COLUMBIA LIBRARIES OFFSITE HEALTH SCIENCES STANDARD HX00044091 Columbia Winihev^itp in tfje €itp ot i^eto gorfe ^ o^v^ ^cfjool of Bental anb d^ral burger? l^eference Hitirarp '7> Digitized by tine Internet Arcliive in 2010 witli funding from Open Knowledge Commons (for the Medical Heritage Library project) http://www.archive.org/details/compendofdentalpOOburc COMPEND DENTAL PATHOLOGY THERAPEUTICS. Henry H. Burchard, M.D., D.D.S, SPECIAL LECTURER UPON DENTAL PATHOLOGY AND THERAPEUTICS, PHILADELPHIA DENTAL COLLEGE. PHILADELPHIA : The S. S. White Dental Mfg. Co. 1896. S5 N^ovau \ Copyright, 1896, by The S. S. White Dental Manufacturing Company. DEDICATED TO THE MEMORY OF THE author's FRIEND, 5a6. JE. (BarretBon, 'B./Ifc., /IR.I)., 2).D.S., WHOSE LIFE-WORK WAS THE TEACHING OF PRINCIPLES. PREFACE. T^HIS little volume is not prepared as an aid to students in memorizing answers for an examination ; the end of the book would be defeated were it used for any such purpose. In framing the questions and answers an endeavor has been made to have each of them represent a guiding prin- ciple in dental pathology or therapeutics. It is essentially a student's note-book, to which additions and details are to be made m conformity with didactic teachings. Prepared primarily for students attending his own lectures, the writer ventures the hope that the book may be found useful to dental students in general, and incidentally to other teachers. H. H. B. CONTENTS. PAGE General Principles i Hyperemia or Congestion 13 Inflammation iS Bacteria . . 19 Fever 24 Septicemia and Pyemia 27 Embolus and Thrombus 28 Necrosis 28 Regeneration 29 Dental Histology 30 Dental Anatomy 36 Dental Embryology ^4 Malformations of the Teeth . . . . - 49 Primary Dentition So Eruption of the Permanent Teeth ... 55 Diseases of the Enamel .57 Green-Stain 58 Diseases of the Dentine and Pulp ... 59 Dental Caries . 67 Therapeutics of Caries . . . . . .71 Hyperemia of the Pulp — Grades and Effects . 75 Inflammation of the Dental Pulp . . . 77 Pulp-Capping 79 Extirpation of the Pulp 82 Suppuration of the Pulp 88 Diseases of the Pericementum .... 92 Calcic Inflammation and Calculi .... 109 Pyorrhea Alveolaris . . . . . .111 Erosion of the Teeth 120 Dental Pharmacology and Materia Medica . 121 Dental Medicine Cabinet 130 CoMPEND OF Dental Pathology and Therapeutics. 1. What is patholog-y? It is the science which treats of the natural his- tory of disease; it is morbid biology. The word is derived from the Gr. pathos, disease, and logos, a discourse or treatise. 2. What is biology? It is the science which treats of life : derived from the Gr. bios, life, and logos. 3. What is meant by life? It is a distinctive and persistent energy always associated with a substance called protoplasm. 4- What is protoplasm? The physical basis of life. Its exact chemical composition is unknown. It contains C, O, H, and N, combined with S and P, in enormous molecules. 5. What are cells? Small masses of protoplasm which exhibit the sum of phenomena called life. ,6. What are these phenomena? They are called the functions and properties of cells. They are irritability, contractility, and the 2 COMPEND OF power of growth-maintenance and reproduction, together Avith the nutritive functions of secretion, digestion, and excretion. 7. What is the anatomical composition of a typ- ical cell? It has a definite boundary outlining its form, called the cell-wall. A small spherical body occu- pies some portion of the cell; this is the nucleus; surrounding the nucleus and inclosed by the cell- wall are what are known as cell contents. The cell contents are traversed by a line reticulum, the nucleus by a more dense one. The substance of the net-w^ork is by some supposed to be the proto- plasm, the fluid or semi-gelatinous substance oc- cupying the net-work, the pabulum. 8. What are the necessary conditions for the proper performance of cell function? The cell must inherit fro;ii its parent the stand- ard measure of vitality. It must receive a proper food supply; it must be maintained at the proper temperature, and its waste products must be re- moved. 9. What are the conditions and offices of foods? They are in solids, liquids, or gases. Cell func- tion is largely manifested in a process of oxida- tion. A supply of the gas, oxygen, is therefore necessary. Water is necessary as a circulating me- dium, and to hold the various solids in solution, which are required for the nutrition of the cells. 10. What are the observed chemical phenom- ena attendant upon cell life? DENTAL PATHOLOGY AND THERAPEUTICS. 3 Materials of knoAvn and complex chemical com- position are taken into the cell as food; these are in part built into still more complex form by the cell becoming part of it; substances are discharged which have a more simple composition than the food. The chemical action through which this de- composition is brought about is oxidation, which is manifested by the production of heat. II. Under what heads may the conditions of life be placed? Under innervation; in the cell, the power resid- ing in that body of performing function. Circula- tion; including the proper food supply, and the re- moval of waste products. Respiration includes the supply of oxygen and the removal of the carbon dioxid. .12. In what three ways is vital energy mani- fested? In nutritive, functional, and reproductive action. The first includes the three conditions of life. The work or office of the cell is embraced in the sec- ond; the power of generating bodies similar to itself in the last. 13. What term do we apply to the normal per- formance of the functions of cells? Health, — vital equilibrium, or a condition of ease. 14. What term is applied to their abnormal per- formance? Dis-ease, dis-health, or a disturbance of vital equilibrium. 15. How are diseases divided? 4 COMPEND OF Into functional and structural. Structural dis- eases are those in which there is a demonstrable al- teration in the structure of the cell. Functional diseases are those in which structural change can- not be demonstrated, and yet there is evidence Oi disturbance in one or more of the cell functions. 1 6. Have all cells an equal resistive power to the causes of disease? No: some are weak, inheriting the weakness from parents, and from a variety of other additional causes they yield to disease, — that is, they have a predisposition toward disease. 17. Of what importance is an exhaustive knowl- edge of cell function and structure? The functions of any animal body are comprised in the functions of its cells. 18. What is the difference between a simple or- ganism, such as an amoeba, and the highest or- ganism — man ? The essential nature of vital activity is alike in both, but the simple functions which are performed by the general body of an aniaba are multiplied and elaborated progressively in higher animals; certain portions of the body are outlined for the performance of single functions. An animal is classified in the zoological scale according to the extent to which it possesses organs for special func- tions. These functions, no matter how subdivided, may still be included under the three heads, inner- vation, circulation, and respiration. This is the tripod of life. (Bichat.) DENTAL PATHOLOGY AND THERAPEUTICS. 5 19. To what systems in the human body do these correspond? Innervation, to all the functions of the nervous system, from the simplest reflex act to the highest thought. Circulation, to the alimentary, circula- tory, and excretory systems. Respiration, with the pulmonary system, including the blood-corpuscles and the organs in which they are formed. It is es- sential to health that all three of these functions, no matter how subdivided, be properly performed. Any interference with either constitutes disease. 20. What is a collection of cells of one type called? A tissue. 21. What is an organ? Organs are tissues of several types built into def- inite forms, the ofQce of the organ being the per- formance of a distinct function. 22. What power is inherent in all vital tissues? The power of repair after injury. 23. In the study of disease what elements are first considered? Hereditary influences, the food supply, the vas- cular system, the nervous mechanism, and excre- tion. 24. What knowledge is an essential preliminary to the study of disease of a part? A familiarity with its anatomy, both macroscopic and microscopic, with its embryology, or its mode of origin and formation. Its physiology must be known; that is, the student should be familiar with the mode of performance of its function. D COMPEND OF 25. What are the two general classes of influ- ences affecting vital activity? Stimulation, or agencies which tend to increase activity. Sedatives, those which decrease it. 26. What is the effect of stimulation upon cells? It depends upon tlie degree. A mild stimulus in creasciS the functional activity; over-stimulation produces paralysis of cell function. 27. What is the effect of sedation? A lessening of cell function, of vital activity; if prolonged, it produces paralysis of cell function also. The stimulation or sedation may be of any of the cell functions. 28. What is meant by etiology? It is the science which deals with the causes of disease. (Gr. cctios, cause.) 29. What is meant by semeiology? The science which treats of the signs and symp- toms of disease. It is derived from the Greek of semeion, a mark or sign, and logos. 30. What are signs and symptoms? Signs are the objective evidences of disease noted by the practitioner. Symptoms are the subjective evidences elicited from the patient. 31. What is meant by the pathology and mor- bid anatomy of a disease? Morbid anatomy describes the changCiS which have occurred in tissues as the result of disease; pathology describes the vital actions through which these changes have been brought about. 32. What is meant by the clinical history of dis- ease? DENTAL PATHOLOGY AND THERAPEUTICS. 7 It is the natural histor}^, dealing with the first evidences of disease and describing its natural pro- gress to the termination. 