the bifurcation), as a perice- mental abscess. This form corresponds to the cases of Class 2, but is apt to be more acute. It is also quite rare. The pulp is, of course, dead, at least partially in such a case. The subject of pericemental abscess is in some confusion because writers have described all these varying phases as pericemental abscess, which indeed they are, yet they require differentiation into: 1. Cases occurring as a sequel to a distinct pyorrhea alveolaris, Class 1. 710 PERICEMENTAL ABSCESS 2. Cases associated with marginal pyorrhea cases but distant to them in all probability, having a source of infection in the pyorrhea pockets, Class 2. 3. Cases beginning on their own account the relation of the calculus if present as a cause or result being in doubt. Class 3 (Figs. 658 and 659). 4. Cases beginning in an apical abscess infection, travelling via the pericementum to another portion of the pericementum. Class 4. Kirk's studies show that in a few cases of pericemental abscess the pneumococcus may be found in pure culture. This suggests a Class 2 case as they are found complicated by other pyogenic bacteria in the ordinary pyorrheas. Garrod found crystals of urates in the serum of blisters in gout}^ patients. In gouty patients they are found in joints, and they con- stitute the common tophus. (See p. 97.) "Urates of sodium are also discharged through the skin in gouty abscesses, either in liquid or solid form, and with or without pus." (Musser.) Musser^ states that a number of these abscesses may discharge without impair- ment of the general health or even with benefit to the system. Calculi scraped from the roots in pericemental abscesses exhibit in a varying degree a response to the murexid test, the test for urates. (Peirce.) The reaction may be very faint in some cases, being overshadowed by the calcium phosphate which makes up the bulk of these masses; in others it is pronounced — i. e., urates made up a portion of the deposits. Black^ by test found urates in nearly all concretions, salivary and serumal, about the teeth. While he claimed that this proved that urates have no causal relation to pyorrhea, the findings seem rather to point to frequent presence of urates in the salivary and serumal excretions, which may really be a cause of irritation even when no obvious symptoms of gout are present. Miller's demonstration of a calculus upon an unerupted tooth is to be recalled It seems fairly reasonable, therefore, to suppose that in rare cases such a calculus may be the result of either gout or a local degeneration and act as an exciting cause. (See p. 624.) Morbid Anatomy .^ — Aside from the state of the teeth which show evidences of a tendency to secondary dentin and nodule formation, it has been noted that the abscess is intrapericemental, not sub- pericemental. Figs. 660 and 661 show the infiammatory swelling of the pericementum, the central abscess cavity, and the loss by resorp- tion of the alveolar process may easily be calculated. The original 1 Medical Diagnosis. ^ Dental Review, 1894. PERICEMENTAL ABSCESS 711 chronic nature of the local irritation in this case is evidenced by the presence of hypercementosis. Symptoms. — These have been largely foreshadowed in the dis- cussion of the pathology. Upon some vital tooth there appears an uneasiness, at first not very painful, followed later by an inflamma- tory swelling which may produce acute pain and then discharge a Fig. 658 Fig. 659 r.'/.-;*r.«- A and C, vital pericementum; B, gouty calculus; D, a subgingival calculus. Fig. 660 A, calculus in area of necrosis; S and C, vital pericementum. Two \'iews of an intrapericemental abscess. Pulp vital. (Kirk.) glairy fluid or purulent matter. There is an absence of the phleg- monous inflammatory involvement of contiguous tissues common in cases of acute apical abscess. The fistula may persist after the discharge and the case may first be seen in this condition. If it discharges at the gum margin it establishes an ordinary pyorrhea. D. D, Smith calls attention to the absence of marked pain upon tapping and the production of a feeling of apprehension upon the 712 PERICEMENTAL ABSCESS Fig. 661 Transverse section through buccal roots and pericemental abscess shown in Fig. 660, showing intrapericemental abscess cavity with fistulous outlet and nearby areas of nodular hypercementosis. (Kirk.) Fig. 662 Pericemental abscess. (Talbot.) (Photograph by Latham.) PERICEMENTAL ABSCESS 713 part of the patient during tlie stages preceding the formation of the fistula. In other cases the shifting of the tooth from its position is the first noticeable symptom, followed later by the pain, and later still by the discovery of a pocket alongside the tooth. Diagnosis. — In making the diagnosis the symptoms described are to be borne in mind, but the disease may be confounded with several diseases having somewhat similar symptoms. An acute apical abscess due to gangrenous pulp may be differentiated by obtaining evidences of pulp death, previous root-canal treatment, etc. There is also much greater pain upon percussion than in pericemental abscess. If slowly and painlessly formed it may be still more con- fusing, but the pulp is dead. If the apical abscess be in the third stage it may be differentiated, if any doubt exist, by incision and subsequent exploration. An acute lateral abscess due to a root perforation is more difficult of differential diagnosis, but after incision evidences of perforation Fig. 663 A, calculus. may be sought externally, or the root canal may be opened. In these acute conditions the a:-ray may render valuable aid. The pulp being found alive by any reliable test is evidence that the case is either one of pericemental abscess or of acute traumatic perice- mentitis. In a few cases of partial gangrene of the pulp the pulp may test as vital, yet really the symptoms be due to apical abscess. Acute traumatic pericementitis usually has a history of traumatism and presents more pain upon tapping. Any abscess is usually the result of infection due to rupture of the pericementum. As stated, a form of pericemental abscess is sometimes found existing as a secondary process dependent upon a primary pyorrhea of the first class. The pus burrows from the gum pocket into the gum tissue and excites an abscess which discharges upon the lateral aspect of the gum. The connection of the sinus at the gum margin with the fistula will demonstrate their relation (Figs. 625 and 626). 714 PERICEMENTAL ABSCESS Again, a pericemental abscess may be caused by metastasis of pyogenic organisms from an acute apical abscess — e. g., an abscess in the bifurcation of the roots of a molar may have been caused by bacteria from an apical abscess; the presumption is that the bacteria have followed the pericemental tract, perhaps via the glands of Black or by way of the bloodvessels, and, finding a suitable location in the bifurcation, have there developed. Of course, in such a case the pulp of the tooth in question, or of that in an adjoining tooth, will be dead. Failing a positive differential diagnosis, the case should be treated upon general principles — i. e., counterirritation, derivation, etc., and decisive developments awaited. Treatment. — If the pericemental abscess discharge by way of the gum margin, infection from the oral cavity occurs and the pocket originally formed becomes deeper. The case simulates then a pyor- rhea alveolaris beginning at the gum margin. The treatment is then conducted accordingly. If the swelling occur upon the gum, at a point more or less midway upon the root, it should be opened under antiseptic precautions. An injection of cocain solution should be made, if necessary, and a semicircular flap raised. The diseased area should be explored for calculus and, whether found or not found, the necrotic tissue should be curetted away. Next, the pocket should be syringed out with an antiseptic and filled with balsam of Peru or Beck's bone paste (see p. 703). The flap is next laid into place. The mouth should be kept in an aseptic condition during the healing of the parts. Whether the exciting cause of this condition shall be finally shown to be bacterial or not, the predisposing cause in a general malnutrition or intestinal toxemia should be sought for, and, if possible, corrected. In the elimination of the waste products which act as irritants the best results seem to be attained by measures directed to an increase of the general eliminative functions, increase of tissue oxidation, and a restriction of diet. Such measures in general cause the elimination of existing waste products from the circulation, and prevent the for- mation of an excess of new waste products (see pp. 92, 99, and 655). Recognizing the predisposition which exists in gouty persons to active pericemental degenerations, the operator should guard against injuries to the pericementum, which might induce a weak articulation and precipitate gouty pericementitis. Any malocclu- sion should be corrected. Such teeth should not be violently wedged; injury to the gum or gum margins, by the use of improper rubber dam clamps, ligatures driven beneath margins, etc., may excite the first stages of a degeneration, which will end only in the loss of the abused tooth. CHA'PTER XXVI REFLEX DISORDERS OF DENTAL ORIGIN Recognizing pain as a condition produced through the over- excitation of sensory nerves, a reflex pain may be defined as a pain referred to some point other than that of its origin. Pain referred to the distribution of a sensory nerve may be due to overexcitation of any portion of the nerve in its terminal distribution, to diseases affecting any portion of the nerve trunk, or to disorders affecting the central termination of the nerve. Again, irritation of one sensory nerve may be referred to some other sensory nerve. The condition is called neuralgia. When muscular motion or glandular secretion is excited by irritation of sensory nerves the condition is called a motor reflex. Both motor and sensory reflexes are also classed under the heading of Reflex Neuroses. As both the upper and the lower teeth and their surroundings receive their neural supply from branches of the fifth pair of cranial nerves, discussion of this subject is confined to causes operating within the distribution of that nerve. As such general conditions as malaria, syphilis, and forms of anemia operate to produce neuralgia which may be referred to the teeth, or the parts about them, only those cases will be regarded as dental which have undoubtedly a dental origin, as evidenced by disappearance of the neuralgia following cure of the exciting dental condition. It should be noted, however, that vague and sometimes severe pains referred to the teeth may entirely disappear after the cure of some constitutional disorder. For example, cases of periodic- ally recurring dental pain have been entirely relieved through the administration of quinin or arsenic; the pains were clearly of malarial origin. Pain about the teeth in syphilitics has disappeared after the administration of iodids. Pain referred to the teeth in anemic patients has disappeared after a long course of chalybeates. The treatment of localized disorders other than dental has relieved neuralgia about the head or face. Reflexes of dental origin are both motor and sensory, the latter far outweighing the former in importance. Motor reflexes may be noted in the quick spurt of saliva from the ducts of the salivary glands upon infliction of pain in the teeth, and by the occasional spasmodic 716 REFLEX DISORDERS OF DENTAL ORIGIN contraction of the muscles about the mouth when the pulp of a tooth is deliberately irritated. Twitching of the muscles about the face is a common accompaniment of trigeminal neuralgia. Before direct association of dental diseases with pains in other parts can be clearly demonstrated, a review of those conditions of the teeth attended by pain must be made. Dental pain arises in consequence of disorder of the sensory struc- tures; these are situated in the pulp, and are continuous throughout the dentin and in the pericementum. Dental pains, therefore, may be discussed, first, in connection with affections of the dentin and pulp, and secondly, with those of the pericementum. It was stated, in discussing the diseases of the dental pulp, that this organ is not the seat of tactile sense, and that, like other organs having a kindred physiological relationship, irritation excited in it is not located, but is referred to some other part. While all reflex dental disturbances are, as a rule, located in some part of the great nerve branch supplying the source of irritation, the irritation may be reflected to distant parts; first, of the same cranial nerve, and secondly, to other nerves. That is, pain having its origin in one of the upper teeth is most likely to be referred to a point or points in the distribution of the superior maxillary division of the fifth nerve. Disturbances in or about the lower teeth are usually referred to the distribution of the inferior maxillary division. In affections of either upper or lower teeth the pain may be referred to the ophthal- mic division. In all of these cases, but most notably in connection with disturbances of the upper teeth, the usual symptom of trifacial neuralgia — tenderness of the supra-orbital and infra-orbital nerves at their points of emergence upon the face, the supra-orbital and infra-orbital foramina — is commonly present. Cases are extremely rare where the reflex pain is referred to the opposite side; so unusual is this occurrence that its mention warrants suspicion that other sources of irritation exist upon the side referred to. The extent of acuteness of reflex pain bears no direct relation to the apparent extent of the source of irritation. As might be surmised from the function of the dental pulp, painful reflex dental disorders are more common in connection with diseases of the pulp than with those of the pericementum. REFLEX NEURALGIA FROM EXPOSED DENTIN The exposure of the dentin to external sources of irritation is followed by reactions governed, first, by the degree of sensitivity Fig. 664 — Plan of the fifth cranial nerve, showing the relationships of the dental nerves. (After Flower.) 718 ■ REFLEX DISORDERS OF DENTAL ORIGIN inherent in the protoplasm of the tissue; and secondly, by the degree of hypersensitivity induced in it. Reflex disturbance due to these irritations is more common in the class of persons called "neuralgics," i. e., in those whose nervous irritability is exalted, a condition which may remain even in nervous exhaustion (see p. 104), Like direct pulp pains, unless actual pressure be exerted upon the affected tissue, there is no localized pain. In the absence of deliberate irri- tation, the pain may be referred to any portion of the peripheral distribution of the fifth nerve upon the face, but if an acid liquid, such as lemon juice or vinegar, or sugars be taken into the mouth, pain is excited, which is referred indefinitely to the teeth of one side, frequently of one jaw. Reflex pains due to this cause often appear when there is but little loss of dentin. When carious cavities have proceeded to any depth evidences of direct pulp disturbance are obtained through the increased response to thermal changes. Reflex pains from exposed dentin appear most commonly in con- nection with exposures at the neck of the tooth and upon abraded areas. Obstinate and persistent ^^°- 665 neuralgia, positively referred to I another nerve branch, may appar- ^^^^^^ f^^'^^\ ently owe its origin to so slight a r \ V ^illL vJI"^— - cause as exposure at the neck of a (^^^ ^^^kj ll^lf^l tooth of a line of dentin (Fig. 665). \ ii'ii/ ^^%^^kK '^^^ proof of the connection be- \iu# ^'^..