33. What is meant by diagnosis? The discrimination of a disease, the determining of its nature. It is derived from the Greek dia, through, and gignosko, I know (gnosis, knowledge). 34. What is meant by prognosis? Foretelling the probable course and termina- tion of a disease. It is derived from the Greek pro, before, and gignosko, gnosis. 35. What is meant by pathogenesis? It deals with the origin and development of dis- ease. Pathos, disease; gennao, I produce. It com- prises etiology, the science of the causes of disease, with pathology, morbid anatomy, and semeiolog3^ 36. What is meant by therapeutics? It is the science and art of the treatment of dis- eases. Greek tJierapeucin, to take care of, to heal. ■Tfy. How is therapeutics divided? Into rational and empirical. Rational therapeu- tics aims to cure disease by removing its cause, remedies being applied with a full knowledge of their mode of action. Empirical therapeutics ap- plies remedies without such knowledge. 38. How may the causes of disease be divided? Into extrinsic, or those which affect the organism from without ; and intrinsic, those which have origin Vvathin the organism. 39. How may the causes of disease be again di- vided? Into predisposing and exciting. iS COMPEND OF 40. What is meant by predisposing causes? Influences which lessen the resistance of a part to the attacks of disease. The usual order of the in- fluence of predisposition is: i. Heredity: defective structure of a part, either inherited or acquired. The defect may not be discoverable, except through such evidence as imperfect function. Heredity is markedly shown in phthisis, gout, cancer, syphilis, asthma. 2. Existing disease, by lowering the vital tone, may predispose to other disease. 3. Previous disease; a part once subjected to inflammatory dis- turbance has lessened vitality. Immunity from dis- ease may be acquired through an attack of the disease, or by inoculation. The exanthemata are examples of this. 4. Debilitating influences, in- cluding hereditary influences. 5. Temperament. 6. Age; certain diseases have a predilection for a definite period of life. 7. Sex; anatomical and physiological differences of the sexes predispose to certain disorders. 9. Occupation ; for example, ex- posure to cold and wet will predispose to rheuma- tism, exposure to phosphorus fumes to necrosis of the jaws. 41. What is meant by a diathesis? A constitutional predisposition toward some dis- ease. 42. What is meant by cachexia? The constitutional manifestations of hereditary disease, such as syphilis or tuberculosis. 43. What are exciting causes of disease? Those which give direct origin to a malady. DENTAL PATHOLOGY AND THERAPEUTICS. 9 44. Under what heads may they be arranged? Abnormal blood-supply; an excess or deficiency in the blood or of its constituents, including prod- ucts present as the result of faulty excretion; those present in consequence of the introduction of para- sites or their products, or due to faults of blood- formation. 2. Abnormal physical conditions, in- cluding injuries from any cause whatever, acting either froin without or within. 3. Altered nerve- influence. 45. What is the great clinical division of dis- eases? General and local. The first, those which exhibit widespread disturbance; the second, those which afifect but a limited area. 46. Why is this division delusive? Many local diseases are attended by general dis- turbance ; many general diseases have a local origin, a focus of disease. 47. What three factors must be considered in the study of disease in a part? The condition of its anatomical parts and its physiology. This includes a study of the cells and intercellular substance of a part; its vascular supply, including any aberrations in the blood or blood- vessels, and the removal of waste products; the condition and action of the nervous supply. 48. What is the primary consideration? The nutrition of the part, intimately associated with the vascular supply. 49. What factors are first considered in this con- nection? The composition of the blood, and its distribution. 3 lO COMPEND OF 50. What is the normal composition of the blood? A viscid, opaque, red, and sHghtly alicaline fluid, S. G. 1055, and a mean temperature of 99° F. or about 37° C. It contains — Water, 78.16 per cent 781 Dry corpuscles, 13.50 per 1000 135 Albuminoids, 7.00. 70 Fibrin, 0.25 2.5 Fats, 0.17 1.7 Extractives, 0.84 8.4 Earthy phosphates, 0.03 0.3 Iron, 0.05 o 1000 Its composition varies as to time and situation. Blood contains the supply of food, including oxy- gen, for the nourishment of the tissues, together with waste products to be eliminated. 51. What is the composition and ofifice of the red corpuscles? They are oxygen-carriers; the body of the cor- puscle is made up of a reticulum, in the meshes of which is contained hemaglobin, the oxygen-carrier. Any deficiency in this substance is followed by defective oxidation, or faulty nutrition of cells. They are present in the ratio of about 500 to i of the white corpuscles. 52. What is an important function of the white corpuscles? The devouring of foreign bodies which gain ac- cess to the body. DENTAL PATHOLOGY AND THERAPEUTICS. II 53. What is this process called? Phagocytosis (see under Bacteria). 54. What is meant by plethora? An excess of the volume of blood. It may be sthenic or asthenic. 55. What is meant by anemia? An increase of the number of white corpuscles as compared with the red. Anemia may be benign or pernicious; acute or chronic. Acute anemia re- sults from hemorrhage. Chronic anemia may be due to repeated hemorrhage, as, for example, from menorrhagia. All debilitating diseases may be at- tended by anemia; malaria is a prominent cause. Improper food-supply is a prolific source of a usually benign anemia. 56. What abnormal constituents of the blood are productive of disease? Waste products, retained in the circulating blood, and which should be excreted; such as urea, uric acid (urates), and other products of tissue metabol- ism, and an excess of other waste products. The waste products arising through the action of bac- teria. 57. What are these substances called? Intoxicants and poisons. 58. What is the most prominent cause of the presence of an excess of waste products? Failure of the excretory apparatus in their elim- ination. The kidneys are more often at fault than any other organs. An increased production is the next cause. 12 COMPEND OF 59. What factor is next considered as regards the blood-supply? The vascular mechanism, including the action of the heart, blood-vessels, and lymphatics. 60. What is the usual method of noting the con- dition of this mechanism? By the pulse. Noting the force, volume, and fre- quency with which the blood is driven through the vessels. 61. How is the pulse noted? By pressure upon a superficial artery of sufificient size to give a well-marked pulsation. The radial, temporal, and facial arteries are those usually se- lected. 62. What may be learned from the pulse? The force, frequency, and regularity of the heart- beat; also the condition of the walls of the artery. The average pulse is 75 per minute, which gives the sensation, when felt, of a gradually and quickly rising and subsiding wave. It is susceptible to changes of volume, frequency, and regularity. 63. How are the conditions of the pulse desig- nated? Full or small, relating to volume. Hard or soft, relating to tension. Quick or slow, relating to frequency. Regular or intermittent, relating to regularity. Increased volume, and frequency, are indicative of a full vascular supply to the organs. Smallness and softness to a diminished supply. Increased frequency is an associate of smallness and softness, in conditions of debility. DENTAL PATHOLOGY AND THERAPEUTICS. 1 3 Increase in frequency, volume, and tension are associates of sthenic inflammation. 64. What local vascular conditions follow upon conditions of the pulse? Increase of the heart's action is followed by a filling of the arteries and emptying of the veins. A decrease of its action is followed by the reverse con- dition — a filling of the veins and a diminution of the blood in the arterial system. Hyperemia or Congestion. 1. What is meant by hyperemia? It is an excess of blood in the more or less dilated vessels of a part. 2. What types of congestion are recognized? Arterial, or active; and venous, or inechanical hyperemia. 3. What is active hyperemia? It is an excess of arterial blood in a part, with an acceleration of flow. 4. What is its immediate cause? Diminished arterial resistance. 5. To what may this be due? ~ Fatigue of muscular walls of the artery, due to overwork or injury, or the removal of support to which the arteries have been accustomed. Second, to vaso-motor influences; the vaso-con- strictor nerves are paralyzed, or the vaso-dilator nerves are stimulated. 6. What is the accompaniment of arterial hyper- emia? Increased redness and swelling of a part. 14 COMPEND OF 7. How is hyperemia produced as a reflex? The irritation of a part is followed by a constric- tion of the neighboring arteries; if the irritation is continued, the reflex is weakened and the vessels dilate. 8. What are the symptoms of hyperemia? An increase of the functional activities of the parts supplied by the dilated artery occurs; sensa- tion and nutrition are increased. There is a sub- jective sense of throbbing, and the part is reddened. 9. What are the results of continued hyperemia? Hypertrophy and permanent dilatation of the af- fected arteries. 10. What is its treatment? Removal of exciting cause. Derivation, a draw- ing of the blood to other parts, by means of cathar- tics, diaphoretics, and counter-irritants applied at a distance from the affected part. Lessening of the pulse and of nervous excitation, by means of arterial and nervous sedatives. 11. Define these agents and explain their modes of action. Cathartics are agents which increase the activity of the bowels; administered to produce watery evac- uations. Diaphoretics increase the flow of per- spiration. Diuretics increase the flow of urine, the general volume of the blood being lessened by all of these means. Counter-irritants are agents which cause a flow of blood to the part where they are applied. Vesicants cause a pronounced irritation, producing a blister. Arterial sedatives reduce the DENTAL PATHOLOGY AND THERAPEUTICS. 1 5 frequency and strength of the heart's pulsation. All of these measures tend to lessen the amount of blood carried to an inflamed part in a given time. 12. What are the distinguishing features of venous congestion? An increase of blood in the dilated capillaries and veins of a part; its motion diminished. 13. What is its cause? Usually, mechanical interference with the re- turn of the blood through the veins; it is called, in consequence, mechanical hyperemia. 14. How are the causes divided? Into those which lessen the propelling force, the vis a tergo; and those which form an impediment to the return of the blood to the heart, introducing a vis a -f route. 15. What are the effects? An accumulation of waste products in the re- tained blood, diminished nutrition of the part, and serous effusions into the lymph-spaces. 16. What is its treatment? Support to the dilated veins; the means of secur- ing the support will depend upon its anatomical situation. Bandages, massage, and elevation of the congested part are indicated. Astringents are em- ployed in some situations. Inflammation. I. What is inflammation? The succession of changes which take place in a living tissue as the result of some kind of injury, l6 COMPEND OF provided this injury be insufficient to immediately destroy its vitality. (Sanderson.) It is essentially a local tissue degeneration, com- bined with pathological exudations from the blood- vessels, followed sooner or later by tissue prolifera- tion, leading to regeneration or hypertrophy. (Ziegler.) 2. What are its causes? The presence of an irritant acting locally and with a greater intensity than productive of hyper- emia. 3. Under what three heads is the process of simple inflammation described? Changes in the blood-vessels and circulation. Exudation of fluid and of blood-corpuscles from the vessels. Changes in the inflamed tissues. 4. Describe the process as seen under the mi- croscope. A transient contraction of arterioles is followed by their dilatation. The blood flows with increased velocity through the vessels. Soon a disposition is exhibited by the white corpuscles (leucocytes) to cling to the walls of the small veins. It is around these vessels that the phenomena of inflammation are observed. The leucocytes appear to cling to the walls of the venules, which seem to exhibit an affinity for them. They mass in such numbers that the central blood-stream is obstructed. An exuda- tion, rich in albumin, is nourcd from the vessels into the tissues, and next leucocytes may be seen DENTAL PATHOLOGY AND THERAPEUTICS. 1/ passing through the walls of the veins (diapedesis). The cells accumulate in the tissues about the ves- sels. Some of them are taken up by the lymph- stream. The subsequent history depends upon the nature of the inflammation. 5. What are the symptoms of inflammation? Redness, heat, pain, and swelling, with altered function of the inflamed part. Any of these symp- toms, except the last, may be absent. 6. What are the causes of these phenomena? The presence of an increased amount of arterial blood causes redness and heat. The swelling is caused by the exudation: the pain is probably caused by pressure upon nerve-filaments. 7. What are the terminations of inflammation? Resolution, or a gradual cessation of the symp- toms ; necrosis, or a death of tissues in the inflamed territory; chronic inflammation, or a persistence of inflammatory action, Avith an absence of acute symptoms. 8. What is the treatment of inflammation? Removal of the exciting cause and reestablishing the equilibrium of the circulation. 9. What is the principle of abortive treatment in acute inflammation? The removal of the stagnation in the vessels of the inflamed area. 10. HoAV is this accomplished? By removing the cause of its stagnation, remov- ing the blood from the venous side of the area. 4 lo COMPEND OF Experiments have shown that lessening the amount of blood carried to the part, though a depression of the heart's action, is less effective, as also are means called derivation, except in the very early stages of inflammation. 11. How is the first object accomplished? By local blood-letting. 12. How is this done? By means of leeches, scarification, and wet cups. 13. Describe these. The leech is applied beyond the margin of the inflamed area; by means of its tripartite toothed jaws it effects an opening through the slcin, and bv means of its sucker abstracts blood. The Swedish leech removes about half an ounce of blood; the American leech half as much. The operation of scarification consists of making a series of inci- sions with a lancet, producing a flow of blood which tends to unload the engorged vessels. Wet cupping is done by drawing a volume of blood by means of dry cups, and scarifying the cupped areas. Blisters and counter-irritants (applied at a distance) are milder means of producing the same effect in a less degree. 14. What are the means and measures adopted for combating inflammation called? Antiphlogistic treatment. 15. What is the most usual of these means, and what end does it serve? Applications of cold. By contracting the blood- vessels it leasens the symptoms of inflammation. DENTAL PATHOLOGY AND THERAPEUTICS. 1 9 " i6. What agents are administered in the early- stages of inflammation to overcome the vascular symptoms? Ergot and arterial sedatives, aconite, veratrum viride, and gelsemium. 17. What effect have these agents after vascular stagnation occurs? They increase the stagnation. Administered after local blood-letting they lessen the volume of blood carried to the inflamed area. 18. When are hot applications made? W^hen the temperature is low, the circulation sluggish, and the color of the parts dusky. Warmth dilates the blood-vessels; heat contracts them. Bacteria. 1. What are bacteria? Minute unicellular plants, many of them invisible under very high powers of the microscope. They are called fission fungi, also schizomycetes. They are devoid of chlorophyll. 2. How are they classified? According to their forms. The spherical or oval forms are called cocci; rod-shaped forms are called bacilli; long thread forms, leptothrix; screw-like rods, spirillse; those having the coils drawn out, vibrios; those with long, narrowly-twisted screws, spirochsete. 3. How are the cocci classified? According to their mode of grouping : in pairs or 20 COMPEND OF double, they are called diplococci; arranged in chain form, streptococci; in clusters, staphylococci. (These are the spherobacteria of Cohn.) 4. What is the composition of bacteria? They are made up of a plasma, a limiting cell- wall, both composed of an albuminous substance called mycoprotein. Many of them contain a nu- cleus. The cell-wall of some varieties consists of cellulose. Some of the bacteria (not the cocci) have flagellate threads, which bring about mobility. 5. How do bacteria multiply? By transverse division. The cells elongate and divide in two. Others divide in two diameters; the sarcina dividing into fours. Under certain condi- tions some varieties of bacteria appear to produce spores. 6. What is the source of their nutrition? Ready formed organic substances, soluble in water. They require, in addition, certain mineral substances, sulfur, phosphorus, potassium, and other elements. They can derive their carbon from carbohy- drates, which are soluble in water. Their nitrogen is derived from albuminous matter. The fungi give ofif a ferment which peptonizes the albuminous matter prior to assimilation. They all require an abundance of water. 7. Into what two classes are bacteria divided? Into saprophytes and parasites. Saprophytes live upon dead organic matter; parasites derive their nutrition from living organisms. DENTAL PATHOLOGY AND THERAPEUTICS. 21 8. What relation has the supply of oxygen to the development of bacteria? To some free oxygen is essential; they are aero- bic. Others derive their oxygen from formed organic matter, anaerobic; free oxygen is fatal to them. Still others develop with or without the presence of free oxygen, facultative aerobics. 9. What are the conditions necessary to the life of fission fungi? As with all protoplasmic masses, a proper food- supply, definite temperatures, and an inherent vital- it}^ The physiological properties can change under modifications of nutrition. 10. What are the agencies and substances called which kill the fission fungi? Germicides. Mature organisms are more sus- ceptible to their action than are their spores. Dif- ferent varieties of organisms exhibit wide differ- ences in their resistance to different germicidal agencies. 11. What is meant by fermentation? Destructive changes which occur in nutritive media as a consecjuence of the growth of the fission fungi. It is not known whether this decomposition occurs inside the cells or on their surfaces. Fer- mentative processes are the cause of nearly all de- compositions of organic matter, the putrefaction of albumin. They change milk into lactic acid; sugar, starch, etc., into lactic, then into butyric acid; alcohol into acetic acid; urea into ammonium car- bonate. 22 COMPEND OF 12. How is the decomposition of albumin ef- fected? Peptones are first formed; next ptomaines; fol- lowing this, nitrogenous bases are formed, the amins, leucin, etc., together with organic fatty acids; next aromatic products; and, finally, the end prod- ucts are hydrogen sulfid, ammonia, carbon dioxid, and water. Bodies of increasing simplicity of chem- ical composition are formed. 13. What great oiBce is performed by bacteria in the economy of nature? They break down the complex organic matters, producing substances assimilable by plants. 