^ tween the two is made clear by a Sites of dentin exposure frequently associated , . p . i i • with reflex pains. disappearance 01 the neuralgia after the exposed dentin has been subjected to the action of powerful caustics (especially silver nitrate), destroying the dentinal filaments to some depth. The connection between the two may be revealed only by accident; the contact of a toothpick, a dental instrument, or the finger-nail may induce a paroxysm of pain. In one case, after removal of calculus, the necks of the lower incisors became a cause of severe neuralgia, compelling the use of silver nitrate. While in some cases the dental origin of reflex pain may be made clear by the induction of a painful response in the area of reflection, by irritating a tooth pulp, this reaction is not constant. The causal relation is only certain when the cure of localized dental disease is followed by a disappearance of the neuralgia without further treatment. This proof should be exacted in all cases. The most common sources of neuralgic attacks about the face are diseases of the eyes and teeth. In general terms, diseases of the eye REFLEX NEURALGIAS FROM PULP DISEASES 719 give rise to reflex pains referred to the distribution of the first branch of the fifth nerve; diseases of the teeth usually cause reflex pains in either the superior or inferior maxillary divisions, according as the upper or lower teeth are affected. In all painful affections of these nerves attention should at once be directed to the organs named. REFLEX NEURALGIAS FROM PULP DISEASES The disturbances require classification according to the distance between their source and their manifestations. In the Fifth Pair of Nerves. — Pain referred to a different spot or area than its origin is a characteristic of all pulp diseases. The extent of its reflection depends, first, upon the patient, as noted in connection with the reflex pains from exposed dentin ; and secondly, upon the variety of pulp disease. In neuralgic patients any variety of pulp disease may cause comparatively distant pains. But, as Black has pointed out,^ the general rule is, that the more chronic and profound degenerative diseases of the pulp are much more liable to give rise to distant reflex pains than are acute pulp diseases. The pains of acute hyperemia and of acute inflammation of the pulp are usually referred to the region of the tooth aft'ected, or to a corresponding nerve trunk. In conditions of venous hyperemia, nodular calcifications, chronic inflammation, and, later, pulp degen- erations, the pains may be of such character that their dental origin is only determined after persistent search. Particularly is this true of the growth of pulp nodules. The source of the reflex pains is all the more obscure from the fact that in these chronic degenerations direct dental symptoms may be entirely absent, and are only elicited upon the most searching examination and exhaustive tests. In some cases of pulpitis even removal of the pulp b}' cocain has been fol- lowed by a neuralgia due to irritation of the nerve trunk in the pulp stump at the apex, so proved by cure through strong sedatives applied via the canal. In one case the neuritis lasted several days. There is no constancy in the location of the pain due to any of these causes; but tenderness of the eyeball upon pressure; iritis or conjunctivitis; persistent pain in the temporal and anterior auricular regions, particularly in connection with pulp diseases of the lower posterior teeth; in the ear itself, a common site of the reflex pain excited by chronic pulp inflammation and suppuration of that organ; 1 American System of Dentistry, vcl. i. 720 REFLEX DISORDERS OF DENTAL ORIGIN Fig. 666 Spots of tenderness in reflex neu- ralgias of dental origin. behind the ear, back of the lower border of the mastoid processes, tender spots may develop; tenderness to pressure may appear at the supra-orbital and infra-orbital or mental foramen, and about the chin. In the same class of diseases the pains may frequently radiate as far as the shoulder. Many of these cases receive attention from the general practitioner, and the painful attacks recurring at irregular intervals are re- lieved by analgesic remedies — phenacetin, acetanilid, exalgin, etc.- — and no attention paid to a probable dental source of the disorder. It should be a routine practice to examine the teeth in cases presenting pains of the tjqje and in the situations described. Acute diseases of the pulp, including suppuration, notably abscess of the pulp, usually have attention directed to the teeth through pain induced by thermal changes, so that their diag- nosis is quickly made. Not so, however, with the chronic degener- ative changes, except possibly of pulp nodules; for if the pulp is in the late stages of degeneration, it may require repeated applications of cold and heat to elicit a response from teeth which do not respond by tenderness upon percussion. Failing to obtain evidence of pulp disorders, examination should be made for eiq)osed and hypersensitive dentin. Then, examination of the pericemental reaction of each tooth should be made, and for any evidences about the teeth poinling to pericemental disturbance. (See later.) Lauder Brunton^ records that, in his own case, temporal neuralgia accompanied by tender eyeball was found due to exposed dentin upon the posterior cervical surface of a lower third molar (see Fig. 665) . The same writer- announces that " so frequently are headaches dependijnt upon decayed teeth, that in all cases of headache the first thing I do is to carefully examine the teeth;" as should every- one else. Brunton explains the painful reaction upon the accepted hypothesis of the pathology of megrim, that it is due to spasmodic contraction of the peripheral end of an artery, with dilatation of the proximal portion. " Irritation in the tooth is reflected to the cervical sympathetic ganglia and causes spasmodic contraction of the arteries through irregular stimulation of the vasomotor nerves." 1 St. Bartholomew's Hosp. Rep., vol. xix. 2 Ibid. Reprinted in his Disorders of Digestion. REFLEX PAINS FROM DISEASES OF THE PERICEMENTUM 721 An abnormal tooth located in the anterior floor of the nasal cavity was the cause of headache for years, so proved by cessation of head- ache after its surgical removal. REFLEX PAINS FROM DISEASES OF THE PERICEMENTUM. As a general rule, pericemental pains are located at the affected tooth ; but in some of the disorders the teeth may not be tender upon percussion, and yet excite reflex pains in other parts, the proof of the connection being determined by a disappearance of the pain upon extraction of the tooth. The roots in such cases usually present either an hypertrophy of cementum or show that resorption of a portion — it may be a major portion — of the root has occurred. In cases of hypercementosis it is assumed that the source of the irritation is pressure upon the nerves of the pericementum by the hypertrophic growth. Very widespread disorders may arise from this source. Flagg^ records many varieties of trifacial neuralgia; pains in remote parts of the body; grave functional disorders of the eye and ear; and motor disturbances — chorea, epilepsy, and paralysis — having a direct demonstrable connection with hx-percementosis. Insanity has also been produced. He mentions \aolent attacks of trifacial neuralgia as the most common reflex disturbance from this source; and next, long-continued pains in the ear or eye of the affected side. The existence of acute disease of these organs is usually diagnosticated by the general practitioner. He states that oral and ocular disturbances, both functional and painful, are of gradually increasing severity. In examining for a dental source of such pains, exposed dentin, pulp diseases, and inflammatory affections of the pericementum should be first excluded. In examinations by percussion a different response may be obtained from some one tooth than from the others. Hypercementosis of a particular tooth may be suspected by finding the gum line slightly receded and the tooth attachment unusually firm; if, in addition, vague, heavy dental pains have persisted at intervals over a long period, the diagnosis is probable. It is only certain when tapping upon the tooth brings on a paroxysm of neural- gia, or where a skiagraphic view actually exhibits the hypertrophic growth. The remedy is extraction. Any root fragment left unex- tracted may perpetuate the reflex disorder. The writer has recently ' Dental Cosmos, 1S78 46 722 REFLEX DISORDERS OF DENTAL ORIGIN treated a case of neuralgia due to a lingual root of a left upper first bicuspid which was retained in the gum after extraction. The gum had healed perfectly over it. It was only discovered by the use of the x'-rays. Painful affections referred to the neighboring region of the affected tooth, or diffused through the distribution of the corresponding nerve trunk, or to the eye or ear, may accompany the process of resorption of the roots of permanent teeth. Gillman^ records a case where facial paralysis disappeared upon extraction of a tooth which had long been the seat of disturbance and which, upon extraction, revealed resorption of its root. In these obscure cases the skiagraph, if taken at once, will be a great aid in the exclusion or diagnosis of pericemental and root abnormalities. All of the acute or chronic, septic or non-septic, inflammations of the pericementum may give rise to reflex pains. The most common causes of the reflex pains are found in that stage of pericemental irritation which antedates acute septic apical pericementitis. Unless an exacerbation of the reflex disorder, or symptoms referable to that region, be induced by pressure or percussion on the tooth, a causal relationship is only made out b}^ either relieving an existing dental disorder, an x-ray skiagraph, or extracting the teeth. IMPACTED TEETH AS A CAUSE OF NEURALGIA Neuralgia of varying degrees of severity is a common accompani- ment of impacted teeth. It is most frequently noted in connection with eruption of the lower third molars, not only because this tooth is the one most frequently impacted, but because of the anatomical relations of its roots with the inferior dental nerve. In the milder forms of impaction, those in which eruption, though delayed, is subsequently completed, the pains are commonly local- ized and associated with but occasional attacks of rigidity of the masseter muscles. If, however, the crown present horizontally or nearly so, and its progress is arrested by impaction against the posterior wall of the lower molar, or if its progress be arrested by permanent imprisonment of the advancing crown between the pos- terior surface of the second molar and the base of the coronoid process, not only may intense local pains be induced, but severe reflex disturbances of both a sensory and motor character may occur. In some of these cases root formation is completed, although the I Boston Medical and Surgical Journal, 1867. PARALYSIS OF THE SENSORY TRACTS 723 crown of the tooth does not advance, in which case compression of the inferior dental canal and its contents may occur and cause grave reflex disturbances. The local irritation about the root, due to root growth, may excite continued constructive action by the peri- cementum, and the hypertrophic growth in its turn may be the source of reflex neuralgias. Complete imprisonment of the entire tooth has been found to be the exciting cause of facial neuralgias, for the cure of which extensive surgical operations have been performed. Impacted cuspids and other teeth may excite no other symp- toms than reflex neuralgia. The possible connection between an impacted tooth and neuralgia is made out after excluding other dental causes, w^hen it may be observed that one or more of the permanent teeth are absent from the dental arch, at dates long after their normal time of eruption. A condition equivalent to partial impaction, in which dental irri- tation may be the source of reflex neuralgia, is seen when the teeth are crowded — jammed into arches too small for their accommodation. During the period of eruption severe maxillary pains may recur at intervals. The diagnosis is by means of the .r-rays. The production of insanity as a reflex condition has been discussed on page 279. PHANTOM ODONTALGIA This is a form of neuralgia in which symptoms similar to tooth- ache appear in the edentulous jaws or in locations from which teeth have been extracted. The name was applied by J. Foster Flagg. It seems to be due to the compression of nerve-endings by dense bone. It may, of course, be a reflex neurosis from some other focus of pulp or pericemental or nerve trunk irritation. Any history obtainable of a previous local inflammation should be obtained, and if the pain is localized in any spot the bony tissue may be broken up by operation with a view to removal of such a cicatricial inclusion of nerve terminals. At least in troublesome cases such a simple operation is admissible. PARALYSIS OF THE SENSORY TRACTS The operation of extraction and occasionally disease of the pulp and pericementum have produced a temporary paralysis of a branch of the fifth pair and loss of sensation in the lip or cheek may result. 724 REFLEX DISORDERS OF DENTAL ORIGIN So far as observed the cases are of not more than a few months' duration and may be ameliorated by massage, either passive or vibratory or by faradization. PAIN REFERRED TO NERVOUS TRACTS OTHER THAN THE FIFTH The most common disturbance appearing in other cerebrospinal nerves than the fifth, due to dental diseases, is an affection of the eighth or auditory nerve. Cases of deafness have been recorded due to diseases of both pulp and pericementum, notably to hyper- cementosis. Deafness which has persisted for a long period has been markedly lessened by the extraction of teeth the seat of disease. Cases of suppurative otitis media have been regarded as having pathological association with septic diseases about the teeth, from the fact that the aural trouble subsided immediately after extraction of the diseased teeth. Sensory disturbances of the eye, associated with dental diseases, have been alluded to; in addition to these, grave structural and functional diseases of the eye, traceable to dental causes, have been recorded, such as motor and trophic disorders.^ Among the latter may be mentioned corneal inflammation and ulceration and phlyc- tenular conjunctivitis. These are probably due in part to reflex trophic disturbances. Irregular paralyses of the third, fourth, and sixth nerves of the affected side have been noted. Amblyopia and functional blindness without retinal conditions to account for it have been found to arise from notably advanced degenerative changes in the dental pulp, sight returning to the eye after loss of a diseased tooth. DeWitt^ records a most instructive case where temporary blindness was associated with septic apical pericementitis, disappearing after evacuation of the abscess and reappearing when secondary inflammatory action arose in the peri- cementum. The ocular affection disappeared permanently and almost entirely with the loss. of the tooth. The history of this case illustrates the important causal relationship of reflex disturbances with late pulp degenerations; for the blindness arose two months after some teeth were filled, and existed for twelve years before the septic apical pericementitis appeared. ' See Brubaker, American System of Dentistry, vol. iii, for very full and detailed discussion of these subjects. 2 Quoted by Brunton, Disorders of Digestion. MOTOR DISTURBANCES FROM DENTAL DISEASES 725 A careful examination of these and all other reflex disturbances shows that pulp degenerations outnumber all other affections as causes. Many or most of the cases are recorded by general prac- titioners, who make no distinction between diseases of the pulp and those of the pericementum, but a reliable diagnosis of the conditions is made possible by the accompanying descriptions. Cases of ovarian and uterine neuralgia and sciatica and cases of obstinate pains in the knee, toes, and fingers have been traced to dental irritation of some one of the varieties named, the proof of association being disappearance of the pain with loss of the tooth, though this is now not always necessary for a cure. MOTOR DISTURBANCES FROM DENTAL DISEASES Motor disturbances due to dental irritation may occur as recurrent or persistent contraction or paralysis of muscles, together wdth more or less chorea; in rare instances epilepsy and hystero-epilepsy. Twitching of muscles of the affected side of the face, ranging from slight affection of the occipitofrontalis or orbicularis palpebrarum to recurring spasm of the elevators and depressors of the lower lip, are far from uncommon phenomena attendant upon pulp and peri- cemental diseases. In one case mentioned by Guilford^ a pulp nodule was the cause of tic douloureux (painful muscular contrac- tions) of two years' standing. Contraction of the masseter muscle is a common accompaniment of retarded eruption of the lower third molar, which may be inten- sified until the condition is fitly termed trismus, in some cases of partial impaction of the teeth. Partial trismus has been found due to a general overcrowding of the dental arch.^ Records of cases of torticollis, due to dental diseases, are also given by Brubaker. Cases of facial paralysis, and cases of paralysis of one arm, of paraplegia and hemiplegia, and even of general paralysis, have been noted as disappearing after the extraction of diseased teeth. It is noteworthy that in these cases, as well as in several cases of tetanus recorded, the probability of an infection entered into the patho- genesis of the nervous diseases. Stellwagen^ records a case where symptoms of partial hemiplegia followed upon the operation of capping the pulps of tw^o molar teeth ; the symptoms disappeared promptly upon extraction of these teeth. ' Private communication. ^ Brubaker. ' Private communication. 726 REFLEX DISORDERS OF DENTAL ORIGIN Cases of insanity arising from dental diseases have been recorded; they were both maniacal and melancholic. In several of them a restoration to a normal mental state followed promptly upon removal of the offending teeth. In some of these cases a preexisting maxillary neuralgia directed attention to the teeth as possible sources of the nervous diseases. Dr. E. Ballard Lodge^ reports a case from the practices of Drs. Upson and Stephan in which a lady had suffered from acute melan- cholia and insomnia. A skiagraph revealed an impacted upper third molar pressing against the distal side of the second molar. Extraction effected a cure. Upson^ reports a number of like cases, as well as some due to pulp and pericemental disease. The local conditions were painless. Trophic Disturbances following Dental Diseases. — Two cases of localized alopecia (loss of hair) have been reported^ obstinate during the dental disease and cured by the cure of a pulpitis in one case and extraction of a root for suppurative pericementitis in the other. Such cases show a vasomotor disturbance in the distant part. A case of facial paralysis followed extraction of seven roots upon one side. It was successfully treated by eight applications of a weak galvanic current.