14. What are pathogenic organisms? Organisms which, developing in the tissues of the living body, produce disease. 15. What are the effects of these organisms? At the point of multiplication, degenerations, ne- crosis, inflammation, and new growth of tissues, while the toxalbumins produced cause manifesta- tions of poisoning. According to the variety of organisms, any one or more of these results may predominate. 16. What is the fate of these organisms? In many cases they die out, and the diseases caused by them proceed to recovery. Other forms may be preserved for a long time in the body, and cause continued disease process. 17. What are pyogenic organisms? Those whose development is attended by the formation of pus; those which cause suppurative processes. DENTAL PATHOLOGY AND THERAPEUTICS. 23 18. What are the most common of these? Staphylococcus pyogenes aureus (the coccus which exists in ckisters and produces orange- colored pus) ; the Staphylococcus pyogenes albus — appears white in cultures; the Streptococci py- ogenes, or the chain cocci, and the diplococci, or double cocci. 19. Describe the process of suppuration. The pyogenic cocci growing in a tissue produce irritating waste products; and the results of irrita- tion follow, viz : increase and multiplication of fixed cells, followed by the phenomena of inflammation. The organisms excrete a ferment which peptonizes and liquefies the exudation and intercellular sub- stance; the cells die and form pus-corpuscles; these cells are themselves liquefied. The inflammatory symptoms are usually more pronounced than in simple inflammation. 20. What is the difference between suppuration produced by the staphylococcus and that by the streptococcus? The former usually produces circumscribed, the latter diffuse, suppuration. 21. Name some of the usual forms of bacteria found in the human mouth. The bacilli of lactic and butyric fermentation, the pyogenic cocci, the pneumococcus, the organisms of actinomycosis, and many others. *rhe conditions of the human mouth containing carbohydrates, dead albuminous matters, a temperature of about 37° C," and abundance of moisture are such as to favor the development of many organisms. 24 COMPEND OF 22. What is meant by lactic fermentation? The process through which carbohydrates are spHt up into lactic acid, sugar CgHiaOs becoming lactic acid 2(C3H603). 23. Why is this process of extreme interest to the dentist? Lactic acid is the substance which effects the so- lution of the calcium salts of the teeth, inaugurating the process of caries. 24. What factors are essential to the process? The presence of the bacillus of lactic fermenta- tion: soluble carbohydrates, such as sugar; nitro- genous material, and a proper temperature, all of which conditions are almost constant in the human mouth. 25. What are the general effects of the develop- ment of pathogenic organisms in the body? The products of their action upon albuminous substances gain entrance to the circulation, and fever, septic intoxication, or septic poisoning oc- cur. Should the organisms themselves gain en- trance to the veins, they may be carried to distant parts, and form disease foci. This is pyemia. Fever. 1. What is fever? A general condition, characterized by an eleva- tion of the bodily temperature as its most promi- nent symptom, and which fluctuates or persists for a variable period. 2. What are its causes? DENTAL PATHOLOGY AND THERAPEUTICS. 25 As a rule the absorption from a focus of disease and presence in the circulating fluids of the pro- ducts of specific fermentations. 3. What are the symptoms of fever? Increase of the bodily temperature, increased fre- quency of the pulse, usually a feeling of illness, con- stipation, a decrease in the amount of urine ex- creted, and an increase of the urea contained in it. 4. What causes the elevation of temperature and increase of urea? There is an increase in the amount of CO, ex- creted and exhaled; an increase in the amount of O inhaled, so that increased oxidation occurs, elevat- ing the temperature; the urea is the product of the oxidation. 5. Into what classes are fevers divided? Into periodic and continued. Periodic fevers are those which have periods during which the ele- vation of temperature is almost or quite absent. Continued fevers, those in which the temperature is subject only to the daily variations, associated with the normal temperature. The normal tem- perature, morning, is 98° F. ; evening, 99° F. ; the average temperature being 98.8° F. to 99.3° F. 6. How are fevers graded in severity? First by the amount of temperature elevation; 100.5° to 101.3°, sHghtly febrile; 101.3° to 103.1°, moderate fever; 103.1° to 104.9°, marked fever. Any temperature above 105.8°, hyperpyrexia. 7. What is the prognostic significance attaching to temperature? 5 26 COMPEND OF The higher and longer continued the tempera- ture the greater oxidation, hence the greater loss of the nitrogenous constituents of the body. Con- tinued high temperatures are attended by granular degenerations of the glands and muscles. Tem- peratures as high as io8° F. to 113° F. have been noted in sunstroke cases. As a rule, temperature above 106° F., continued, denotes a fatal ending to a malady. 8. To what is death from fever usually due? To cardiac failure. Fevers are dangerous in the degree that they are attended by weakened heart-action, evidenced by weak heart-sounds, a frequent and soft pulse. 9. What is the general therapeutics of fever? F"irst, reduction of temperature. The most effi- cient means of attaining this end is removing the source of infection where and when possible; if from a local inflammatory focus, removing the cause of and subduing the inflammation. If the source be irremovable, the employment of cool baths and antipyretic drugs to reduce the temper- ature, and sustaining the action of the heart by the administration of stimulants. 10. With what form of fever may the dentist meet? Surgical fever, due to the absorption of pyro- genous (fever-producing) material from a focus of disease about the jaws. 11. What is its treatment? The removal of the local sources of fermentation, DENTAL PATHOLOGY AND THERAPEUTICS. 2/ and the treatment by sedation or stimulation of constitutional symptoms. (See Septicemia.) Septicemia and Pyemia, 1. What is meant by septicemia? The entrance into the blood, the circulation of and effects of the products of bacterial decompo- sitions upon the body. 2. How is it classified? Into septic intoxication, septic poisoning, and pyemia. These express grades of severity of the septic process. The intoxication is probably caused by one or more sets of waste products, or by the same products which cause septic poisoning, when they are present in lesser amounts. The septic poisoning is due to the entrance of bacterial alkaloids or toxalbumins into the blood; the pyemia, due to the entrance of the organisms themselves to the circulation and their multiplication in distant parts. All three of these processes may exist at the same time. 3. What are the symptoms of septicemia? In general, a chill, followed by a rise of tempera- ture, headache, nausea, vomiting, and perhaps di- arrhea, followed by delirium and coma. The symp- toms depend upon the nature of the poison, — i. e., the character of the infecting organisms. 4. What is the treatment? The removal of the source of disturbance, the use of antiseptics to destroy any organisms present in 28 COMPEND OF accessible parts, the washing out of their products. The strength of the patient is maintained through the use of quinine and stimulants until the excre- tory organs shall have eliminated the poison from the circulating fluids. Embolus and Thrombus. 1. What is an embolus? A plug closing the lumen of an artery. 2. What are its efifects? If in an artery which has no anastomosis, there is death and degeneration of the tissues supplied by the artery. The general effects depend upon whether the embolus is septic or non-septic. If septic, it becomes the focus of disease processes. 3. What is a thrombus? A plug forming in a blood-vessel which causes the obstruction and occlusion of the vessel. 4. What are its effects? Those of an embolus, but the symptoms are of gradual growth. As thrombi usually form in veins, there is an increasing severity of the symptoms of mechanical hyperemia. 5. What is an infarction? The area of tissues supplied by a terminal artery is deprived of nutrition when an embolus occludes the artery; the area undergoes degeneration; the area of degeneration is known as an infarct. Necrosis. I. What is meant by necrosis? Death of the cellular elements of a part. DENTAL PATHOLOGY AND THERAPEUTICS. 29 2, What are its causes? Anything which interferes with the supply of nutritive material to a part, or which directly des- troys the vitality of the cellular elements. Ob- structions of arteries, of capillaries, or of veins are causes. Diminished cardiac power is an element in causation. Inflammation is a common cause. Physical forces, such as excessive heat or cold, acids and caustic alkalies, and the waste products of bacterial life, are causes which destroy the vital- ity of cellular elements. 3. What is a predisposing cause? Debility of tissues. Regeneration. ' 1. What is meant by the regeneration of tissues? The process through which lost tissues are re- placed by the vital parts. 2. How is this accomplished? For example may be cited the filling of an ab- scess-cavity after the evacuation of the pus. The cells forming the walls of the cavity undergo pro- liferation; first the nuclei undergo changes of form, and finally divide into two ; the cell body itself next divides, and the cavity becomes filled with small round cells. Blood-vessels grow in loops from adjoining vessels, and penetrate the mass of new cells, which go on to organization, replacing the lost parts. 3. What is necessary that this may occur? Sources of irritation must be removed, or else the new tissue degenerates instead of organizing. 30 COMPEND OF 4. What is the new tissue called? Scar tissue. 