^ Facial paralysis has also followed the eruption of teeth, as of a second molar. Infantile paralysis has also been caused by dentition (see p. 194). DENTAL PAIN ARISING FROM OTHER THAN DENTAL SOURCES Conditions of pain the reverse of those discussed — i. e., pain definitely or indefinitely located in teeth which exhibit no morbid conditions whatever — demand occasional attention at the hands of the dentist. Chronic malarial poisoning, as stated in the beginning of this chapter, may give rise to periodical attacks of maxillary neuralgia. As in the gouty cases, the constitutional cause of the disturbance is made clear through the therapeusis most effective, viz., the periodical recurrence of the pain leads to the inference of a malarial origin, and to the administration of quinin. Anemia and other conditions in which there is accumulation of products of metabolism also cause it. Syphilitic pains in the jaws have a pericemental character, and other evidences of syphilis are present which point to a diagnosis. Pains in or about the teeth are occasional accompaniments of 1 Dental Summary, 1908. 2 Dental Cosmos, 1910, p. 526. ' Mounier: Le Laboratoire, 1907. * Griefswald: Cosmos, 1906, p. 356. DENTAL PAIN FROM OTHER THAN DENTAL SOURCES 727 diseases of the brain or its vessels, and of pregnancy or diseases of the uterus, kidneys, and bladder. Disease in any portion of the fifth cranial nerve may cause pain referred to the teeth, for example, inflammation of the nerve trunk, a tumor in the nerve, or a tumor pressing upon the nerve trunk, or a portion of fractured bone so pressing, or a cicatrix contracting up a nerve. Dental pain during pregnancy, without any direct evidence of dental disease, is relatively common. Disorders of the lower bowels, causing constipation, may give rise to pain referred to one or more teeth, the pain ceasing promptly upon the administration of an active evacuant. La grippe occasionally produces antral empyema or neuralgia about the dental region as one of its sequelae. Pain may appear in one or more teeth either with or without association with pain about the maxillae or tenderness at the foramina of emergence. If there be possible causes in defective teeth or teeth with fillings in which pulp irritation is a possibility, there may be difficulty of diagnosis. There may be a history of an attack of influenza or even of coryza, with the common variety of which dental pains are often associated. It may occur after la grippe has seemed to have disappeared. The pain is at first generalized over the entire head, but gradually local- ized in one or several upper teeth, more frequently in the second molar, occasionally the bicuspids. It sometimes is so severe that the patient thinks an abscess is forming. There is almost always pain in the molar region when pressure is made upon the inner alveolar portion of the hard palate, and sensi- tivity of the external alveolar region. For the pseudoodontalgia Roy recommends a capsule containing the following: ^ — Antipyrin gr. vij Quinine hydrobromid gr. iij Sodium bicarbonate gr. iij Sig. — One dose. Increase and prescribe four times a day. Locally he recommends: ^ — Mentholis gr. x Acidi borici 3iij Vaselini 5J — M- Sig. — A small portion to be applied within the nostrils on rising and retiring. Treatment of Facial Neuralgia. — The cause should be sought for, and, if possible, removed. If due to disease of the teeth, these should 728 REFLEX DISORDERS OF DENTAL ORIGIN be relieved; if due to eye disease, or other cause, this should receive attention. Should one not discover the cause, yet desire to afford a relief pending its discovery, the accepted remedies antipyrin, acetanilid, and phenacetin, combined with caffein or the bromids, are useful. IJ — Antipyrini (vel phenacetini vel acetanilidi) 5J Caffeinse citratis gr. x Potassii bromidi 3iij — M. Ft. in chart No. x. Sig. — One every thirty minutes until reUeved (Hare.) If the patient be constipated, the bowel should be freed of toxic substances by the use of castor oil, repeated as necessary. Castor oil in small doses is antineuralgic. In obstinate neuralgia and other painful affections with unremov- able cause, the application of the a;-rays has been urged by Morton as highly efficacious in relieving pain often for a considerable time. The blue ray is also used. A remedy of exceedingly simple nature was introduced by Verge and Pitres in 1902, It consists of injecting into the mucous membrane or skin, about where the pain seems to originate, 1 cm. of alcohol (85 per cent, plus 1 per cent, cocain is preferred by Lenson) at the temperature of 60° C. by means of a hypodermic syringe. Asepsis must be provided for. A slight humming sensation and swelling of tissue occurs about the area of injection. The pain disappears for a long period after one or two injections a week apart. A deep injection also relieves. A case in which the face became black on the side of injection was also followed by relief and sub- sidence of the congestion. The method has been objected to by some. It has been recorded that myosis, and prickly or tingling sensation or paralysis of the part or nearby muscles of temporary nature are by-effects. Aconitin internally in minute doses is also antineuralgic. Injection of the nerve trunk with dilute osmic acid has been practised by surgeons. Strychnin in fairly large doses has been employed under medical supervision. When the cause cannot be determined the nerve itself may be resected. CHAPTER XXVII INFECTIONS OF AND FROM THE MOUTH, AND STERILIZATION The conditions found in the human mouth, as pointed out in Chapter III, are of a character which afford lodgement to, and opportunities for multipHcation of, many forms of bacteria, both saprophytic and parasitic. The oral conditions are, however, not entirely constant, so that at different periods they may favor the development of some special bacterial forms more than others. The nature of these variations has not been made out, although their effects are indubitable. Again, the oral bacterial inhabitants are not constant as to species, for while there are many forms which appear to be invariable occupants of the oral cavity, man}' patho- genic forms are but accidental residents. Becoming resident, they may or may not develop according as they find in the mouth a suit- able soil. The nature of what constitutes a suitable or unsuitable soil has not been determined, although in some cases extra-oral culture experiments furnish some indications. Bacterial growths, as causes of dental caries and diseases of the pulp and pericementum, have been discussed in connection with those several diseases. It was shown that the pyogenic cocci are almost constant inhabitants of the human mouth. There appeared also evidence that some of the reflex disorders of distant parts are directly traceable to septic processes about the teeth, and, in addition to these, suppurative diseases in other parts become curable after removal of a septic tooth, such conditions representing infection from a local dental infection, an important aspect of dental pathology. The notable fungus of the blastomycetes is the saccharomyces albicans; this organism, when classified by mycologists as a thread fungus, was known as the oidium albicans (Fig. 667). The growth of this organism illustrates forcibly the influence of soil on the growth of fungi. It does not occur in the mouths of healthy, well- nourished, and clean children with good surroundings. It is a disease of childhood, particularly of nurslings, and its occurrence is almost always confined to bottle-fed babies whose feeding bottles are kept in an unclean condition. Debility of the oral tissues is established in consequence of the fermentations arising from the source just named, furnishing a favorable condition for the development of the 730 INFECTIONS OF AND FROM THE MOUTH saccharomyces (oidium) albicans. The condition produced is known as thrush. The infection may be carried from one child to another, and if the fungus be brought in contact with an abraded mucous surface of an adult it may develop. Fig. 667 Fig. 668 Saccharomyces albicans, thrush fungus. (Miller.) The fungus burrows between the epithelial cells of the mucous mem- brane (Fig. 668), not beyond it. It first appears in small spots which coalesce, until large patches- of a membranous-like growth cover exten- sive surfaces, spreading by continuity to all of the mucous surfaces asso- ciated with the- mouth. As bud fungi flourish only in media of acid reaction, the use of alkaline washes is indicated in the treatment of this condition. Wiping the patches with dilute phenol-sodique is effica- cious. Small spots may be cauterized with silver nitrate or trichlor- acetic acid. Hydrogen dioxid or 25 per cent, iodin in glycerin are also useful. Pavement epithelium covered with spores of the odium albicans. (Ch. Robin.) INFECTIVE BACTERIA OF THE MOUTH Bacteria, being ever present, must always play a part in either originating, modifying, or associating with all oral diseases. That the progressive decomposition of albuminous substances, always present in the mouth to a greater or less degree, by the action of saprophytic fungi, must give rise to derivatives of albumin. STOMATITIS 731 many of them toxic in effect, would be surmised even in the absence of experimental demonstration, a suspicion confirmed by experiment. Vulpian^ produced septicemia by vaccinating animals with the , saliva of a healthy man. Griffin^ showed that the parotid saliva (pure) is harmless. The saliva, if boiled, exerts no toxic action, from which it is clear that it derives its toxic substances from the mouth. The saliva of individuals differs at times in the degree of its poisonous action. In some diseases it becomes intensely toxic. Of the many oral bacterial forms, some are cultivable and some are not; hence the specific effects of some are discovered, others are doubtful. With regard to local affections, other than those described in the body of this book, a bacterial causation has been made out in some, but in others it has not. STOMATITIS Definition. — By stomatitis is meant an inflammation of the mucous membrane of the mouth. If secretion is markedly increased it may be termed catarrhal stomatitis. Varieties.— It may be localized, as in marginal gingivitis, or be diffuse; and, again, be accompanied by localized tissue destructions — ulcerations; the character of the ulceration differs according to its probable causes. Occurrence. — ^Most of these diseases belong to the period of child- hood, although localized ulcerative stomatitis may appear in the adult. Causes. — The causes of stomatitis are so many and varied as to suggest a classification under heads according to assignable causes. While it is true that bacterial infection has not been shown to be a direct cause of all of these conditions, some degree of causal relation- ship is probable in all of them. The disease may, however, be included under two heads according as they are or are not localized, and necrotic. The less localized cases appear as a diffuse catarrhal affection, affecting wide areas of the oral mucous membrane; the others appear as spots of localized tissue destruction attended by surrounding hyperemia. 1 Quoted by Miller. 2 Ibid. 732 INFECTIONS OF AND FROM THE MOUTH Simple. Catarrhal stomatitis Local Symptomatic Ulcerative stomatitis Local Symptomatic Fermentations. Diphtheria. Gonorrhea. Infective Eruptive fevers. Syphilis. Tuberculosis. Typhoid fever. Drug action . Aphthae. Thrush. Noma and gangrenous stomatitis. Herpes. Syphilis (primary). Secondary. Tertiary. Syphilis . . . . Gonorrhea. Tuberculosis (local). Scurvy. Simple Local Catarrhal Stomatitis. ^ — The general symptoms of catarrhal inflammation — heat and swelling, with deepened color of the mucous membrane, followed by increased secretion and exudation — attend several types of oral irritation, such as the irritation induced by erupting teeth, particularly of the deciduous teeth. Inflamma- tion of any degree may follow the taking into the mouth of caustic chemical substances, such as caustic alkalies, mineral acids, carbolic acids, etc., which are occasionally taken by children. Other irritant drugs and very hot fluids may produce similar results. General catarrhal stomatitis is a frequent affection of confirmed smokers, and of drinkers of distifled liquors. The cure of these conditions consists in the removal or neutrali- zation of the cause, and the use of local sedatives and antiseptics to allay irritation and prevent infection. The most effective method of treating the inflammatory condition is by antiseptic sprays, such as diluted Dobell's solution, followed by sprays of strong solutions of potassium chlorate. If much pain exist, phenol-sodique is an admirable sedative antiseptic, used in 10 to 20 per cent, solution, as a spray. Infective Local Catarrhal Stomatitis. — This in some degree is a common, perhaps the necessary, antecedent condition to many of the ulcerative forms of stomatitis. It is probable that many of the cases of stomatitis found in infants, children, and adults are due to unusual fermentations occurring in the mouth. Children whose nursing bottles are not kept clean; those who at a later age suffer from neglect of the teeth and from the effects of improper food; adults in whose mouths dental disease is widespread, and whose STOMATITIS 733 oral hygiene is very faulty; all exhibit abnormal conditions of the oral mucous membrane — more or less swelling, softness, and deepened color of the mucous membrane, a coated tongue, and offensive breath, with an increase of oral secretions. The complexus of oral symptoms is commonly, and also by the general practitioner, regarded as symptomatic of gastric, intestinal, and hepatic disorders, as doubtless they are, but the causal relation- ship is in many cases probably the reverse of that implied in such opinions, for it is probable that the disturbances of digestion are fermentative in character, and the organisms causing them find their way to the stomach from the mouth, which was first affected. The treatment of this condition consists in the correction of its causes, their non-repetition, and the continued use of oral antiseptics. ^Yhile the point of first attack of the diphtheria bacillus is most marked about the soft palate and tonsils, the false membrane form- ing there and spreading to the pharynx, more or less general inflam- mation of the oral mucous membrane also occurs. The gonococcus may be lodged in some portion of the oral cavity and excite its specific effects upon contiguous mucous membranes. Symptomatic Catarrhal Stomatitis. — Stomatitis in its catarrhal form usually accompanies the early and later stages of the eruptive fevers, scarlet fever, smallpox, etc. In scarlet fever and smallpox evidences of direct infection of the mouth exist and the inflammatory reaction is pronounced. Catarrhal stomatitis is one of the manifestations of secondary and tertiary syphilis, antedating the appearance of tissue necrosis (ulcerations) . ^Nlore or less catarrhal stomatitis, confined, it may be, to the mucous membrane of the gums, is common in the mouths of phthisical patients; tubercular ulcers may arise or threaten. In some cases the palate has been perforated. Curtis states that these are usually fatal. The stomatitis of typhoid fever may be regarded as an almost essential feature of the disease. The effects of drug elimination by the oral tissues have been already discussed (see p. 618). ^Mercurials in excess produce gingivitis with puffy gums which bleed readily; there is coated tongue, fetid breath in marked cases, swollen tongue and cheeks, and exfoliation of the teeth. The history of administration of mercurials, and, possibly, of syphilis, as a reason for it affords a diagnosis. The mercury should be stopped; atropin sulphate, 5 minims of a 1-grain to 1-ounce solution in water, admin- istered as an antisialagogue every four to six hours; a 5 per cent. 734 INFECTIONS OF AND FROM THE MOUTH potassium chlorate solution in hydrogen dioxid makes a useful mouth wash for reducing the local inflammation. Ulcerative Stomatitis. — It has been customary to describe ulcera- tive stomatitis as simple and infective; in all probability these ulcera- tions are always infective. Like catarrhal stomatitis the ulcerative disease may have only a local significance or be indicative of some general disease. Ulcerative Stomatitis of Local Significance.— The more usual or infantile forms of these disorders are a sequel of catarrhal stomatitis, at least of an acquired debility of the oral tissues, and their primary cause is, therefore, the cause producing a condition of mucous mem- brane which permits the growth of infective organisms. One of these diseases, thrush, has already been described. The others, aphthae, herpes labialis, and noma, are all probably due to the action of organisms. Aphthae. — This affection is common in its isolated form, as the canker sore. In the catarrhal stomatitis of children, during or after dentition, multiple sores frequently make their appearance. The condition can best be studied when it appears as an isolated sore in the mouth of the adult. The most common situation of the sore is at the junction of two mucous surfaces, such as that of the gum with the lip or cheek, or that of the floor of the mouth with the gum or tongue. Redness diffused over a limited area, followed by a nodular hardening, occurs, during which local pain is annoying; the centre of the hardened area breaks, the epithelium disappearing, forming a raw surface, which quickly acquires a rough, yellowish white coating which is easily removable. The sores are very painful. The mouth is usually otherwise healthy, and there is an absence of associated throat and skin affections. This condition follows so constantly upon the taking of very indigestible food,, such as lobster, Welsh rarebit, etc., that acute indigestion must be regarded as having some causal relationship with it. It is also of frequent occurrence in the mouths of dyspeptics ; that form of gastric disturbance attended with a deficiency of hydro- chloric acid in the gastric juice appears to have a constant association with it, though it is probably caused by the oidium albicans. The appearance of ulcerative stomatitis in children, together with its treatment, was discussed in the chapter on Dentition. The general treatment of these ulcerations appearing in the mouths of children is the administration of a laxative, and the subsequent administration of listerine, gtt. x, every two hours. Locally the mucous membrane is to be sprayed with hydrogen dioxid, followed by sprays of strong solutions of potassium chlorate. NOMA, CANCRUM ORIS, GANGRENE OF THE MOUTH 735 Localized aphthous patches in the adult are ])romptly relieved by the administration of calomel, gr. ij, at night, followed in the morning by a mild saline. The local sore is dried and touched with pure carbolic acid. The administration of alkalies before meals, and hydrochloric acid after meals, usually remedies the gastric condition, unless it be of long standing. A variety of aphthous sore is called, from the anatomical situation of the ulcers, follicular stomatitis. Irritation and swelling of the mucous follicles in the palatal, buccal, and labial mucous membrane are accompanied by more or less localized inflammation; the follicles become ulcerous, the small ulcers having a uniform size. This con- dition quickly disappears under the treatment advised for ulcerative stomatitis. An indication of the bacterial origin of all of these dis- turbances is seen in the efficacy of antiseptics used in their treatment. A form of stomatitis is due to artificial dentures resting upon the mucous membrane, and either by pressure or light friction, or possibly by preventing radiation of heat, they cause desquamation of the epithelium. The part beneath the plate assumes a more or less reddened or ulcerated appearance. Vulcanite plates that are not smooth upon their surfaces of adaptation may produce this physical irritation, but oftentimes such surfaces are covered with infective mucous plaques, so that this may in some cases be an added cause. Treatment. — The treatment consists of rest and healing mouth washes. Antiseptics are usually included. (See Gingivitis.) Stomatitis Aphthosa Epizootica.^ — This is the oral expression of foot-and-mouth disease occurring in cattle and rarely fatal, and usually lasting about eight weeks. The germ is not fully determined as yet. Diagnosis. — The diagnosis rests upon the presence of the disease in nearby cattle and the prodromata and later presence of fever, pustules on the mucous membranes of the lips, tongue, and sometimes on the hard palate and throat, occasionally between fingers, around nails, or on nipples. These later burst, leaving ulcers with a grayish yellow coating. The pustules dry up without scars in the second week. Treatment. — The treatment rests upon antisepsis in so far as the local manifestations are concerned. NOMA, CANCRUM ORIS, GANGRENE OF THE MOUTH In ill-fed, ill-nourished, and ill-kept cachectic children, the debili- tation of the oral tissues may exceed the grades given, and a disease, 1 Lartschneider: Dental Cosmos, 1908, p. 880. 736 INFECTIONS OF AND FROM THE MOUTH probably bacterial in origin, may arise which leads to widespread necrosis of the cheeks and maxillae. The condition is called gangrene of the mouth, noma, or cancrum oris; the latter term has been applied to the less severe varieties. Hillesen obtained a diplococcus which developed in pure culture, produced noma in an animal into which it was injected, and from the lesion a pure culture of it was obtained which in like manner was put through four animals.^ Fig. 669 Noma. (J. Lewis Smith.) This disease may make its appearance as an ulcer at the junction of cheek and gum; in other cases a severe stomatitis arises without a primary ulcer. A greater or less extent of the cheek acquires a board-like hardness, becoming livid; the overlying mucous mem- brane breaks, exhibiting a large slough. The necrosis extends toward cheek and jaw, destroying further tissue. The sloughs undergo putrefactive decomposition, emitting a stench. The destruction of tissue may be arrested, or may proceed, destroying in a few days the entire cheek and bony tissues. In the more severe cases the disease is almost invariably fatal, because the extent of the tissue destruction bears a constant relation to the underlying debility of the patient. It will be seen that the disease resembles malignant pustule or carbuncle in several of its features. 1 Dental Cosmos, 1908, p. 180. SYPHILITIC AFFECTIONS OF THE MOUTH 737 While no specific organism has been isolated as pathogenic of this condition, Schimmelbusch^ found a bacillus (pure culture) ui)on the borders of the necrosis which may prove pathogenic of noma. These cases are purely medical; so that their full discussion is not warranted in these pages. The principle of treatment is to improve the general condition of the child, destroy the probable infection in the borders of the still vital tissue by cauterization, and promote sloughing of the necrosed tissue by the use of antiseptic applications. Dr. L. Fisher (New York) reported a case upon the inside of the cheek, cured by applications of ichthyol in lanolin four times a day over the entire area.^ SYPHILITIC AFFECTIONS OF THE MOUTH The recognition of syphilitic lesions about the mouth is of vital importance to the dental operator, first, because by the recognition he may take steps to prevent the carriage of infection to innocent patients; and secondly, that he may avoid inoculation of himself by the poison. In the minds of many, syphilis is associated with the lower class of persons, who are confirmed debauches. While it is undoubtedly true that its prevalence is most marked in this class of persons, it appears, and with horrible frequence, in persons who would be little suspected of having such infection. The operator is to be guided in his opinions and precautions in this matter, not by the social status of the patient, but by the nature of the morbid conditions existing. The cause of syphilis is the Spirocheta pallida discovered by Schaudin and Hoffman, and present in its lesions, transmitted from one person to another directly or through the medium of an inani- mate object which has been infected. The diagnosis may be made by microscopic examination. The sore is washed and the serum later exuded used to make a smear on a glass slide. This is first dried in the air, then stained with Hastings' stain. After a minute distilled water is added until a metallic film is formed. After five minutes more they are washed in running water and dried. The Spirocheta pallida stains a faint blue.^ Syphilis is usually divided into three stages, primary, secondary, and tertiary; to these may be added a fourth stage, viz., in patients who have been discharged as cured mild manifestations of disorders, particularly of the skin and mucous membranes, make their appear- i Miller: Dental Cosmos, September, 1891. 2 Dental Cosmos, 1902. ' McKee: Dental Cosmos, 1909, p. 1437. 47 738 INFECTIONS OF AND FROM THE MOUTH ance from time to time, and disappear promptly upon the adminis- tration of iodids. The first stage of syphihs — primary syphiHs^consists in the form- ation of the primary sore or chancre, and the involvement of the nearest lymphatic glands. Secondary syphilis is attended by fever, eruptive inflammations of the skin, inflammation and superficial ulceration of mucous structures. In tertiary syphilis destructive inflammation of the skin, mucous membranes, and connective tissue occurs, together with the formation of specific tumors — gummata. Some differences of opinion exist among syphilographers as to the relative infective power of the secretions from the several lesions of syphilis. All are agreed, however, that the secretions from the secondary lesions observed in and about the mouth are highly infective. It is the part of prudence to regard all syphilitic lesions as infective. All these stages of syphilis may be seen in the human mouth. It is to be remembered that if the mucous membrane of the mouth be infected from a mucous patch (a secondary lesion), the acquired disease will appear, not as a mucous patch, but as a chancre. It is from mucous patches that infection is most to be feared. Primary Syphilis of the Mouth. — Causes.— The primary lesion of syphilis, chancre, when found in the mouth is a consequence of direct infection from a syphilitic. The infection occurs from contact of the mucous surface of the mouth with a syphilitic lesion upon another person: It has been transmitted by kissing; it may occur from using a glass or cup previously used by a syphilitic, by smoking cigars or cigarettes which have been made by syphilitic cigarmakers, who have applied the tongue to the tobacco in attaching the wrapper. Any of the articles named, or the contact of any article which has been in contact with a syphilitic lesion, if brought in contact with an abraded mucous surface, may cause infection.^ The infection may be transferred from patient to operator if the fingers have any abraded surface, or if the surface is broken acci- dentally by an instrument. Infection may be transmitted from one patient to another by any instrument, appliance, or article used by a syphilitic being afterward used by an innocent person. Drinking glasses, mouth mirrors, exploring instruments, rubber dam, rubber dam clamps, saliva-ejector tubes, lancets, forceps, or any other instruments may be the medium of communication. During and 1 Metchnikoff and Roux found that an ointment composed of 10 parts calomel and 20 parts, lanolin, applied by inunction to an intentionally infected part, prevented the appearance of syphil- itic infection if used within one hour after inoculation. Mercuric chlorid was of no avail. Dental Cosmos, 1907, p. 1007. SYPHILITIC AFFECTIONS OF THE MOUTH 739 since the time of Hunter the use of teeth from syi)hilitic patients in plantation operations has been a clearly recognized medium of communication. About 32 per cent, of all primary chancres appear within the dental field either upon the lips or within the mouth. Dentists have been inoculated upon the hand. Appearances and Diagnosis. — "The primary lesion of syphilis never makes its appearance before ten days after infection; the maximum period is about ninety days; the average is twenty-one days."i It usually appears as a single, elevated, hard papule. In cases of dental infection, most frequently about the lips, the papule loses its epithelial coating after some days. The induration surrounding the papular mass increases until the papule, which is now raw and in a process of ulceration, appears surrounded by a ring of cartilaginous hardness. This induration is the one distinguishing feature of the chancre, which is not painful. In about a week after the appearance of the primary sore, swelling of the submaxillary lymphatic glands is observed. In case the chancre appears upon the tongue, the sub- hyoid lymphatic glands are swollen.- Unless pyogenic infection has occurred, the lymphatic involvement is not inflammatory, there being no pain present. In from three to four weeks the sore disap- pears, leaving no signs of its site in some cases; in others, some induration may persist. The diagnosis of this condition is the important consideration, so far as the dental practitioner is concerned, its tceatment being the province of the general surgeon. The elevation of the sore, its induration, and, if obtainable, the time of inoculation, are diagnostic data. The sore is single, as a rule, and there is hard, nodular, painless sw^elling of the neighboring lymphatics. A single ulcer of ulcerative stomatitis may in some degree simulate the appearance of a very small chancre. It may exhibit slight induration, but its irregular form, situation, painful- ness, and the usual absence of lymphatic involvement, together with its prompt disappearance after sterilizing the mouth and cauter- izing the ulcer, will differentiate the two sores. If the chancre be upon the tip or sides of the tongue, where it is subjected to irritation, it may become very large and bear a close resemblance to epithelioma of that organ. In epithelioma there are apt to be pains of a lancin- ating character, the induration follows ulceration, and the ulcer has hard edges and often a warty-like growth. It is a wise precaution to view all sores about the mouth as possibly ' Gross: System of Surgery. - Park: Surgery. 740 INFECTIONS OF AND FROM THE MOUTH infectious. All errors of diagnosis in this direction will be more than compensated for by the assurance of non-transference of infection. Secondary Syphilis of the Mouth. — The secondary manifestations of syphilis are observed in and about the mouth, no matter what the location of the primary lesion may have been; they are the result of a general, not a local, infection. Chancre of the Up. Secondary infections of the mucous tissues appear in from four to twelve weeks after the appearance of the primary lesion. Sore throat, due to inflammation of the mucous membrane of the pharynx and parts about, is almost constant; together with syphilitic hoarse- ness, due to the extension of the affection to the mucous membrane of the larynx. The appearance of copper-colored areas upon some portion of the mucous membrane, on the tonsil, pharynx, soft palate, lips, or bucco- labial surface, precedes the loss of epithelium over these surfaces, which soon occurs, forming the most virulently contagious lesion of syphiHs, the mucous patch. The patches become covered with a grayish-white, opalescent, pasty covering, resembling the ulcera- tions of non-specific stomatitis. So close is the resemblance that a differentiation can only be made at times by additional evidences of secondary syphilis. Single patches may coalesce, forming large, irregular areas covered by a grayish-white pellicle. These patches are rarely painful. Ulcerations having ragged, irregular outlines may appear at the sites of the original patches or in other situations, and exhibit a tendency to spread. In healed cases the cicatrices present a whitish pellicle and contracted scar, indicative of old healed ulcers. In the skin little pits and linear scars are symptomatic. The diagnosis of the condition is determined by a discovery of other lesions of secondary syphilis; iritis, headache, neuralgia, SYPHILITIC AFFECTIONS OF THE MOUTH 741 paralysis of muscles of eye and face, chorea, brittle, cracking nails are often early symptoms;^ also the lymphatic glands will be involved; skin eruptions, falling out of the hair (alopecia), and the areas of copper-colored eruption upon the mucous membrane of the pharynx and soft palate. Hugenschmidf- has observed among syphilitics, who presented no local lesions, the frequent nocturnal occurrence of indefinitely located dental pains, spreading to the palatal region. Tertiary Syphilis of the Mouth. — The syphilides of the secondary stage arise in, and are confined to, the mucous and dermal structures; those of the tertiary stage arise in the deep connective tissues, and are frequently associated with periosteum. Tertiary lesions, as seen by the dentist, are usually in the form of ulcers of, first, the soft or hard palate, and of the tongue or lips. In the earlier stages hard, nodular formations may be noted as ante- cedents to the ulcerations. Chronic periostitis of the palatal processes may occur, leading to the formation of localized thickenings. In other cases, in the soft palate, upon the tongue, or in the hard palate, localized sw^ellings may occur, having a livid red appearance; the overlying mucous membrane breaks, establishing an ulcer, which may perforate the soft palate and destroy a portion of the palatal process, or form large ulcers on the tongue. The condition is one of gumma. These lesions appear in from two to five years after the secondary manifestations. Tertiary Lesions. — The sight and hearing may be affected, the throat diseased, causing loss of voice, necrosis of the bones and tissues of the nose causing deformity. The brain or spinal cord affected may cause paralysis, locomotor ataxia, or loss of reason. These are usually the result of failure to follow treatment to a conclusion. The tongue may have either a localized or widespread parchment like hyperplasia of the mucous membrane, and muscular tissue w^hich may cause it to become indented by the teeth, to lose its papillae, and become dry and red. Pedersen^ calls attention to the fact that the indentations do not disappear when the tongue is stretched, while if due to ordinary debility they may be. Although there is much doubt as to the degree of infectiveness of these tertiary lesions, precautions as to sterilization should be taken as with the primary and secondary lesions. A defined, ragged ulcer occupying the hard or soft palate, which has persisted for a long time, should always be view^ed with suspicion, and a search be made for other evidences of syphilis. > E. Whitney: Dental Cosmos, 1911, p. 524. ^ Dental Cosmos, 1S92. 