5. What relation does the scar tissue bear to the normal tissue? Tissues of the highest order are reproduced by fibrous connective tissue, not by those of their orig- inal form. Dental Histology. 1. Of what tissues is a human tooth composed? Of a general body called dentine, which is covered upon its crown by enamel, upon its root portion by cementum. A nervo-vascular tissue occupies and fills an interior chamber in the dentine; a fibrous, nervo-vascular tissue called the pericementum sheathes the cementum. 2. What is enamel? It is the hardest substance of the animal body, containing from 2 per cent, to 5 per cent, of organic matter; from 95 per cent, to 98 per cent, of inor- ganic matter. 3. What is its chemical composition? Calcium phosphate and fluorid 89.82 " carbonate 4.37 Magnesium phosphate 1.34 Other salts 88 Cartilage 3.39 ?Fat 20 (Von Bibra.) The inorganic constituents are combined with an albuminous substance, forming calcoglobulin. DENTAL PATHOLOGY AND THERAPEUTICS. 3 1 4. What is its anatomical composition? Enamel is made up of wavy hexagonal prisms, arranged with their axes pointing toward the center of the pulp-cavity. Seen in sections, magnified, the prisms are crossed obliquely by a series of parallel brown stripes, the stripes of Retzius. A series of irregular pigmented markings cross- ing the former almost at right angles are called the stripes of Schreger. 5. What is the sub-enamel membrane? A structure, the existence of which is questioned, which marks the boundary between the enamel and the underlying dentine. 6. What is the dentine? Dentine is the substance of which the body of a tooth is composed. 7. What is its composition, chemical? It differs with the age of the patient and in the several teeth of the individual. Under fifteen years — S. G., 2.066; per cent, of water, 11.89; organic matter, 25.92; inorganic matter, 62.26. Average — over 60 years — S. G., 2.106; water, 10.66; organic matter, 24.81; inorganic matter, 64.56. (Black.) When dry, its average chemical composition is — Organic matter 27.61 Fat 0.40 Palcium phosphate and fluorid 66.72 " carbonate 3.36 Magnesium phosphate 1.18 Other salts 83 32 COMPEND OF 8. What is the anatomical structure of dentine? It consists of a calcified basis-substance, traversed by tubuli radiating from the pulp-chamber in curved lines to the under surface of the enamel. The tubuli, averaging i-ioooo" in diameter, are branched, so that the dentine represents a net- work of tubules. Each tubule has around it a covering more resistant to the action of acids than the basis- substance of the dentine; these coverings or walls are called the sheaths of Neumann. Properly pre- pared sections exhibit a fibrous basement-structure to the dentine (gelatin-yielding fibers). 9. What are interglobular spaces? These are defined areas of non-calcification found in the substance of the dentine. The dentinal tubuli may be continuous on either side of them. 10. What occupy the dentinal tubuli? They are occupied by protoplasmic prolongations from the boundary cells, the odontoblasts (the mem- brana eboris) of the pulp. They transmit sensation to the pulp, and are the seat of nutritive changes and disturbances. 11. What is the dental pulp? It is the contracted papilla over which the dentine was formed. It represents in form an attenuated copy of the tooth form. 12. Describe it. It consists of a loose fibro-cellular net-work, in- closing arteries, veins, and nerves, but no demon- strable lymphatics. The large vessels and nerves enter at the foramen at the end of the root; the ves- DENTAL PATHOLOGY AND THERAPEUTICS. ^^ sels break up into a plexus of capillary loops; the nerve-trunks break up into a net-work plexus be- neath the peripheral cells of the pulp, the odonto- blasts; the exact mode of nerve termination is un- known. 13. What are the odontoblasts? They form a layer upon the periphery of the pulp, formerly known as the membrana eboris. The cells are cylindrical in form; they are placed together like cylindrical epithelium. One, and occasionally more than one, prolongations extend from their distal extremities and occupy the dentinal tubuli. At their proximate ends are large nuclei. These are the dentine-forming cells. Under abnormal conditions, other cells of the pulp may take on a similar formative function. In the body of the pulp its cells are irregularly arranged in a gelatinous matrix; in the root they are arranged with their long axes parallel with that of the pulp. 14. What is cementum? It is a modified bone, covering the roots of the teeth, pierced at the apex by a canal which trans- mits the nervous and vascular supply of the pulp. It overlaps the enamel slightly at its gingival end.. The cementum contains numerous bone-corpuscles and lacunae; occasionally evidences of a Haversian system are seen. The layer o£ cementum is thickest at the apex of the root, gradually thinning toward the enamel. There is no distinct line of demarka- tion between the dentine and cementum. Imme- diately beneath the cementum, in the dentine, an 34 COMPEND OF irregular layer (Tomes granular layer) is seen, its elements lying between the terminals of the den- tinal tubuli; these latter occasionally enter the ce- mentum. 15. What is the pericementum? It is a fibro-vascular membrane, encasing the cementum of the teeth, and forms the ligament which binds the teeth to their articulating surfaces, the walls of the alveoli. It is plentifully supplied with nerve-fibers. 16. Describe the pericementum in detail. Its fibers radiate from the root, and are attached at higher levels in the alveolus, so that the tooth is swung in its socket; the elasticity of the fibers per- mits mobility of the tooth, and draws it into posi- tion, when stress is removed. At the apex of the root the fibers radiate, fan-like, from the root to the alveolus. At their other extremity they merge into the periosteum covering the alveolar wall, forming a thickened layer which has been named the dental ligament. The artery which enters the apical space, which lies between the apex of the root and the alveolus, breaks up into a number of branches ; one or more of these enter the foramen to supply the pulp ; the others peTietrate the substance of the peri- cementum and anastomose with the arteries from the alveolar walls. The nerves follow the same course. 17. What is the apical space; what tissues oc- cupy it? It contains the thickest portion of the peri- DENTAL PATHOLOGY AND THERAPEUTICS. 35 cementum, the arterial and nervous trunks supply- ing pulp and pericementum and the emergent veins of pulp and pericementum. lis. Describe the apical portion of the pulp- canal. It is composed of cementum, and after the de- struction of the ptdp may contain living cells (ce- mentoblasts), while the dentine is dead. 19. Describe the alveolar process. It is a provisional bony structure for maintaining the teeth in position. It is a process growth from the bodies of the inferior and superior maxillary bones; diverging from the body of the bone in the superior maxilla; converging in the inferior. It rises about the teeth so that each tooth is inclosed in a socket, called an alveolus. Its outer walls and alveolar lining are of cortical bone; its substance of spongy bone, the chambers of which are arranged so that they form a chambered, spongy, and elastic bed. The blood-vessels from their outer wall anas- tomose with those of the pericementum. Nerves from the same source follow the same course. Its immediate external coating is a periosteum, a con- tinuation of that of the body of the bone. 20. What are the gums? Firm and elastic coverings to the periosteum of the alveolar process. 21. What is their structure? They are covered above with squamous epi- thelium of unusual depth; this layer rests upon en- larged papillae covered with cuboidal epithelium; 36 COMPEND OF the subepithelial layer is composed of densely inter- lacing fibers continuous with the periosteum of the alveolar process. Dental Anatomy, 1. What are teeth? Hard bodies situated in the anterior portion of the alimentary canal, designed for the purpose of seiz- ing, cutting, or crushing food. In the higher mam- mals they are confined to the cavity of the mouth. 2. How are teeth arranged? Symmetrically upon either side of the median line. 3. What is the median line? An imaginary line dividing the body into right or left symmetrical halves. 4. What is a dental formula? It represents the number of teeth and their ar- rangement into classes. It is distinctive for each zoological family. 5. What is the dental formula of the deciduous human teeth? Molars. Premolars. Cuspids. Incisors. 20 12 6. What is the formula of the permanent teeth? Premolars. Canines. Molars. Bicuspids. Cuspids. Incisors. 3212 3212 DENTAL TATHOLOGY AND THERAPEUTICS. 37 7. What form has the temporo-maxillary articu- lation in man? It is a combination of the rounded head and deep glenoid fossa found in the carnivora, with the flat- tened head and socket found in herbivorous ani- mals. 8. What does this indicate? That man is both a carnivorous and herbivorous animal, — is omnivorous. 9. What is the arrangement of the muscles of mastication? They accomplish a combination of direct up and down movements of the mandible with a well- marked lateral movement. The extent of either movement depends upon the manner in which the teeth occlude ; it varies as the individual. 10. What general forms have the teeth? A combination of forms designed for both cutting and crushing. The occlusion of the teeth, the joint articulation and muscular distribution, are in mutual correspondence. 11. How arc the surfaces of the teeth named? Those which underlie the lip are called the labial surfaces. The outer surfaces of the 12 anterior teeth (6 upper, 6 lower) have labial surfaces. Sur- faces underlying the cheek are called buccal, the outer surfaces of the 20 posterior teeth. The inner surfaces of the upper teeth are called the lingual. The inner surfaces of the lower teeth are called the lingual. The surface of a tooth which presents to the median line is called its mesial surface; that 38 COMPEND OF pointing from the median line the distal. The artic- ulating faces of incisors and cuspids are called their cutting-edges ; those of the bicuspids and molars the masticating surfaces. The sharp points of teeth are called the cusps. The lines at the bases of the cusps are called sulci. The surfaces of adjoining teeth which are in contact are called approximal. 12. From what simple form are all tooth forms derived? From a simple cone. 13. How is the cone modified? By compression, and union with other cones. 14. What is the general form of incisors? The cone is truncated, and its top compressed into a wide, almost straight edge. 15. AVhat is the form of the cuspids? The cone is compressed upon either side of the apex, which projects as a point or cusp. 16. How are bicuspids formed? By the union of two simple cones. 17. What is the relation of the roots of the teeth? Each primitive cone bears a conical root as a gen- eral rule, although the appearance is often obscure. 18. Flow are molars formed? Upper molars by the union of three cones; lower molars by the union of four. 19. Describe the upper central incisors. They possess a tapering root having the general form of a much rounded triangle, its base at the la- bial aspect. The crowns are of spade form, con- vex, labially concave lingually, the concavity being DENTAL PATHOLOGY AND THERAPEUTICS. 39 formed by the presence of two lateral buttresses ris- ing from the middle of the cervical portion and curving outwardly to terminate at the angles of the cutting-edge. Its mesial and distal faces are both triangular, the latter more rounded than the former. The mesial angle of the cutting-edge is almost or quite acute; the distal angle is rounded. 20. Describe the upper lateral incisors. They are much smaller than the central incisors, more rounded labially and more concave lingually, the lateral iDuttresses being more marked. Both mesial and distal surfaces are more rou;ided than ia the central incisor. The mesial angle at the cutting- edge is more acute, the distal more rounded. The root is smaller and rounder than that of the central, and exhibits a tendency to curving, at times ab- ruptly. This tooth is occasionally absent. 21. Describe the upper cuspid. From its resemblance to the typical tooth of the carnivora it is called a canine. Its root is larger than that of the central incisor, longer and more prominent, and has a tapering form, elliptical on section. The crown is much rounded labially, ter- minating in a sharp point, which is mesial to the middle line of the crown. The cutting-edges slope away from the point, the longer edge being distal. The lingual surface is marked by three buttresses, one in the median line, one at either border, the three blending in a rounded prominence at the mid- dle of the conical portion of the crown. 22. What common structural defects are found in the teeth thus far described? 40 COMPEND OF At the points of union of the buttresses with the depressed surfaces of the crowns, pits may be found which become the seats of caries, 23. Describe the upper bicuspids. They are elhptical upon transverse section. Their buccal surfaces are convex in both directions, which is also true of their lingual surfaces. As their name implies, they have two cusps, the outer the sharper and more triangular; the cusps join at their bases, forming a sharp sulcus which is frequently a fis- sure. At each end of the sulcus there is a depres- sion. The outer cusps exhibit a modification of the three buttresses of the cuspid. The inner cusp is more smooth and rounded. The teeth taper from the line marking the bases of the cusps, their point of contact, to the ends of the roots, which are also elliptical on section. The root of the first bicuspid is frequently double or bifurcated toward its apex. The first bicuspid is slightly larger than the second. 24. Describe the upper first molar. It has upon section a rhomboidal form, the inner cone of formation being flattened. The prominent angle of the rhomboid is the mesio-buccal. The opposite angle, the disto-lingual, is not so acute; the other angles, disto-buccal and mesio-lingual, are both rounded. The three primitive cones are marked by the two buccal and the mesio-lingual cusps. The fourth cusp of the tooth is added to the lingual cone distally, and marked ofiF from it by a more or less well-defined fissure. The cusps are bound together by enamel girders, one at the mesial DENTAL PATHOLOGY AND THERAPEUTICS. 4I edge, one extending from the mesio-lingual cusp to the disto-buccal cnsp. The sulci between the cusps frequently exhibit fissures and pits. The buccal cusps, as in all the upper teeth, are sharp; the lin- gual cusps and crown surfaces rounded. The roots are three in number, one for each of the primitive cones, two buccal, the distal the smaller; the palatal or lingual root is large and round. As a rule the roots are divergent, but may be bent into any form. 25. Describe the upper second molar. It is smaller than the first molar, is almost a much rounded triangle on section. The mesio-buccal angle is more pronounced; the lingual surface is rounded in all directions; the form of the lingual cone is more pronounced, the fissure marking the junction of the fourth cusp is less pronounced and more distal. The roots, as a rule, diverge less than those of the first molar, the tooth being altogether smaller. 26. Describe the upper third molar. The three primitive cones are evident. The tooth on section is an oval, slightly flattened upon its mesial and buccal faces. The largest cone and cusp are the lingual, the smallest the disto-buccal. The three roots of this tooth are commonly compressed into one root curving backward, in which the three roots are more or less clearly defined. There may be a pulp-canal for each root, or there may be but one central canal. 27. Describe the lower incisors. 7 42 COMPEND OF They are truncated cones, flattened upon the sides, and having- their tops compressed into thin cutting-edges narrower than those of the upper incisors. They are triangular, viewed either at their labial or lingual or at their distal or mesial faces. The labial faces are almost flat, and marked faintly by three longitudinal ridges. At their necks thev are oval upon section, the lingual surface of the crown concaved longitudinally to form a chisel shape. The lateral incisor is larger than the central. The distal angles of the laterals mark the median lines of the upper lateral incisors. 28. What is the general relation of the lower to the upper teeth? The upper arch is larger, and therefore the outer cusps and cutting-edges of the teeth close out- side of those of the lower teeth. The buccal edges of the upper teeth are the sharper in that denture, the lingual cusps being the sharper in the lower den- ture. The lines of division between the lower teeth mark nearly the middle lines of the upper teeth; the teeth of the lower jaw being one-half a tooth in ad- vance of those of the upper jaw. 29. Describe the lower cuspids. Their general form is that of the upper cuspids, the ridge descending from the cusp to the cervix upon the labial w^all is curved toward the mesial edge. The distal cutting-edge is longer, the mesial shorter, than in the upper cuspid. The lingual sur- face is but faintly ridged as compared with the up- per cuspid, resembling more nearly the lower in- DENTAL PATHOLOGY AND THERAPEUTICS. 43 cisors. Its root is elliptical, and smaller than that of the upper cuspid. 30. Describe the lower first bicuspid. It is not a true bicuspid, but more nearly a cuspid, having an exaggerated lingual tuberosity, the lin- gual cusp being primitive. As in all of the lower posterior teeth, its lingual wall is comparatively straight, its buccal convex in both directions. Ris- ing from the primitive lingual cusp, a ridge of enamel ascends to the buccal cusp; two lateral ridges or girders ascend from the bases of the lin- gual cusp; between these ridges there is a mesial and a distal pit. Its root is elliptical, nearly oval; smaller than that of the lower cuspid and the second bicuspid. 31. Describe the lower second bicuspid. It is larger than the first bicuspid. A semi- circular sulcus outlines the base of the buccal cusp. The lingual cusp more nearly resembles an edge than a pointed cusp, and is frequently marked by a fissure which may divide the lingual cusp into two distinct sections. 32. Describe the lower first molar. It is formed of four primitive cones, two buccal and two lingual. It has five cusps, the bucco-distal cone bearing the extra cusp, which is the smallest of the five, at its distal angle. The shape of the crown is trapezoidal, the long parallel side at the buccal aspect. The crown has four main sulci, two buccal, which pass from the median longitudi- nal sulcus, between the buccal cusps, down upon the 44 COMPEND OF convex buccal wall. A single lingual sulcus passes from the longitudinal fissure to between the lingual cusps, usually terminating at the lingual edge. The roots are two, rounded at their buccal and lingual edges, much flattened at their mesial and distal, showing clearly the four primitive roots. The an- terior root frequently shows a distinct canal for buccal and labial sections of the root. The distal root is rarely thus distinguished, there being, as a rule, but one large elliptical canal. The lower first molar is the largest tooth of the dental series. 33. Describe the lower second molar. It is formed of four primitive cones, each of which is surmounted by a cusp. The sulci are cruci- form, outlining the four cusps. The crown is almost rectangular, and smaller than that of the first molar. The roots are similar to those of the first molar, but curve backward. 