3 Dental Cosmos, 1908, p. 332. 742 INFECTIONS OF AND FROM THE MOUTH These ulcerations appearing upon the side of the tongue may closely simulate epithelioma of that organ. The confusion is increased if, in consequence of the presence of jagged teeth, a continuous irritation is excited. Moreover, leukoplakia of the cheeks, a diag- nostic sign of incipient epithelioma; frequently accompanies tertiary syphilis. In some cases an absolute diagnosis is only made by noting the disappearance of the local lesion following the administration of iodids, the specific treatment of tertiary syphilis. The existence of tertiary syphilis is of great clinical importance to the dentist in that a condition of lessened resistance of tissues is established, and disease processes which in the healthy person are comparatively circumscribed, in the syphilitic run a riotous course. A septic pericementitis by extension may involve a wide area of periosteum, leading to extensive maxillary necrosis. Treatment. — The treatment of syphihs has been largely by the administration of mercury for a long period until the Spirocheta pallida shall have been killed out. If not so continued the tertiary lesions may reappear with serious results. The latest development in treatment is the use of Ehrhch's preparation of arsenic, dioxy- diamedoarsenobenzol, "606," or salvarsan, for which positive claims as a prompt cure are made. In obscure cases diagnosis is made by Wassermann's reaction. (See p. 247.) TUBERCULOSIS OF THE MOUTH The bacillus of tuberculosis, under favorable conditions, develops in the tissues of the mouth, producing its characteristic lesions. Finding a suitable soil, such as is furnished by the heredity which predisposes to phthisis pulmonalis, the bacillus may find entrance to the deeper tissues from the mucous membrane of the mouth and excite tuberculosis in the deep structures, the bone, etc. A number of perforations of the hard palate have occured. According to Curtis these are usually fatal. What part is played by local oral and dental lesions in tuberculosis of distant parts, by establishing pathways for the entrance of the bacilli into the circulation, is at present conjectural, but that such infections occur is very probable. ACTINOMYCOSIS The condition produced by the development of the ray-fungus, the actinomycosis, in the lower jaw and cervical regions of cattle and GENERAL SEPTIC DISEASES OF DENTAL ORIGIN 743 swine — lump-jaw — is not unknown in human beings. It may be derived by chewing straw or grass in wliich tlie ray-fungus has produced "rust." Miller^ gives 203 cases reported in German medical literature between 1886 and 1891. In at least 120 of these cases the point of entrance of the fungus was found to be in the region of the mouth or throat. Actinomycosis threads have been repeatedly found in the saliva and in carious teeth, and notably in the tonsils. Whether the path of entrance to deeper structures is ever through carious teeth is undetermined, but certainly lesions or wounds about the mouth furnish an entrance. The disease has yielded to the action of sulphate of copper, | grain, plus iodid of potassium, 10 grains, internally four times a day> together with local irrigation of 0.1 per cent, solution of copper sulphate.- GONORRHEA Undoubted cases of oral infection by the gonococcus of Neisser have occurred. The oral mucous membrane and the gums may undergo intense suppuration with its accompaniment. Fever and its accompaniments may be present. The mouth and eyes are very subject to secondary infection in an individual suffering from gonor- rheal urethritis. The hands are a medium of transference. Babes may be directly infected by the mother, and blindness often results. The law now requires the instillation of a mild solution of silver nitrate as advocated by Crede. The diagnosis can be made by microscopic examination of the bacteria. (See p. 644.) The toxins and the germs formed in the mouth may be swallowed. GENERAL SEPTIC DISEASES OF DENTAL ORIGIN The effect of the existence of dental diseases upon the body at large, particularly as regards secondary infection, is a matter increas- ing in importance as the possibilities of their connection are made out. At present the organisms of greatest demonstrable patholog- ical interest are the pyogenic cocci. The almost constant presence of these organisms in the mouth, carried thence into the pharynx, posterior nares, larynx, lungs, and stomach, furnishes the reason for the pyogenic and phlegmonous inflammations which occur in these • Dental Cosmos, 1891. * Brophy: Dental Cosmos, 1908, p. 78. 744 INFECTIONS OF AND FROM THE MOUTH organs. The diplococcus of pneumonia, a frequent organism, but waits a favorable opportunity to establish high inflammations and fibrinous exudations in the lungs, and possibly in other structures. The most important clinical associations of dental with general infections are diseases of the pericementum. The pulps of teeth, having no lymphatics, do not appear to take up and transmit the products of the action of septic organisms; but while the evidences of such absorption, involvement of the neighboring lymphatics, are not present, it must be remembered that the veins may transmit the poison, and, in addition, may perhaps convey organisms from a diseased but still vital pulp to distant parts. When, however, the pulp is dead and the pericementum is invaded, there is no doubt of general infection from this local source. More or less septic intoxica- tion is a common attendant upon severe septic apical pericementitis, and septicemia accompanied by inflammation of the neighboring lymphatic glands is of sufficient frequency to emphasize the need of the vigorous antiseptic treatment recommended in all of these cases. Pyemia is far more uncommon.^ Pyogenic organisms, gaining access to the blood current from the local source of infection, establish suppuration in distant parts; in other parts of the bone, or in other bones (osteomyelitis), in the lungs, meninges, and substance of the brain. One case^ has been reported where abscess of a toe, ear, and forearm ceased, and recovery took place after treatment and filling of septic root canals. Several cases are tabulated by the same author in which extensive necrosis and death resulted from pyemic infec- tion from septic pericementitis. Some of these cases recorded were associated with acute, some with chronic, septic pericementitis. In addition to the usual pyogenic cocci. Miller has isolated several forms of cocci, bacilli, and spirilla, forming products which, if injected into the circulation of animals, cause death from septicemia in from hours to days. As many of these forms may be brought into rela- tion with deep parts by the anatomical conditions created by pulp death, the possibilities of many types of infection via pulpless teeth are evident. The possibilities of local as well as general infections through the conditions estabhshed in the several forms of pyorrhea alveolaris should not be forgotten. The pockets formed by the soft tissues overhanging lower third molars whose eruption is impeded invite the passage of septic organ- 1 Miller: Dental Cosmos, 1891. " Ibid. LEUKOPLAKIA BUCCALLS 745 isms to deep parts. Local pyogenic infections are common in these cases, and may extend into the pharynx and the submaxillary tissues, as in Ludwig's angina. HERPES LABIALIS (HERPES SIMPLEX) This consists of a vesicular eruption upon the lip, tongue, mouth, cheeks, or alse of the nose. The vesicles are filled with a clear fluid which soon discharges. An excoriation is left often covered by a light crust, which is never followed by a scar. The condition may cause little pain or considerable burning and itching. It may accom- pany colds, fevers, exposure to heat, draughts, and gastric disorders. It follows either a direct irritation of the nerves, as after the use of rubber dam or other dental operations in susceptible persons, or may be of reflex origin; in either case localized peripheral neuritis being the initial lesion.^ There is some reason to believe that infection plays a part in its production. As a preventive it is well to lubricate the lips with glycerin and rose water or with cold cream when much stretching or other irritation is necessary. Leprosy. — During the progress of leprosy, an infective disease, characteristic nodules and ulcers appear about the oral structures. As many parts of the head are affected in like manner, these are but symptoms of the progress of the effects of the Bacillus lepra .^ HERPES ZOSTER This is a probably infectious disease, almost invariably mono- lateral, associated with a neuritis usually of a spinal ganglion or with a peripheral neuritis, which produces, first, a hyperesthesia of the integument, macules, and later vesicular eruptions not usually beginning on a mucous surface. They appear in groups and may coalesce, forming patches. Desiccation forms a crust; pus may form. The interest to dentists lies in the fact that in zoster of the head exfoliation of the teeth is said to be associated in rare cases.^ LEUKOPLAKIA BUCCALIS Upon the inner surface of the cheeks or lips, and upon portions of the gum and the dorsum and edges of the tongue, may appear sharply ' Hyde and Montgomery: Diseases of the Skin. ' For an exhaustive article see Oliver, Dental Cosmos, 1908. ' Hyde and Montgomerj': Diseases of the Skin. 746 INFECTIONS OF AND FROM THE MOUTH outlined, dull, whitish, slate-colored or silver-whitish points, disks, streaks, bands, ribbons, or patches of irregular shape, either flattened or slightly elevated, above the general level of the mucous surface. They may crack or fissure, and inflammation of the derma and pain result. Ordinarily they are simply rough and without much dis- comfort. It occurs almost exclusively in males. They differ from the mucous patches of syphilis in that the latter are soft and tend to ulcerate, and, while they may accompany syphilis, may occur in its absence or of any history of it. They simulate the keratosis of lichen planus, which should also appear as papules upon other parts of the body. Apart from syphilis, it is due to irritation such as that from tobacco or rough teeth, and with syphilis, tobacco, and rough teeth may be additional excitants. The use of alcohol and spices are also a cause. The pellicle is closely adherent, and consists of an hypertrophied and hyperkeratinized epithelium, with more or less inflammatory infiltration of the derma and with partial obliteration of the papillae. The chief danger in the disease is the tendency to epithelioma, some authors estimating 30 per cent., especially in the cases in which exfoliation and ulceration occur. The removal of the pellicles by suitable caustics, galvanocautery, or bur, and the avoidance of all irritants, especially tobacco and alcohol, and the use of soothing mouth washes, together with a hygienic regimen, is the usual treatment to avoid epithelioma. The diagnosis lies clearly within the province of the dentist who may note it before the patient. The treatment is usually conducted by the physician, and is often unsatisfactory as to permanent cure. Cases with syphihtic history, of course, require antisyphilitic treatment, especially with mercury. Leukoplakia has been also called buccal psoriasis, but psoriasis does not affect mucous surfaces, hence it is a misnomer. LICHEN PLANUS This condition, which may simulate leukoplakia,^ is characterized by an eruption consisting of glistening flat-topped polygonal papules with tendency to form irregularly arranged groups. On the mucous surface they appear as whitish macules, strise, or flat papules on both sides of the tongue at the points in contact with the molar teeth. I Hyde and Montgomery: Diseases of the Skin. PHOSPHOR NECROSIS 747 They are the result of an arterial or venous hyperemia of the papillffi of the corium, a secondary thickening of the lower part of the rete, and a tertiary flattening of the papule by pressure. A proliferation of cells in the granular layer and a deposit of keratohyalin in whitish spots occur. This causes a similarity to leukoplakia. It usually occurs in the nervously exliausted, though many patients may have a fair degree of body nutrition while yet nervouslv exhausted. PHOSPHOR NECROSIS This disease is a more or less extensive necrosis of the maxillae due to the entrance of phosphorus or its fumes into contact with the periosteum or pericementum of a tooth. It was formerly frequent in match factories, when white phosphorus was used, though now less when the red is employed, but has occurred through the chewing of match heads, and a case has been reported in which a half grain taken in three days caused it.^ As it does not ordinarily occur in the mouths of those having sound teeth, it is generally regarded as of local origin, the phosphorus gaining entrance either through the pulp canal of a tooth, or, possibly, through some point of injury external to the tooth. Abscesses containing oft'ensive pus cause great swelling and exces- sive salivation, and may cause several fistulse, while the swallowing of the discharge causes general toxic disturbance, and infection such as pneumonia or cerebrospinal meningitis may have rapid effect. The periosteum remains unaffected as to its vitality, while the bone proper undergoes osteoporous necrosis, becoming like rotten sponge. As the sequestrum is separated, there is a tendency to formation of new bone by the periosteum. The necrosis of bone may be very extensive, involving in the lower jaw the entire horizontal portion, while the ramus may remain unaffected. In the lower jaw, after exfoliation, the bone may be almost entirely restored to an amount nearing fair comparison with the ordinary edentulous mouth, while in the upper jaw no repair occurs. This new bone may undergo atrophy if not put to work by artificial teeth. ^ As a pro- phylactic sodium bicarbonate solutions are recommended by Arnone.^ ' Arnone: Dental Cosmos, 1910, p. 425. ' For consideration of treatment the reader is referred to Garretson's System of Oral Surgery, sixth edition, and other writings upon the subject. ' Dental Cosmos, 1909. 748 INFECTIONS OF AND FROM THE MOUTH SCORBUTUS This is scurvy as described on pages 103, 205, 619, and 649. PURPURA H-fflMORRHAGICA This is the appearance of small purplish spots beneath the skin and mucous membrane, and is dependent upon infection and toxic conditions. Brown,^ following Schamberg, presents the following clear differ- entiatial symptoms: Scorbutus Purpura Hemorrhagica 1. Occurs in those subjects due to lack of 1. No such etiological relationship. vegetable food and to bad hygiene. 2. Definite antecedent symptoms, weakness, 2. Antecedent signs slight or absent. impaired circulation, etc. 3. Onset slow. 3. Onset sudden. 4. Gums spongy, swollen, and bleeding; teeth 4. Gums often bleeding, but not swollen. loose. 5 Severe muscular pain. 5. Less marked. 6. Brawny infiltration of lower extremities. 6. Not present. 