34. Describe the lower third molar. It is formed of four primitive cones, surmounted by four distinct and usually an extra faintly-marked cusp upon the disto-buccal cone. The outline of the crown is nearly oval; the flattened broad end of the oval mesial, the small end distal. The sulci resemble those of the first molar, but usually have numerous irregularities. The two roots are usually more or less fused together, and curve backward. Dental Embryology. I. What is the first stage of tooth formation? An involution of the epithelium covering the summits of the embryonic jaws. DENTAL PATHOLOGY AND THERAPEUTICS. 45 2. How soon is it formed? In the sixth week of intra-uterine life. 3. From what embryonic layers do the dental tissues arise? From the epiblastic and the mesoblastic. 4. What tissues are formed by each? The enamel by the epiblastic; the dentine, ce- mentum, pericementum, alveolar walls, and pulp from the mesoblastic. 5. What is the tooth sac? It is a fibro-vascular structure inclosing the en- tire developing tooth, and which subsequently be- comes, in part, the pericem.entum. 6. What cells form the enamel? Elongated cells from the deepest epithelial layer, which are called the ameloblasts. 7. What is the composition of the enamel- organ ? It consists of a double layer of epithelial cells, the layer separated by a quantity of myxomatous tis- sue, owing to the peculiar appearance of which, when seen in sections, it is called the stellate retic- ulum. 8. What is the vascular supply of the enamel- organ ? Its external epithelial coat is covered by a layer of fibrous tissue, in which ramify numerous blood- vessels. The pabulum of the ameloblasts, therefore, passes from the vessels through the external epi- thelial covering, into the stellate reticulum, from which it is taken by the ameloblasts, passing to 46 COMPEND OF them through a membranous structure covering them. Later the outer epithehal coating and stel- late reticulum disappear, an4 the ameloblastic layer is separated from the vascular supply by Avhat appears to be a glandular tissue. 9. How is the enamel formed? At the distal ends of the ameloblasts numerous glistening globules are seen ; apparently external to the cells is a structureless mass, resting upon the dentine, but separated from it by what appears to be a membrane. This mass becomes the enamel. As the ameloblastic layer recedes from the dentine, the oldest portions of the deposit take form and become enamel-prisms. The process begins about the sixth month of intra-uterine life. 10. What is calcoglobulin? If a solution of a calcium salt be slowly added to a solution of albumin, the calcium unites with the albumin in small glistening microscopic bodies, which have a structure similar to that of an onion. These globules are calcoglobulin. They are mark- edly resistant to the action of acids. From the globules the enamel and dentine are built. 11. Describe the dentinal papilla. In its descent into the substance of the embryonic jaw, the epithelial infolding appears to meet a re- sistance which forms it into a representation of the future tooth. The outlined portion of mesoblastic tissue covered by this formed epithelial cap is called the dentinal papilla. 12. What are its peripheral cells called? DENTAL PATHOLOGY AND THERAPEUTICS. 47 As soon as the epithelial boundary cells of the enamel-org'an assume their prismatic form, the boundary cells of the dentinal papilla become ar- ranged in a layer, called the odontoblasts. Their function is the formation of the dentine, 13. How is dentine formed? Masses of calcoglobulin are excreted from the ends of the odontoblasts, which recede as the de- posit occurs, each leaving a prolongation in the de- posit, about which the walls of the dentinal tubuli are formed. 14. When is the alveolar process formed? Its development is coincident with that of the enamel and dentine. 15. How is the inferior maxilla formed? Extending from the embryonic middle ear are two rods of cartilage acting as a support to the arches of the embryonic lower jaw. These are the cartilages of Meckel. They are surrounded by a mass of mesoblastic tissue, in which islands of cal- cification are found, which coalesce, and become the inferior maxillary bone. 16. How are the superior maxillary _bones formed? The right and left visceral arches above those forming the embryonic lower jaw extend forward, and are met by a pair of processes growing down- ward from the frontal projection. These latter, joining the lateral projections, form the upper jaw. Any failure of tne parts to unite with one another causes hare-lip, or it may be cleft palate. 48 COMPEND OF * 17. How is the antrum of Highmore formed? An invagination of the mucous membrane of the middle meatus occurs, which marks the site of the nasal opening to the antrum; the interior of the bone is excavated through a resorptive process, the cavity being lined by the invaginated mucosa, which follows the direction of the excavation. 18. How is cementum formed? The fibrous layer inclosing the developing tooth becomes a periosteum; it is at the extremity of the enamel-organ in contact with the periphery of the dentinal papilla. A layer of odontoblasts abutting with a layer of cementoblasts (osteoblasts), the de- velopment of the cementum is then sub-periosteal. 19. How are the teeth erupted? The progressive growth of the tooth-root, to- gether with the alveolar process beneath and about it, forces the tooth outward, its apex causing ab- sorption, by pressure, of the overlying tissues. 20. What influences affect the developing enamel? Many of the conditions affecting general nutri- tion. The several eruptive fevers. Scarlet fever, smallpox, measles, being forms of specific derma- titis, the teeth, as part of the tegumentary system, are affected. 21. What are Hutchinson teeth? Malformed upper central incisors; they are crude cones, deeply notched upon their cutting-edges, and are evidences of hereditary syphilis. dental pathology and therapeutics. 49 Malformations of the Teeth. 1. What are malformed teeth? Teeth whose outward forms or whose tissues vary from the normal. The term is applied alone to gross aberrations from the normal standard. 2. What are the causes? Influences which affect any portion of the tooth- follicle at any period of its growth. Owing to un- known causes, the enamel-organ may assume a form entirely different from the typal form, and the entire tooth may have its form widely different from that of a normal tooth. Aberrations in the formation of the roots are very common. An enamel-organ may partially divide into two, and form what outwardly appear to be double, or twin teeth. The ce- mentum of two adjoining teeth may fuse. 3. What evil follows upon malformation of the teeth as regards their outward forms? The creation of pockets about and between the teeth, which retain food debris and become the seat of lactic fermentation. 4. What histological malformations are found? Deficiencies of enamel : these may be slight or ex- tensive; a failure to perfectly close a sulcus or pit; ^nd, on the other hand, teeth forming during the oc- currence of one of the eruptive fevers may be almost devoid of enamel. The general structure of the enamel may be faulty, owing to imperfect organiza- tion. The dentine may contain spaces in which cal- cification has not occurred, — interglobular spaces. 8 50 COMPEND OF 5. Why are the teeth affected by the eruptive fevers? These diseases are ah expressions of dermatitis; the teeth, as dermoid structures, are also involved. Primary Dentition. 1. What is meant by primary dentition? The cutting of the temporary or milk teeth; the process through which the developing temporary teeth emerge from the gum and assume their posi- tions in a dental arch. 2. In what order and at what times do the tem- porary teeth emerge through the gum? ^ ^ , . . f Lower, s to 7 mos. Central mcisors | ^pper, 7 " 8 " Lateral incisors ] L-^' ^ L' 9 : ( Upper, 9 10 X-. , 1 ( Lower, 11 " 12 " r irst molars ^ t t - u u \ Upper, 13 14 CusDids I ^°'^'^^' '7 " 18 " ^^^P'"^^ 1 Upper, 19 " 20 " Second molars 23 " 30 " These are the average periods. Children may be born with teeth erupted; others may not "cut" teeth until several years of age. 3. Describe the process of eruption. ■ The partially-formed teeth are within the sub- stance of the fibro-osseous tissues associated with the alveolar process. Above are the dense fibrous structures of the gum; these nmst be pierced to free DENTAL PATHOLOGY AND THERAPEUTICS, 5I the tooth. On all sides is the developing alveolar process. Beneath, the partially-formed root con- tains a large pulp mass which communicates with the vital tissues beneath it; the periphery of the apical foramen is now the periphery of the root. The developing root thrusts the apex of the crown against the overlying tissues, which, pressed upon, undergo resorption as the crown advances until the latter emerges through the gum. 4. What may be said of this process? Like parturition, that although a physiological process, pathological manifestations are frequently noted. 5. What are some of the manifestations of path- ological dentition? Local disturbances, irritative stomatitis, next more general disturbance of the gastro-intestinal canal, manifested in vomiting and diarrhea, or it may be by obstinate constipation; skin eruptions may occur; fever is not uncommon, and, finally, re- flex disturbances associated with the central ner- vous system. The local symptoms are frequently red and swollen gums, inability to nurse, and hyper- secretion of saliva. General symptoms may appear without any evidences of local disturbance, the gums not being inflamed. It is probable that the backward pressure upon the pulp, caused by the failure of tissue removal in advance of the crown, may cause the symptoms referable to the central nervous system. 52 COMPEND OF 6. What is the severe expression of these reflex disturbances? Convulsions. 7. What is the general treatment of pathological dentition? Removal of the source of irritation. If the symp- toms are mild, a piece of ice wrapped in a handker- chief is given the child to suck in lieu of a teething- ring. Cases not relieved by such means usually re- quire lancing. 