7. Hemorrhages from mucous membranes, 7. Hemorrhages from mucous membranes so not profuse, as a rule. severe as to sometimes prove fatal. ANGINA Angina is usually defined as a sense of choking or suffocation, a symptom which accompanies inflammatory affections of the pharynx as well as the paroxysmal neuralgic affection of the heart known as angina pectoris. Angina Simplex. — This is inflammation of the pharynx, with, of course, more or less swelling and inflltration of exudate. Swallowing may be difiicult. Local depletion and sedation washes, with general derivation, are indicated. If chronic, stimulant washes are useful combined with general tonic treatment. Ludwig's Angina. — In 1836 Ludwig described a disease which is considered to be an infectious cellulitis in the submaxillary region, which may extend deeply into the tissues of the neck. The infection is thought to be due to the Streptococcus pyogenes or bacillus of malignant edema, though the staphylococci and Diplococcus pneu- moniae are found, and probably enter the cellular tissue of the 1 Dental Cosmoa, 1911, p. 296. DENTAL STERILIZATION 749 submaxillary region and neck through the oral or pharyngeal mucous membrane or a wound. An apical abscess, also, the repeated impac- tion of food into the peridental region, especially about a third molar, and its fermentation has caused a deep infection resulting in this disease. The patient has lassitude, chilliness, and fever. A hard swelling appears beneath the mandible after several days, and extends toward the neck and under the tongue. There is mus- cular rigidity and the head is inclined in one direction. The skin is not much reddened. Later edema is marked and may extend upward toward the parotid gland or the glottis. Breathing and swallowing are rendered difficult by oral and pharyngeal swellings. There are the usual oral symptoms of inflammation. Upon incision the connective tissues are found to be sloughing, grayish black in color, and may ooze pus. The spread of the infection being by continuity of cellular spaces, the glands are much enlarged. A large abscess may form and discharge. Pneumonia, septicemia, and pyemia are complications to be feared as the result of spreading infection. Incisions for drainage and antisepsis are usually con- joined with systemic treatment, but as the case is often of dental origin the cause should be removed. Vincent's Angina. — This is an edematous tonsillitis, which may affect also the mucous membrane of the mouth and pharynx, fol- lowed by the formation of a pseudomembrane as in diphtheria, later ulceration and hemorrhage may appear. There are the usual accom- paniments of inflammation in this locality, together with fever and sometimes rigors. It usually lasts about two weeks. The differential diagnosis from diphtheria and syphilis is made by microscopic examination. Vincent's bacilli, spindle-shaped, pointed at extremities, and 6 to 10/^ in length, are usually associated with a long thin spirillum. They take several stains, but not the Gram. In diphtheria, Loeffler's bacilli, and in syphilis the Spirocheta pallida would be found. In the treatment hydrogen dioxid, and tincture of iodin locally, and potassium chlorate internally are of value. DENTAL STERILIZATION It must ever be borne in mind that the dental operator constantly works in a field of infection, and unless extraordinary precautions be taken every instrument which touches this field— the fingers of the 750 INFECTIONS OF AND FROM THE MOUTH operator, his mirrors, glasses, napkins, rubber dam, rubber dam clamps — becomes immediately infected as soon as it is brought in contact with the mouth of the patient. The likelihood of infection varies with the patient and the particular instruments; mouth mirrors, rubber dam clamps, scalers, and all instruments used in the treatment of pulp canals are likely to become more promptly and extensively infected than other instruments. Again, the forms of the instruments determine whether or not increased opportunity is given for the retention of infective material. The fingers of the operator may be the medium through which infective material is transferred from one patient to another. Infection may be carried from superficial areas of the mucous membrane of the mouth, from the enamel and the saliva, into deeper structures, where conditions are favorable for the development of sepsis. The scheme for dental sterilization, therefore, includes the steriliza- tion of the operator, instruments, apparatus, appliances, etc., used in operations, and the sterilization of the field of operation prior to operating. The Operator. — Extreme personal cleanliness upon the part of an operator is clearly the first step in asepsis. The best class of dentists are exceedingly neat as regards personal habits; daily bathing, care of the nails and of the skin, and immaculate linen form as much a part of the day's labor as dental operations per se. The virtues of soap and water, wherever they may be applied, are regarded as a very important item in preventing infection. Linen which has been boiled prior to wearing may be regarded as safely sterile; so that the matter of personal steriHzation relates to the hands, particularly to the finger-nails. The space under the nails is a favorable habitat for many organisms, notably the pyogenic cocci, the staphylococcus pyogenes aureus being commonly present in this situation. It has always been advised that the finger-nails be trimmed short, and be made smooth to avoid mechanical injury to the soft tissues of the patient. Since the advent of aseptic and antiseptic surgery these precautions have an additional significance; nails kept short and smooth may be more readily cleansed than if long and ill-kept. The nails should be cut so that they nowhere project beyond the tips of the fingers. Their mechanical cleansing should be done with smooth instruments, not sharp knife-blades; the latter produce rough surfaces, which furnish spaces for lodgement of bacteria. There is but one effective method of washing beneath the nails; it is that followed by the general surgeon. After dipping the soap in water as hot as can be borne by the hands, all of the finger-nails should be DENTAL STERILIZATION 751 made to scrape the soap until the spaces under the nails are filled with soap. After this coarse hand-brushes are used to scour every part of the hands with soap and water as hot as can be borne. Special nail-brushes are next used to scrub beneath the nails, driving out piecemeal the soap masses there. The general surgeon continues the scrubbing until the nails are scrupulously clean. The soap usually used is Castile, or soap made from palm oil, etc., but antiseptic soaps, such as ethereal soaps, may be substituted with ad\'antage. Tincture of green soap is effective (see below). Sterilization of the cleansed hands is insured by immersing them for five minutes in antiseptic solutions, such as 50 per cent, alcohol. The hands should be sterilized after treating each patient; rubbing the hands with a paste of flour, mustard, and water for three minutes and washing oft* with sterilized water is effective. (Nancrede.) If the patient dismissed has possessed an unusually septic mouth, or has been a syphilitic, for example, the time for hand cleansing and sterilization is to be prolonged; if syphilitic, every instrument used is transferred to separate vessels containing antiseptic solutions or boiled, and the hands are viewed as highly infected; they are scrubbed with mercuric chlorid solutions to prevent personal infection or the carriage of infection. Chancres have from time to time appeared upon the fingers of dentists as well as physicians. In a syphilitic case one might use the rubber gloves worn by surgeons. Sterilization of Apparatus. — The scrupulous cleanliness of the operating chair, whose head-rest should receive frequent changes of boiled linen coverings, metallic parts rubbed, and general covering cleansed; the cleansing, polishing, and sterilizing of cuspidores; the changing of paper coverings upon instrument tables, etc., are part of the general scheme of sterilization. The floor of the operating room also requires attention; instead of being covered with carpet, it is preferable to have it made of parquetry material or cement, over which rugs are laid, which may be removed from the room for cleansing, the floor proper being scrubbed. Napkins used about the mouth are certain to become infected, so that their boiling should be prolonged at least fifteen minutes. For many operations it is preferable to substitute strips of muslin for linen napkins, which after being used may be thrown away. If a hydraulic saliva ejector be used, the glass mouth tubes should be changed for each person, a sterilized tube being substituted directly before its use is required. A number of these tubes should be in use, and may be sterilized after washing by placing them in a 50 per cent, solution of Listerine or a formaldehyd solution for a few hours. Tumblers and mouth mirrors may be sterilized in like manner. 752 INFECTIONS OF AND FROM THE MOUTH The cloudiness of saliva tubes is produced by the formation of salivary calculus, and may be removed by the use of acidulated water,^ At the close of each day a large cup should be filled with an anti- septic solution, which is to be drawn through the tubing of the ejector to keep it in a reasonably aseptic condition. Rubber dam may be sterilized by boiling water, but it is more safe and cleanly to use a new piece for each patient. It should be washed and then dusted with borated talcum powder. The possi- bilities of infection through this medium are great, particularly in syphilitic cases. The water used for douching cavities should be boiled previous to placing in the warmer, and should have a little pleasant antiseptic added to it. Nancrede^ states that all pyogenic cocci, and even anthrax spores, are killed by boiling instruments for two minutes in a 1 per cent, solution of sodium carbonate, which also prevents rusting. Mouth mirrors and other instruments which can be wet may be placed for one-half hour or longer in a covered jar containing 20 per cent, formaldehyd, to which borax has been added to saturation. Rusting is prevented by borax (Williams). Broaches, trephines, and other small points requiring to be kept sterile may be placed in a bottle such as are sold containing gold cylinders, and kept wet with any essential oil or carbolic acid. G. Zederbaum^ suggests sticking the shanks in the cork; when to be used the cork is to be transferred to another bottle of like size containing alcohol and shaken to remove the antiseptic. They may then be washed in sterilized water. Extracting forceps require careful mechanical cleansing and pro- longed boiling after each use, for perhaps more cases of infection, and of many kinds, have resulted from unclean forceps than from all other causes combined. Instruments, such as hand-pieces, which cannot be conveniently wet may be subjected for ten minutes to formaldehyd gas, developed in a Low or Schering apparatus.^ If desired, all the instruments may be so sterilized. The entire instrument case may be disinfected by burning a Low lamp in one drawer of the dental cabinet for one- half hour at night. The drawers should be made communicating by small perforations at one or more points. Miller found that placing a formalin tablet in each drawer sufficed to sterilize its contents. 1 Thornton: Dental Review, 1903. 2 Park's Surgery by American Autho'-s. 3 Dental Cosmos, 1907. ^ See American Text-book of Operative Dentistry. DENTAL STERILIZATION 753 Sterilizing the Field of Operation.^ — To insure sterilization of the field of operation antiseptics should l)e used freely about the mouth prior to operating. The thoroughness of the sterilization will depend in great degree upon the personal liabits of the patient. If by the systematic use of the agents and measures described under the pro- phylaxis of caries tlie patient's mouth be kept in a reasonably aseptic condition, sterilization of the oral cavity can be accomplished with sufficient readiness. The choice of antiseptic will depend in great degree upon the state of oral hygiene ; in ill-kept mouths, with deposits of foreign materials about and between the teeth, on the gums and tongue, much more active and penetrating germicides will be required than if the parts are clean. The presence of putrefactive decom- position in the mouth, made evident by ill odors, amid which that Fig. 671 Low sterilizer: A, sterilizing chamber; B, perforated tray on which instruments to be sterilized are placed; C, glass dome and cast aluminum support; 0, condensing chamber for removing all moisture from gas; D, formaldehyd burner; E, platinum cone, which generates the gas from Columbian spirit; F, lamp body. The course of the gas through the apparatus is indicated by the arrows. of hydrogen sulphid may be detected, needs for its treatment the immediate and free use of preparations from which nascent oxygen may be disengaged. A good method is to forcibly spray the mouth with a 1 to 3 per cent, solution of hydrogen dioxid, in order to force infective material from about the teeth. The other solutions, as a solution of potassium permanganate or mercuric chlorid or alcohol may then be used. This spraying or washing should be somewhat prolonged when the mucous membrane is likely to be injured, as in extractions which often result in infection from the patient's own secretions. Many operators keep a stock of inexpensive tooth- brushes for such cases, which are thrown away after the patient has used them, who is directed to scrub the teeth well with the brush and the antiseptic solution. ' 48 754 INFECTIONS OF AND FROM THE MOUTH For very thorough disinfection thoroughly cleanse the teeth and use the antiseptic between them upon floss silk. For surgical work or etherization very active work should be done. Wadsworth/ in an investigation of mouth washes and their action on pneumococci, found but little value in the ordinary wash or even solutions of formalin, lysol, or H2O2. He found that 1} — Alcohol 30 parts Water 70 parts Glycerin and salt, a small quantity added, was very effective in destroying the bacteria. In a series of tests upon the devitalizing power of germicides for streptococcus, gonococcus, pneumococcus, and Bacillus typhosus, Post and NicolP found tincture of "green soap" (a brownish liquid composed chiefly of alcohol and caustic potash), alcohol in solutions above 50 per cent., silver nitrate solution from 1 to 1000 to stronger, tincture of iodin, Senn's solution (iodin 1, potassium iodid 1, water 100 and even 400), phenol, 5 per cent., and chloroform were effective in one minute. Potassium chlorate, mercuric chlorid, 1 to 500, failed in ten minutes. Boric acid failed in two hours. As some of these germicides are for the mouth and some for the hands the information is of great practical value. The routine practice of scaling and polishing the teeth and pre- scribing an antiseptic mouth wash prior to the commencement of a series of sittings is to be highly commended. Before scaling absolute disinfection is impossible. The writer uses the antiseptic freely during the entire operation. If ulcerations or inflammatory conditions exist, the sterilization is to be prolonged. If a suspicion of syphilis exist, not only should the mouth be freely washed with strong antiseptics, but special instruments should be used, preferably an old set, kept sterilized and used only in special cases. If the hands of the operator have abra- sions or irritated spots, these should be covered with collodion, and after the operation should be carefully sterilized to prevent personal infection, of which a number of cases have been recorded (see p. 751). A deep infection may usually be prevented during the treatment of pyorrhea alveolaris and pulp gangrene by attention to the steril- ization of the infected tract before beginning work upon the parts or during its progress. These methods have been indicate^ in the discussion of these subjects. 1 Dental Cosmos, 1907. 2 Spence: Dental Cosmos, 1911, p. 548. INDEX Abrasion, 284 in animals, 284 of calculus, 290 degrees of, 285 during sleep, 295 effects of, 291 from clasp, 290 gritty powders as cause of, 287 labial and approximal, 286 lingual, 290, 291 occlusal, 284 relation to caries, 287 tooth-brush in, 287 treatment of, 293 Abscess, apical, acute, 561. See Peri- cementitis, chronic, 584. See Pericemen- titis, scar from, 603 septicemia from, 568, 579, 582 systemic complications from, 603 around third molar, 573 extraction in second stage of, 577 fistula in, 128 perforation of bone in, 576 pericemental, 708 pointing in, 128, 567 of pulp, 471 pus in, 126 Absorbent organ, 208 Acacia, use of, 198 Acetanilid as cause of hemorrhage, 115 use of, 115, 132, 381, 466, 580 Acidity, hyper-, 88, 298, 393, 421 Acidosis, acids in, 89, 95, 96, 100 Aconite, tincture of, 118, 131, 452, 575 Aconitin, use of, 728 Actinomycosis of mouth, 743 Aerogenic bacteria, 41 Adenoids in mouth breathing, 218 Adrenalin, use of, 384, 490 Agenesia of enamel, 238 Agglutination, 57 Albumin, fermentation of, 43 Albuminuria, 105 Alcohol, injection of, 728 use of, 144, 381, 495 Alexins, 49 Aloin compound, use of, 655 Alopecia, from dental disease, 726 Alum, use of, 465, 534 Alveolar process, fracture of, 639 Alveolitis, postextraction, 640 Amalgam, copper, use of, 403, 408, 536 facing, 503 Amboceptors, 56 Ameba, properties of, 18 Ameloblasts, 154 Ammonol, use of, 381 Ameba of dysentery, 35 Amputation of roots, 598, 691 Amyl nitrite, use of, 495 Anemia, 108, 109, 110 Anesthesia of apical tissue, 496 general, use of, 490 diploetic, 496 by pressure, 465, 482, 490 nerve trunk, 388 of pulp, 490 Angina, Ludwig's, 748 simplex, 748 Vincent's, 749 Angle, classification of malocclusion by, 213 Ankylosis, dental, 625 Anomalies of teeth. See Malformations. Antikamnia, use of, 381 Antipyrin, use of, 727 Antiseptic powders, use of, 131 Antiseptics, mouth, 749 Antitoxin, formation of, 55 streptococcus, use of, 144, 580 Antrum, empyema of, 600, 604 Aphtha;, 734 Aqua regia, use of, 513, 525 Aristol, use of, 131, 381, 485, 558, 596 Arsenic, accidents with, 504 action of, on gum tissue, 504 on pulp tissue, 497, 502, 504 variations in, 499 apical hyperemia from, 497 coverings for, 503 iodide of, use of, 462 mummifying paste and, 505 objections to, 500 pocket for, 503 pulp hyperemia from, 497 in pulp nodule, 440 second application of, 500 suffusion from, 498 use of, 466, 482 756 INDEX Arsenic, use of, danger of, 393, 497, 504 ^Irsenical fiber, 502 Arterial hyperemia, 116 Asperin, use of, 466 Astringents, use of, 120 Atrophy, 74 general, 75 local, 74 marginal, of gum, 656 Harlan's method in, 656 Atropin, use of, 381, 619 Attachment of teeth, 253, 639 Autointoxication, general malnutrition as causes of, etc., 88 oral effects of, 650 B Bacteria, action of gastric juice upon, 49 aerogenic, 41 in blood, 40, 45 as cause of disease, 34 of inflammation, 121, 125 chemical composition of, 37 chromogenic, 41 conditions antagonizing, 60 of dental caries, 326, 349, 358 destruction of, by tissue, 49 division in blood, 40 effect of blood reaction upon, 60 external antagonistic agencies, 60 facultative, 41 fermenting action of, 41 ferments of, 42 forms of, 39 immunity to, 52, 56 intoxication by, 95 life conditions of, 38, 40 localization of, 49 media of, 39 motility of, 38 of mouth, 47 general infection, by, 142 obligate, 41 parasitic, 40 pathogenic, 40, 46 penetration of root tubules by, 611 position in vegetable kingdom, 34 predisposition to, action of, 29 pyogenic, 45, 126 saprophytic, 40 specific, 44 spore formation of, 39 spreading of, in tissue, 45 toxic effects of, 40 products of, 43 universality of, 44 zooglea of, 39 Bacterial plaques in dental caries, 330, 343 Balsam of Peru, use of, 596 Band, dental, 153 Bandage, use of, 120 Benzoic acid, use of, 646 Benzoin, use of, 457, 465 Bilein, use of, 655 Bismuth, subnitrate, use of, 198, 596, 599 Black, glands of, 184 Black's 1-2-3 mixture, use of, 703 operation for scar, 603 Bleaching agents, use of, 317, 556 Blindness, dental, cause of, 724 Blisters, use of, 118 Blood, alterations in, 107 bacteria in, 40, 45 coagulation of, 110 extravasation of, 113 pressure of, 116 reaction of, as immunizing factor, 60 supply to teeth and jaws, 171, 181 Bloodletting in inflammation, etc., 118, 131 Blue light, use of, 381, 574 Bone, caries of, 84, 137, 592 of face, embryology of, 147 infection of, from dental lesions, 604 inflammation of, 136, 604 of jaw, development of, 147 necrosis of, 84, 136 from alveolodental abscess, 606 from syphilis, 570, 607 perforation of, in abscess, 576 regeneration of, 136, 139 resorption of, 136, 137, 138 in gingivitis, 667 Boric acid, use of, 726 Boroglycerin, use of, 646 Brewers' yeast, use of, 131 Broaches, Downie, use of, 508 Swiss, 529 use of, 509 varieties of, uses of, 508 Bromural, use of, 381 Brush, use of, 416 Bruxomania, 285, 295 Caffein, use of, 580, 678 Calcareous infiltration, 82 Calcific degeneration of pulp, 441 Calcium chloride, use of, 115 salts in blood, 662 in pus, 677 Calcoglobulin, 83, 155 Calcospherites, chemical composition of, 155 in dentin, 430 in pulp nodule, 434 Calculi, basis of, 83, 659 Calculus, analyses of, 660 hematogenic, 677 origin of, 659, 663 INDEX 75- Calculus, pyogenic, 677 salivary, 658 analysis of, 660 foreign bodies in, 662 hardening of, 665 mode of deposit, 659, 663 occurrence of, 659 origin of, 659 pathological effects of, 667 removal of, 668 scalers for, 668, 676 structure of, 659 treatment of, 668 varieties of, 658 sanguinary, 677 subgingival, 673 Calendula, use of, 646 Calomel, use of, 305 Campho-phenique, use of, 450, 465, 618, 703 Canada balsam, use of, 402 Canals, imperfectly filled, results of, 544, 558, 603, 609 root, enlargement of, 510 Cancrum oris, 755 Cantharides, use of, 507 Capping, for pulp, 408 Capsicum plaster, use of, 576 Carbohydrates in dental caries, 325, 328, 340 Carbolic acid, use of, 197, 391, 395, 397, 465, 495, 507, 618 Carbon dioxid, defective elimination of, 89, 299 paper, use of, 634 Carcinoma, 73 Caries of bone, 84, 137, 592 dental, 320 acids in, lactic, 325 neutralization of, 356, 418 age in, 337, 352 alkalies in, 328 bacteria of, 326, 349, 358 bacterial plaque in, 312, 342 bodily condition in, 338 carbohydrates in, 325, 328, 340 causes of, bacterial, 325, 358 exciting, 323 predisposing, local, 330 systemic, 336 in cementum, 364, 372 chemical reactions in, 326 clinical history, 364 deep-seated, 397 dentin in, 351 decalcification of, 356 secondary, 348, 371 diagnosis of, 373 drinking water in, 337 eburnation in, 362 effect of malnutrition upon, 90 in enamel, 335, 342 experiments in, 323 filth as a protection from, 329, 341 Caries, dental, foodstuffs in, 326, 328 glycogenic infiltrations in, 334 heredity in, 336 history of, 320 clinical, 364 inception of, 323, 342, 364 locations of, 342 lactates formed in, 356 liquefaction foci in, 357 loss of crown by, 372, 407 of root by, 372, 410 morbid anatomy of, 342 mucin in, 334 of Nasmyth's membrane, 351 pathology of, 342 penetrating, 371 perforation by, 372, 407 periodicity in, 337 pigmentation in, 362 prenatal influence in, 336 prognosis of, 375 progress of, 365 saHva in, 334, 339 in school children, 337 prophylaxis of, 415 pulp in, almost exposed, 460 exposed, 357, 372, 404 recurrence of, 414 of secondary dentin,. 371 self-healed, 371 simple, 396 spreading, 371 stages of, 396 structure of teeth in, 335 sulphocyanide in, 339 superficial, 395 symptoms of, 373 of temporary teeth, 411 terminations of, 372 therapeutics of, 395 transparent zone in, 360 tube casts in, 359 under fillings, 359 Caroid, use of, 131 Caseation, 78 Castor oil, use of, 198, 728 Catabolism, 23 Cataphoresis as test, 538 in hypersensitive dentin, 385 Cataplasma kaolini, use of, 226, 580 Cathartics, use of, 118, 575 Cautery, actual, use of, 295, 394 electric, use of, 295, 393 Caustics, use of, 131 Cells, chemical changes in, 23, 24 composition of, 17 giant, 62 hypertrophy of, 62 life conditions of, 24 movements of, 19 nucleus of, IS properties of, 19 phagocytic, 19 receptors of, 23, 54 reproduction of, 19 758 INDEX Cells, stimulation of, effects of, 21, 62 stimuli of, 20 Cellulitis, submaxillary, 748 Cement, substance, interprismatic, 156 oxychlorid of zinc. See Zinc. oxyphosphate of copper. See Copper. oxysulphate of zinc. See Zinc. silicate, use of, 306, 397 zinc phosphate. See Zinc. Cementum in dental caries, 364, 372 formation of, 160 histology of, 173 malformations of microscopic, 241 relation of, to enamel, 173 Chalk mixture, use of, 198 use of, 305 Chemotaxis, 51 Chloral, use of, 381 hydrate, use of, 204 Chlorin, use of, 318, 557 nascent, use of, 556, 557 Chloroform, use of, 389, 450, 451, 457 Chloro-percha, use of, 457, 526, 559 Chlorophyll, chemical action of, 36 Chlorosis, 109 Chorea from dentition, 223, 721 Chromic acid, use of, 392 Chromogenic bacteria, 41 Cinnamon, oil of, use of, 703 Circulation, disturbances of, 107 local, 116 Cleansing of teeth, 416 Cleft palate, embryology of, 150 Clot, absorption of, 135 septic, 142 Cloudy swelling, 78 Cloves, oil of, use of, 406, 450 Coagulation of blood, 110, 120, 123 necrosis, 85 Coagulants, use of, 368 Cobalt, use of, 502 Cocain, systemic effects of, 494 use of, 384, 368, 440, 490, 493 Codein, use of, 466 Cold, use of, 118, 131, 226 Colloid degeneration, 81 Color of teeth, 284 Complement, 56 Compress, use of, 114, 226, 581 Concrescence of teeth, 251 diagnosis of, 224 Conical teeth, 242 Constipation, dental pain from, 727 Copper amalgam, use of, 403, 408, 536 oxyphosphate of, use of, 403, 413, 536, 691 sulphate, use of, 702 Cords, dental, 153, 155 Cotton root dressings, dangers of, 544, 610 salicylized, use of, 690 tampons, danger of, 578 use of, as root filling, 528, .529 Counterirritants, use of, 131, 451 Counterpressure in opening tooth, 574 Credo's ointment, use of, 143 Creosote, use of, 532 Crowns, cantilever, use of, 409 removable, 559 Crypts of teeth, relations of, 160 Cup gum, use of, 597 Cups, use of, 118 Curette, use of, 131 Cusps, supplemental, 257 Cysts associated with apical conditions, 589 causes of, 63 dentigerous, 63, 279 dermoid, 64 teeth in, 65 impacted teeth as cause of, 63, 279 varieties of, 63 Deafness, dental, cause of, 623, 721 Decalcification of dentin in dental caries, 356 of teeth, 66, 207, 343 Degeneration, 75 calcific, of pulp, 441 cloudy, of pulp, 488 colloid, 81 of pulp, 488 fatty, 75, 120 of pulp, 488 fibroid, 460 of pericementum, 637 of pulp, 484 hyalin, 79 in mouth, 79 of mucous membrane, 79 lardaceous, 81 mucoid, 80 of mucous membrane, 80 nerve-end of pulp, 488 of pericementum, 630 Dental structure, transparency of, 66 Dentigerous cysts, 63, 279 Dentin in dental caries, 351 decalcification of, 356 secondary, 371 development of, 155 granular layer of, 238 histology of, 167 hypersensitivity of, 375 causes of, 376 diagnosis of, 380 pathology of, 376 symptoms of, 378 treatment of, 380 interglobular spaces in, 238 lines in, 167 of Schreger in, 167, 239 malformations of, microscopic, 238 recalcification of, 403 resorption of, 431, 462, 480 secondary, 426 INDEX 759 Dentin, secondary, bacterial penetra- tion of, 433, 467 caries of, 371 neuralgia from, 432 resistance to acid by, 371, 629 staining of, 316, 362, 554 by putrefaction, 554 stains of, treatment of, 317, 556 tubes of, 167 tubular calcification of, 425 tumor of, 430 Dentinal papilla, 153 Dentition, cause of, 185 constitutional states modifying, 205 normal, 187 pathological, first, 189 as cause of epilepsy, 191 climate and weather in, 191, 192 convulsions in, 194 diet in, 199 headache in, 194 hemophilia in, 197 hemorrhage after lancing in, 196 intestinal complications in, 192, 198 feeding after, 199 lancing in, 195 nervous disturbances in, 193, 204 paralysis in, 194 pulmonary disturbances in, 195 shock after lancing in, 197 skin disorders in, 195, 197 strabismus in, 194 systemic conditions influenc- ing, 205, 222 symptoms of, 191 treatment of, 195 periods of, 188 process of, 187 second, 206 disorders of, 212 irregularities of, 212 necrosis in, 221 pathological, 222 symptoms of, 189 Depletion of gum, 465, 575 of pulp, 457, 465 Derivation, use of, 118, 466, 575, 617 Dermoid cysts, 64 teeth in, 65 Development of face, 147 of teeth, 153 Devitalization of pulp, 497 Devitalizing fiber, use of, 502 Diabetes meUitus, 95 Diagnosis, definition of, 25 forms of, 25 Diathesis, acquired, 87 gouty, 98 hemorrhagic, 113 Diathesis, hyperacid, 60, 87 Dilaceration of teeth, 254 Disease, bacterial causes of, 34 basis of, 21, 24 causes of, 27 clinical history of, 25 existing, as a predisposition, 32 functional, 25 predisposition to, 29 previous, as a predisposition, 32 Discoloration by putrefaction of pulp, 554 Dislocation of teeth, 639 Disuse of teeth, 634 Dobell's solution, use of, 602, 732 Donaldson cleaners, use of, 570 Dover's powders, use of, 575 Downie broaches, use of, 509 Drill, Beutelrock, use of, 612 Gates-Glidden, use of, 513 spear, use of, 573 use of, 508 Dropsical infiltration, 81 Drugs, intoxication by, 94 Dry cups, use of, 118, 596 Dryness, use of, 382 Dwarfism of teeth, 242 Dysentery, ameba of, 35 E Ear, disease of, from dental cause, 623, 724 Eburnation in dental caries, 362, 371 Ecchymosis, 113 Ehrlich's theory of immunity, 54 Electrical disinfection of root canal, 552, 587 Electricity as test, 538 Electrolysis, cataphoric, 515, 552 Emboli, septic, 113 EmboHsm, 112 Embryology of face, 147 of teeth, 153 Emphysema of cheek from air pressure, 550, 594 Empyema of antrum, 600, 604 Enamel, agenesia of, 238 in dental carieS; 324, 344 development of, 156 formation of, effect of exanthemata upon, 234 fracture of, 306, 309 histology of, 157, 233 tubes, Caush's, 165, 167, 232 hypoplasia of, 234, 237 lines of Schreger in, 165 malformation of, macroscopic, 230 microscopic, 233 nodule, 256 opaque spots in, 229 organic matter in, 165 parts of, 164 relation of, to cementum, 173 760 INDEX Enamel, resorption of, 296 sensitivity of, 167 stains upon, 312 strise of, 165, 234 stripes of Retzius in, 234 of Schreger in, 233 tubes of, 165, 233 unusual location of, 255 Endarteritis obliterans, 77, 653 Energy, nerve, loss of, 23, 104 sources of, 23, 93 Epilepsy from dental disease, 191, 721 pathological dentition as cause of, 191 Ergot, use of, 115, 118, 131 Erosion of teeth, 297 acids in, 298 extraneous, 301 causes of, 298 diagnosis of, 303 effects of, 303 malnutrition upon, 90, 299 possible action of glycogen in, 79 systemic factors in, 299 treatment of, 305 Eruption of teeth, causes of. See Dentition Escharotics, effects of, 28, 615 Ether, use of, 384, 389 Ethyl chlorid, use of, 383, 401, 496 576, 579 Etiology, definition of,. 25 Eucalyptol, use of, 529, 549, 552 Eugenol, use of, 406, 450 Evans' root drier, use of, 527 Exanthemata, 145 malformations caused by, 145 necrosis caused by, 145, 221 Exostosis of alveolai process, 623 Extravasation of blood, 113 Extirpation of pulp, 508 Eye, disease of, from dental cause, 623, 724 Face, development of, 147 embryology of, 147 fistula on, treatment of, 602 Fat, degeneration of, 76 infiltration of, 76 necrosis of, 85 Fermentation, bacteria as causes of, 41 definition of, 41 products of, 42, 43 of proteid matter, 43 Ferments organized, 41 unorganized, 42 varieties of, 43 Fever, 139 Fibrin, formation of, 110 Fibroma, 71 Fibrosis of pericementum, 637 Filling materials, use of, 398 Fistulae, 128 in antrum, 600 causes of, 592 on face, threatened, 575, 602 treatment of, 602 healing of, 596 making artificial, 576, 589 packing, 579 premature closure of, 131, 579 Flagg's operation for scar, 602 Fletcher's carbolized resin, use of, 393 Flexion of teeth, 255 Flora, normal, 44 Floss silk, use of, 417, 529 Folhcle, dental, 155, 160 wall of, 155, 158 Food, chemical changes in, 23 supply, abnormal, 27 Foramen, wide treatment of, 529 Formagen, use of, 402, 451, 537 Forma-Percha, use of, 526, 546, 596 Formaldehyd, action of, upon products of putrefaction, 546, 548 uses of, 392, 421, 452, 522, 546, 587, 646 Formo-cresol, use of, 492, 547, 557 Fracture of alveolar process, 639 of teeth, 306 repair of, 308, 431 reunited, 308, 431 treatment of, 309 Fungi as ferments, 41 vegetable, 35 Fusion of teeth, 249 G Gallstones, origin of, 83, 659 Gangrene, 86 circumscribed, 83 dry, 86 moist, 86 discoloration from, 554 of pulp, 537 dry, 537 moist, 540, 558 partial, 545 Galvanism, sterilization by, 552 Gastric juice, action of, on bacteria, 49 Gaultheria, oil of, use of, 703 Gelatin, use and danger of, 115 Gemination of teeth, 254 Geranium-formol, use of, 547 Germicides, action of, 60, 749 Giantism of teeth, 241 Gingivitis, 641 antiseptic washes in, 646 astringent washes in 646 interstitial, 648 resorption of bone in, 652 deeply seated, 648 marginal, 642 systemic causes of, 649 Glycerin, use of, 383 INDEX 761 Glycogen, infiltration of, 79 Glycogenic infiltration in dental caries, 334 Gonorrhea of mouth, 743 Gout, 96 chronic, 97 contrasted with rheumatism, 101 diet in, 99 oral effects of, 568 relation of, to teeth, 710 salts deposited in, 82, 97 treatment of, 99 Goutiness, 98 treatment of, 99 Granulations in regeneration, 132 Grippe, dental pain from, 727 Guards in pericementitis, 452, 574, 618 Gum, depletion of, 465 glycogenic infiltration of, 79 hyperplastic, 478 laceration of, 640 lancing of, 196, 225, 576, 579 marginal atrophy of, 656 Harlan's method in, 657 tissue, action of arsenic on, 504 Gutta-percha, eucalyptol solution of, use of, 400, 526 use of, 400, 409, 451, 526, 530, 596 Halisteresis ossium, 139 Hamamelis distillate, use of, 579 Hands, sterilization of, 750 Harelip, 151 Headache in dentition, 194 from pulp diseases, 720 Healing by second intention, 132 under a clot, 135 Heat, use of, 118, 131 Hematogenic calculus, 658, 677 Hemoglobin, derivatives of, 83 Hemophilia, 113 in dentition, 197 Hemorrhage, acetanilid as cause of, 115 after extraction, 640 pulp removal, 492 local, treatment of, 115, 588, 640 replantation for, 114 treatment of, 115 varieties of, 113 Hemorrhagic diathesis, 113 sex in, 114 Heredity as a predisposition, 31 Herpes labialis, 745 zoster, 745 Histology, morbid, 25 Hoffendahl, electric method of, 552 Hot water, use of, 389 Hutchinson's teeth, 244 Hydrogen dioxid, use of, 137, 226, 471, 580, 597 dangers of, 589 Hydronaphthol, use of, 400, 646, 657 Hydrastis, use of, 115 Hygiene, definition of, 26 Hyoscyaniin, use of, 381 Hyperacidity, 59, 95, 96, 100, 279 Hyj)oracidosis, 89, 95, 96, 100 Hypercementosis, 620 reflex neuroses from, 556, 721 Hyperemia, arterial, 116 collateral, 117 compensatory, 117 degrees of, 117 pathology of, 117 of pulp, 477 arterial, 445 devitalization in, 451 from arsenic, 497 from electric action, 454 idiopathic, 453 thermal toleration in, 453 from root resorption, 623 venous, 455 devitalization in, 451 from hanging, 457 reflex, 116 suffusion in, 455 as a resistance to infection, 1 18 results of, 117 symptoms of, 117 treatment of, 118 venous, 119, 121 suffusion from, 455 Hypernutrition, 61 Hyperplasia, 63 Hypersensitivity of dentin, 373, 375 Hypertrophy, 62 of cell, 62 Hj^phomycetes, 36 Hypnotism, use of, 381 Hyponutrition, 74 Hypoplasia, 74, 243 of enamel, 243 Hypophosphites, use of, 462 IcHTHYOL, use of, 143, 737 Immunity, 33 acquired, 52 and disease, 29 Ehrhch's theory of, 54 influences conferring, 33 local, 33 lost, 33, 51 natural, 51 Impaction of teeth, 269 as cause of cysts, 63, 279 death of pulp from, 279 diagnosis of, 280 neuralgia from, 277 resorption of roots from, 279, 627 symptoms of, 277 treatment of, 223, 281 Implantation, 600 762 INDEX Inanition, 92 Indican as an index of malnutrition, 91 Indol, 94 Infants, feeding of, 199 Infarction, 113 of pulp, 484 Infection, classes of, 45 general septic, 142 of mouth, 729 predisposition to, 29, 30, 33 resistance of tissue to, 49 spreading of, 45 Infiltration, calcareous, 82 dropsical, 81 fatty, 76 glycogenic, 79 pigmentary, 83 Inflammation, 120 bacteria in, 121, 125 bloodletting in, 118, 131 of bone, 136, 604 causes of, 120 derivation in, 118 exudates of, 120, 122, 125 infective, 125 necrosis in, 126 pathology of, 121, 125, 126 of pulp, 458 chronic, 469, 475 resolution in, 124, 126, 131 simple, 120 stimulation in, 131 suppurative, 126 symptoms of, 124, 125, 129 general, 125, 129 treatment of, 131 Inoculation by bacteria, 44 Insanity from dental disease, 726 Insomnia from dental disease, 677 Instruments, sterilization of, 749 Insulator, 295 Intermaxillary bone, failure of develop- ment of, 152 formation of, 147 Interstitial gingivitis, 648 Intestinal complications in pathological dentition, 192, 198 Intoxications, 94 acid, 96 bacterial, 95 drug, 94 intestinal, 94 intrinsic, 95, 96 Intubation of root, 559 lodin, dental, tincture of, 451, 481, 646 use of, 483, 525, 554 Iodoform, use of, 131, 526, 546, 548 lodoglycerol, use of, 646 Iron, chlorid of, tincture of, use of, 333, 580 Ischemia, 116 Joining of teeth, 400, 693 Jugulation of pulp, 456 Kerr broaches, uses of, 509 Krameria, use of, 646 Laceration of soft tissues of mouth, 640 Lactic acid, use of, 513, 524 Lacunae, Howship's, 138 La grippe as cause of antral disease, 604 Lancing for abscess, 576, 579 gum, 196, 225, 576, 579 Lanolin, use of, 143 Laudanum, use of, 118, 198 Lead, oral effects of, 649 use of, 118 water, use of, 118, 575 Leeches, use of, 575 Leukemia, 107, 109 Leukocytosis, 107, 109 Leukoplakia buccalis, 745 Lichen planus, 746 Lime water, use of, 418, 421 Listerine, use of, 198, 647 Lithemia, 100 treatment of, 100 Lithia salts, use of, 655 Liver, functions of, 92 in general malnutrition, 92 Ludwig's angina, 748 Luxation of teeth, 639 M Jaw, enlargement of, cause of, 163 Jodoformagen, use of, 402, 406, 451, 537 Magnesia, milk of, use of, 305, 418, 419 sulphate of, use of, 226, 466 Malaria, dental pain from, 716, 726 Malformations, macroscopic, 241 microscopic, 229 of roots, 258, 516 of teeth, 229 Malnutrition, causes of, 23, 87 general, 87 autointoxication in, 90 cause of, 88 diet in, 91, 99 liver in, 91 from gingivitis, 705 Malocclusion of teeth, 632 causes of, 212 classification of, 213 Malpositions of teeth, 267 Massage, use of, 227 vibratory, 580 Maxillae, embryology of, 147 Maxillary rampart, 153 Meckel's cartilage, 152 INDEX 763 Melancliolia from dental disease, 726 Menthol, use of, 388, 389, 457, 574, 726 Menthol-phenol, use of, 450 Mercury, bichlorid of, use of, 131, 132, 143, 144, 418, 533, 578, 580, 619 as cause of stomatitis, 649 oral effects of, 619, 649 Talbot's experiments on dogs with, 614 Metabolism, diseases of, 87 Metastasis, 144 Methvl chlorid, use of, 383, 496, 576, 579 Microorganisms, as disease causes, 35 Milk, modified, 195, 199 Pasteurized, 195, 196, 199 Morphin, use of, 132, 381, 466, 575 Motor reflexes from dental disease, 725 Mouth, actinomycosis of, 743 asepsis of, 417 bacteria of, 46 general infection by, 142 pathogenic, 46 breathing, 215, 218 gangrene of, 735 gonorrhea of, 743 hyalin degeneration in, 79 infections of, 729 lamp, electric, use of, 373, 538 sepsis from, 419 soft tissues of, laceration of, 640 sterilization of, 514 syphilis of, 737 tuberculosis of, 742 washes, application of, 418, 646 Mucin, characteristics of, SO in dental caries, 334 Mucoid degeneration, SO of mucous membrane, 80 Mucous membrane, glycogen in, 79 hyaUn degeneration of, 79 mucoid degeneration of, 80 overstimulation of, effects of, 79 Mummification of pulp, 493, 537 Mummifj-ing paste, arsenic and, 505 Mustard, use of, 118 Myers' syringe, 493 use of, 387 Myrrh, tincture of, use of, 619, 646 N Xasmtth's membrane, 159. 164 in dental caries, 351 Necrobiosis, 84 Necrosis, 84 after extraction, 578 of alveolar bone, 606 of bone, 138 from alveolodental abscess, 598 from syphilis, 607, 741 coagulation, 85, 127 Necrosis, etiology of, 84 of fat, 85 from exanthemata, 221 from typhoid fever, 221 hquefaction, 86 phosphor, 747 varieties of, 84 Neoplasm of pulp, 489 Nerve energy, loss of, 104 suppl3% abnormal, 28 sensory, of face, 717 trophic influence of, 28 vasomotor, 116 Nervocidin, use of. 389, 496 Nervous disturbances in dental disease, 715 in dentition, 193, 204 Neuralgia, cause of, etc , 715 treatment of, 727 from impacted teeth, 277 from pulp disease, 439, 446, 457, 464, 472, 570 from secondary dentin, 433 Neurasthenia, 90, 104, 105 Neuroma, 155 Neuroses, reflex, 715 Nitric acid, use of, 295, 392 Nitrous oxid gas, use of, 380, 490 Nodule, cemental, 241 in pulp, 434 Noma, 735 Non-conductors, uses of, 400, 450 Nosophen, use of, 131 Nutrition, basis of, 22 deficiency of, 74 disturbances of, 24, 29, 61, 87 excess of, 61 Obligate bacteria, 41 Odontalgia, phantom, 723 Odontoblasts, 154, 167, 172 atrophy of, 429, 477 relation of, to sensor}' nerves, 172 Odontomata, 259 Oligocvthemia, 107 Opiun{, use of, 115, 118, 131, 198 Opsonic index, raising of, 59, 597 Opsonins, 57 Organic matter, decomposition of, 37, 40 fermentation of, 41 Organs, composition of, 22 Orthoform, use of, 606 Osteitis, condensing, 137 rarefying, 137 Osteodentin, 431 Osteomalacia, 420 Osteomyelitis, 137 Osteoporosis, 137 Osteosclerosis. 137 Overarch bar, use of, 632 Overfeeding, 93 764 INDEX Overuse of teeth, 631 Oxaluria, 104 Oxidation, deficiency of, 88 excessive, 88 Oxygen, nascent, use of, 551, 556 Pain, dental, from other sources than dental, 726 postextraction, 624, 640 Palate, cleft, cause of, 150 Papain, use of, 535 Papoid, use of, 131 Paralysis from dental disease, 722, 723, 725 in dentition, 194 Parasitic bacteria, 40 Paraffin, use of, 558, 596 Paraform, use of, 493, 527 Paraglossus, 295 Pathogenic bacteria, 40, 46 Pathogenesis, definition of, 25 Pathology, basis of, 17, 24, 26 dental, definition of, 17 general, definition of, 17 Pediluvium, hot, use of, 118, 575 Peptones, 43, 120 Perforation as cause of abscess, of root, 514, 520, 535, 607 fining of, 536 Perforations by caries, 372, 407 Pericemental abscess of, 708 Pericementitis, 515. See also Pyorrhea alveolaris. acute septic apical, 561 complicated, 603 beginning at gum margin, 641 chronic, effects of, 619 septic apical (non-purulent), 609 purulent, 584 bUnd, 603 with fistula, 589 without fistula, 584 gouty, 710 non-septic, 614 chemical, 615 symptomatic, 618 septic, at bifurcations of roots, 613 in the temporary teeth, 609 traumatic, 614 Pericementum, blood supply to, 171, 181 calcospherites in, 184 cellular element of, 184 flegeneration of, 630, 637 fibroid, 586 development of, 162 diseases of, 562 fibrosis of, 637 function of, 175 glands of, 184 , histology of, 174 Pericementum, nerves of, 182 overuse of, 631 Periostitis, maxillary, 593 proliferative, 136 suppurative, 137 Peru, balsam of, use of, 599 Petechia, 113 Phagocytosis, 19, 50 Phantom odontalgia, 723 Phenacetin, use of, 381, 466, 728 Phenobromate, use of, 381 Phenol camphor, use of, 381, 406, 472 sodique, use of, 194, 418, 640 Phenolsulphonic acid, 597 Phosphates, use of, 305, 421 Phosphaturia, 104 Phosphor necrosis, 747 Phosphorus, use of, 305 Physical condition, abnormal, 28 Physiology, morbid, 25 Pigmentary infiltration, 83 Pigmentation in dental caries, 362 Pigments in tissue, 83 Pilocarpin, oral effects of, 618 Pins, removal of, 550 Piscidia erythrina, use of, 381 Plantation, mode of attachment in, 628 Plaques, microbic, 342 Plaster of Paris, use of, 406 Plethora, 107 Pneumonia, bacterium of, 47 Podophyllin, use of, 602 Pointing, 128 Polycythemia, 107 Potassocain, use of, 384 Potassium bromid, use of, 728 carbonate, use of, 383 chlorate, use of, 194, 619, 646 iodid, ill effects of, 618 Poultices, danger of, 581 uses of, 131 Powder, tooth, use of, 417 Precipitins, 57 Predisposition to disease, 29 general, 29 local, 32, 33, 45 Pregnancy, dental pain from, 727 Pressure anesthesia, 384, 398, 457, 465, 471, 475, 482, 490, 507 hemorrhage after, 515, 615 Prognosis, definition of, 25 Prophylaxis, 416, 420 Proteid, composition of, 18 fermentation of, 44 use of, 23 Protoplasm, composition of, 18 properties of, 22 Protozoa as disease causes, 35 Pseudoodontalgia, 723, 727 Ptomains, 43 Pulp, abscess of, 471 action of arsenic on, 497 anesthesia of. See Pressure. . arteriosclerosis of, 476 blood supply, 169 INDEX 765 Pulp, capping of, 405 cavity duplication of, 254 forms of, 173 constructive diseases of, 423 death of, from impaction, 279 symptoms of, 538, 545, 573 degeneration of, 424 calcific, 441 cloudy, 486 colloid, 488 fatty, 488 fibroid, 484 nerve, 488 depletion of, 575 destructive diseases of, 444 devitalization of, 497 digestion of, 535 exposure of, sj^mptoms of, 404 treatment of, 405 extirpation of, 508 gangrene of, 537 partial, 545 histology of, 167 hyperemia of, 445 arterial, 445 devitalization in, 451 from electric action, 454 idiopathic, 453 thermal toleration in, 453 from arsenic, 497 venous, 455 suffusion in, 455 hyperplasia of, 477 infarction of, 484 inflammation of, 458 chronic, 475 jugulation of, 456 •'knocking out," 506 mummification of, 533 neoplasm of, 489 nerves of, 171 nodules, 434 and arsenic, 440 puncturing of, 471, 457, 465, 507 putrefaction of, 540 removal of, 490, 508 partial, 532 special methods of, 506 replantation of, vitality after, 431 sclerosis of, 475 suppuration of, 466 swelHng of, 462 thermal tolerance of, 424 tissues, action of arsenic on, 497, 502, 504 toughening, 513 ulceration of, 469 vitaUty of, tests for, 538, 545, 573 Pulpitis, 458 acute, 459 chronic, 475 resorption of dentin in, 462 hyperplastic, 477 Pumice, use of, 419 Purpura hsemorrhagica, 748 Pus formation, stages of, in apical abscess, 566 varieties of, 129 Putrefaction, 43, 86, 142, 540 formalin in, 546 germs of, effects of electricity upon, 552 of pulp, 537 Pyemia, 144 Pyocyaneo-protein, use of, 607 Pyogenic calculus, 677 Pyorrhea alveolaris, 678 abscess secondary to, 685 beginning with a marginal gingivitis, 680 bridge and plates in, 700 in bifurcations of roots, 591 causes of, 678 clinical history of, 681 and dental caries, 687 diagnosis of, 688 endarteritis in , 653 gum incision in, 690 heteroplasty of roots in, 691 interstitial gingivitis in, 630 and living pulps, 687, 691 looseness in, 683 malnutritional factor in, 648 not dependent upon calculus, 706 opsonic index in, 704 oral catarrh in, 685 pathology of, 629 prevention of motion in, 693 prophylaxis in, 688, 704 recurrence of, 705 replantation in, 704 root amputation in, 691 splints for use in, 693 systemic effects of, 705 symptoms of, 681 treatment of, 688 medicinal, in, 701 varieties of, 680 Pyrozone, use of, 500, 556, 596 Q QuiNiN, use of, 132, 144, 443, 575, 580 RacHiTis, 103 Rampart, maxillary, 153 Recalcifi cation of dentin, 403 Receptors of cells, 23, 54 Reflex action, 189, 192, 715 disorders of dental origin, 715 of systemic origin, 715, 726 pain, pathology of, 720 Refrigeration in hypersensitive dentin, 383 use of, 576 766 INDEX Regeneration of tissue, 132 Replantation, 599 secondary dentin after, 431 for hemorrhage, 114 of pulp, vitality after, 431 of teeth, 599 Resorcin, use of, 143 Resorption of bone, 138 varieties of, 138, 601 of permanent roots, 271, 625 of temporary roots, 207 teeth, 207 Retzius, stripes of, in enamel, 234 Rhein, root methods of, 520, 550, 596 Rheumatism, 101 chronic, 102 contrasted with gout, 101 muscular, 103 treatment of, 102 Ridge, dental, 153 Robinson's remedy, use of, 295, 391, 691 Root, amputation of, 598 calcification of, 162, 164 canal, accidents in opening, 523 anatomy of, 547 electrical disinfection of, 587 filUng of, 525 inaccessible foramina of, 531, 550 loss of continuity of, 523 development of, 162 drier, Evans', use of, 527 filling, immediate, 515, 525 removal of, 549 implantation, 600 intubation, 559 loss of, by caries, 372, 410 malformations of, 258, 521 multiple, 258 perforation of, 514, 524, 535 permanent, formation of, 210 resorption of, 625 replantation of, 599 resorption of, 207, 625 of permanent, 625 sterilization of, 546 temporary, resorption of, 207 transplantation of, 599 Rose geranium, oil of, use of, 547 S Saccharin, use of, 198 Saccharomyces albicans as disease cause, 35, 730 Salicylic acid, use of, 646 Saliva, analysis of, 661 in dental caries, 334, 339 in general malnutrition, 89, 299 increased flow of, 191, 715 infective bacteria in, 730 non germicidal action of. 48 Salivary calculus, 658 Salivary calculus, analysis of, 660 foreign bodies in, 610 hardening of, 665 mode of deposit of, 663 origin of, 659 pathological effects of, 667 recurrence of, 670, 673 scalers for, 668 structure of, 660 Salol, use of, 132, 144, 198, 527, 580 Salter, lines of, in dentin, 167 Sanguinary calculus, 623 Sapremia, 142 Saprophytic bacteria, 41, 44 Sarcoma, 70 Schizomycetes, 37 Schreger, lines of, in dentin, 167 in enamel, 233 Sclerosis of pulp, 475 Scorbutus, 103, 748 Scurvy, 103 infantile, 205 oral effects of, 619 Sedation, results of, 21 Sedatives, use of, 450, 465, 475 Sepsis, dental, 420 general, of dental origin, 743 intoxication from, 141 Septic intoxication, 141 Septicemia, 45, 142 from apical abscess, 568, 579, 582 threatened, 568, 579, 582 Serres, glands of, 184 Serum therapy, 55, 74, 115 Sheaths of Neuman, 167 Silicate cements, use of, 403, 413 Silver, Crede's ointment, use of, 143 soluble, use of, 144 nitrate, use of, 295, 391, 412, 419, 452 Sinus, 128 Skiagraphy, use of, 440, 572 Skin eruptions in dentition, 195 Slough, 87 Sodium biborate, use of, 646 bicarbonate, use of, 391, 655 bromid, use of, 204 chlorid, use of, 305, 525 dioxid, danger of, 551 use of, 391, 551, 557 and potassium, alloy of, use of, 524 sulphate, use of, 115, 418 Somnoform, use of, 490 Sphacelus, 87 Sponge grafting, use of, 608 Stains, black, 315 in dentin, 316 green, 314 metallic, 312 non-metallic, 314 red, 316 tobacco, 316 treatment of, 317 Starvation of tissue, 92 Stellate, reticulum, 154 INDEX 767 Steresol, use of, 282 Sterilization, dental, 514, 749 Stimulation, effects of, 61 results of, 21 Staples, use of, 311 Stomatitis, 643, 731 classification of varieties, 732 in dentition, 195, 197 infective catarrhal, 732 mercurial, 618 beneficial effects of mercury in, 619 simple catarrhal, 732 symptomatic catarrhal, 733 ulcerosa, 643 ulcerative, 734 Strabismus in dentition, 194 Stratum intermedium, 154 Strychnin, use of, 144, 728 Subgingival calculus, 673 Suffusion, 113, 455 from arsenic, 498, 506 from hanging, 457 from venous hyperemia, 455 Sugar in diabetes, 95, 338 as source of energy, 23, 93 Sulphocyanate, use of, 394 sulphocyanids in dental caries, 339 Sulphuric acid, use of, 115, 492, 511, 524, 597 Sulphurous acid, use of, 558 Supernumerary teeth, 265 Supplemental cusps, 257 Suppuration in inflammation, 126 of pulp, 446 Suprarenal extract, use of, 115 Susceptibility to disease, 29 Symptoms, definition of, 25 objective, 25 subjective, 25 Synostosis, dental, 625 Syphilis, dental pain from, 715, 741 of mouth, 737 necrosis of bone from, 607, 741 oral effects of, 738 Syphilitic teeth, 244 Syringe, Myers', 493 Tannin, use of, 383 Teeth, abrasion of, 284 absence of, 262 accidents to, 639 anomalies of. See Malformations. attachment of, 253, 639 blood supply of, 181 brushing of, 416 change in color of, 284, 554 cleansing of, 416 color of, 289 concrescence of, 251 conical, 742 crypts of, relations of, 160 Teeth, decalcification of, 207, 343 in dermoid cysts, 65 development of, 153 discoloration of, 455 disuse of, 634 dwarfism of, 242 embryology of, 153 erosion of, 297 eruption of, causes of, 185 flexion of, 255 fractures of, 306 fusion of, 249 gemination of, 254 giantism of, 241 histology of, 164 Hutchinson's, 244 impaction of, 269 injury of mechanical, 306 joining of, 400 luxation of, 639 malformations of, 229 malocclusion of, 213, 264, 267, 632 malposition of, 267 overuse of, 631 permanent, development of, 162 eruption of, 206 replantation of, 599 size of, variations in, 241 stains on, 312 structure of, in dental caries, 335 supernumerary, 265 supplemental cusps on, 257 syphilitic, 234, 246 temporary, caries in, 411 eruption of, 187 devitalization of, 507 pericementitis in, 609 resorption of roots of, 207 retained, 212 transplantation of, 600 variations in number of, 262 Temperament, classes of, 31 Therapeutics, basis of, 20 definition of, 17, 25 empirical, 26 rational, 25 Thrombosis, 111 Thymol, use of, 406, 422, 450, 527, 533, 534 Thymophen, use of, 450 Tic douloureux, 725 Tissue, composition of, 22 excessive destruction of, 93 food supply to, 22 regeneration of, 132 resistance of, to bacteria, 49 starvation of, 92 waste, excessive, 93 Tomes, granular layer of, 239 Toxalbumins, 43 Toxemia, 45, 128, 141 in general malnutrition, 94 Toxins, 43 chemotactic properties of, 51 as ferments, 43 768 INDEX Toxins, immunity to, 52 Toxoid, 56 Toxon, 56 Transparency of dental structures, 66 Transparent zone, 360 Transplantation, use of, 599 Trephine, use of, 577 Trichloracetic acid, use of, 481, 606 Tricresol, use of, 503, 561 Trioxymethylen, use of, 392 Trophic disturbance, 28 from dental disease, 726 Tube casts in dental caries, 359 Tuberculosis of mouth, 742 Tubes of dentin, 167, 354 of enamel, 165 Tubular calcification, 425 Tumors, 66 causes of, 68 classes of, 68, 69 definition of, 64 effects of, 67, 70 epithehal, 72 malignancy, 66, 70 metastasis in, 70 morbid anatomy of, 68, 70 sarcomatous, 70 treatment of, 74 U Ulceration, 130 of pulp, 469 Uremia, 95 Urates in pericementum, 710 in tissue, 97 Uric acid in gout, 96 Uvula, bifid, 152 Vaccine therapy, 59, 144 Vapocain, use of, 384 Vascular system, disturbances of, 107 Varnish, use of, 399, 402 Vaselin, use of, 535, 581 Vasomotor nerves, 116 Vegetable fungi, 34, 36 Venous hyperemia, suffusion from, 455 Veratrin, use of, 225 Vincent's angina, 749 W Wall, follicular, 155 Waste removal, abnormal, 28 Wax, use of, 527 Wood points, use of, 673 X-RAY, use of, 440, 572 Zinc chlorid, use of, 596, 646 iodid, use of, 646 oxid and eugenol, use of, 402, 406, 451 use of, 411 oxychlorid of, use of, 401, 402, 406, 527, 556, 558 oxysulphate, use of, 406 phosphate, use of, 399, 401, 451 sulphate, use of, 389 Zooglea of bacteria, 39 COLUMBIA UNIVERSITY LIBRARIES This book is due on the date indicated below, or at the expiration of a definite period after the date of borrowing, as provided by the rules of the Library or by special ar- rangement with the Librarian in charge. DATE BORROWED DATE DUE DATE BORROWED DATE DUE JCTl ^^ I. DEC 6194! I - C28H 14O)M100 COLUMBIA UNIVERSITUIBRARIES (hslslx) RK 301 B892 1912 C.1 A text t)ook of dental patholnqv and ther 2002339153 RK301 I- Burchard B89r^ 1911?