8. How is this done? The incision is made in the line which should be occupied by the cutting-edge of the tooth. Lower incisors are lanced parallel with and inside the cut- ting-edges of the teeth; upper incisors to the out- side. The lower molars and the upper second molar are lanced twice diagonally across the cusps. Upper first molars are lanced crucially. Cuspids are lanced first as incisors, and when their points have emerged, the surrounding ring of gum is di- vided at two points, inside and outside. 9. Wliat precautions are taken? The blade of a curved bistoury is wrapped with linen until its point alone is visible. A thumb and finger of the left hand are placed about the part to be incised. An assistant holds the child upon his left thigh, his right hand holding the child's hands folded across the abdomen, the legs held down by the right arm; the assistant's left hand steadies the child's head. 10. What is the subsequent danger, and how is it treated? DENTAL PATHOLOGY AND THERAPEUTICS. 53 Hemorrhage. A small amount of bleeding is serviceable. It is checked by giving the child a piece of ice wrapped in linen to suclc, touching the bleeding surface with phenol sodique or other powerful styptic. The case is to be examined for oozing hemorrhage. II. At what periods are reflex disturbances most common? The second summer, because winter-born chil- dren cut their cuspids (four) and summer-born chil- dren their first or second molars at this period. (Flagg.) 12. . What is the primary reason for this? These teeth are commonly cut four at a time. 13. What other influence is present? The alimentary tract is kept in a condition of ir- ritation at a period when cholera infantum prevails. 14. What is the treatment of teething convul- sions? Immerse the child to the waist in hot water; place cold water upon the head. In five minutes adminis- ter a rectal injection of a drachm of glycerol. As soon as the bowels have moved give rectal injection: R — Hydrat. chlor., gr. iij; Sodii brom., gr. v; Sol. starch, oz. ij. — M^ The gum over the teeth which should be erupt- ing is incised, whether indications of inflammation be present or not. 15. What is the treatment of caries in tempo- rary teeth? 54 COMPEND OF Excavate as thoroughly as possible, keep the parts dry by means of napkins, syringe with hydro- gen peroxid. Upon articulating faces of the teeth fill with zinc phosphate. Small cavities may be filled with tin or amalgam. Approximal cavities are usually to be filled with gutta-percha. Shallow cav- ities in which undercuts cannot be secured are touched with nitrate of silver after excavating. 1 6. Of what great importance is the early and systematic treatment of the temporary teeth? By checking caries before the pulp is involved, there is not that interference with the resorption of roots which follows upon death of the pulp ; further- more, septic processes do not occur. 17. What is the resorption of roots? A physiological process through which the roots of the temporary teeth are removed, as the perma- nent teeth which lie beneath them advance toward eruption. t8. What dangers are to be apprehended from abscess upon temporary teeth? The immediate danger is a possible involvement of the follicle of the permanent tooth in the process of suppuration. Abscess upon temporary teeth is frequently associated with septic intoxication. The remote danger is interference with root resorption; the process is abortive in pulpless teeth. 19. What is the treatment of pulpless and septic temporary teeth? Free entrance to the canals; a thorough washing with pyrozone. The canals are then filled with DENTAL PATHOLOGY AND THERAPEUTICS. 55 Balsamo del Deserto, and the carious cavity with gutta-percha. 20. What is the treatment of acute abscess upon temporary teeth ? Early and free entrance to the pulp-canals, wash- ing with antiseptics, and early incision of the swell- ing upon the gum. 21. What are the objections to the extraction of temporary teeth? It interferes with the normal enlargement of the jaws, and may mechanically injure the developing permanent teeth. Too long retained, the tempo- rary teeth may cause malpositions of the permanent teeth. In grave septic inflammations the early re- moval of the affected tooth is demanded. Eruption of the Permanent Teeth. 1. What are the periods of eruption of the per- manent teeth? First molars, si to 7 years. Central incisors, 6 to 8 years. Lateral incisors, 7 to 9 years. First bicuspids, 9 to 10 years. Second bicuspids, 10 to 12 years. Second molars, 12 to 14 years. Cuspids, 13 to 15 years. Third molars, 17 to 45, or even 60 years. Lower teeth, as a rule, precede the upper by a few months. 2. What peculiarities associate with the eruption of the permanent teeth? 56 COMPEND OF Malpositions, treated of under the head of Ortho- dontia. The absence of teeth. Cases are common in which no upper lateral incisors are formed. Delayed eruption, and teeth which have been devel- oped in such positions as to permanently prevent eruption (encysted teeth). 3. With w^hat teeth is pathological dentition common? The lower third molars. 4. What is the common cause of the difficult eruption of the lower third molars? Lack of space between the ramus of the inferior maxillary bone and the posterior wall of the second molar. The eruption is also delayed on account of the density of the bony structures about the tooth. 5. What are the usual evidences of abnormal eruption? Inflamed and tumid gums; ill-defined pains about the parts, often becoming acute; more or less dififi- cvdty in opening the jaws, leading upon the part of the patient to the belief that trismus is imminent. Severe symptoms may appear and septic processes occur before the appearance of the crown. Exten- sive inflammatory disturbances are far from com- mon, the neighboring parts participating. 6. What is its treatment? Depends upon the conditions. If a flap of gum overlies the almost emerged crowns, the mouth is sterilized and the flap excised. If the tooth be par- tially imprisoned by gum, the latter is incised freely; a crucial incision may be required. In se- DENTAL PATHOLOGY AND THERAPEUTICS. 57 vere cases, in which it is evident that the tooth is firmly impacted between the ramus of the jaw and the second molar, the latter tooth is to be extracted. Marked general symptoms may require treatment. The administration of morphia may be indicated, but it is preferable to employ gr. x of ammonol and give sulfonal as a hypnotic when required. The removal of large flaps may be accomplished pain- lessly by injecting the parts with about 1-16 gr. co- cain in a large volume of listerine and water. Tense flaps may be removed through applications of trichloracetic acid, full strength. 7. Which of the permanent teeth is of greatest clinical importance? The first permanent molar. First, on account of its- function, it acts as a bulwark which, when re- moved, interferes with the general dentition. Its sulci and pits are the situations in which caries is first found. Diseases of the Enamel. 1. What is the relation of enamel to disease causes? When fully formed it is passive. 2. To what diseases is it subject? Malformations, due to errors of development; it is the seat of deposits of fungi and calculi, and sub- ject to chemical solution through the action of acids, 3. How are malformations of enamel divided? Into topographical and histological. Topo- 9 58 COMPEND OF graphical malformations affect the general form of the enamel-cap; they are termed anomalies. His- tological malformations are characterized by an ex- cess or deficienc}^, usually the former, of the enamel- cap, 4. What are the prominent causes of the most pronounced of these affections? The occurrence of the eruptive diseases at the time the enamel is developing. Smallpox, scarlet fever, measles, are all forms of specific dermatitis, so that the teeth, as dermoid structures, are affected. Syphilis of the infant causes topographical mal- formation of tooth-crowns. 5. How are these latter teeth named? Hutchinson teeth. The permanent central inci- sors are dwarfed, notched, and in some cases coni- cal; they are regarded as pathognomonic of hered- itary syphilis, 6. What is another distinct cause of malforma- tions? Mechanical violence to the dental follicle during tooth-formation. Green-Stain, I. What is green-stain? The term is usually applied to the green deposits covering the cervical portion of the enamel of chil- dren's teeth, the upper anterior teeth being most commonly affected more than the other teeth. Its common situation is in the cervical remnants of the enamel-cuticle. DENTAL PATHOLOGY AND THERAPEUTICS. 59 2. What is its origin? In great part due to the growth of fungi in the remnants of the enamel-cuticle. The coloring mat- ter is not chlorophyll. It is usually found asso- ciated with soft white deposits in ill-kept mouths; the enamel surfaces to which the stain is at- tached are roughened, probal)ly before the deposits of green-stain are formed. 3. What is- its effect upon the enamel? Apparently not injurious; the roughness of enamel found beneath the deposits is probably the partial cause rather than the effect of the deposits. 4. What is its treatment? The removal of the deposits and the polishing of the rough enamel surfaces by means of abrasives, followed by increased hygienic precautions. 5. What are other causes of colored deposits upon the enamel? Staining by metallic salts, — copper, iron, man- ganese, mercury, and nickel. Diseases of the Dentine and Pulp. 1. Into what two classes are affections of the dentine divided? Into constructive and destructive. 2. With what organ is the first class asso- ciated? With the dental pulp. 3. What are the functions of the dental pulp? They are formative and sensory. 4. How is formative activity evinced? 60 COMPEND OF Originally, in the formation of dentine; abnor- mally, in secondary growths of dentine, which may obliterate the dentinal tubules; from protuberances or excrescences upon any portion of the wall of the pulp-chamber; or, again, the products of secon- dary activity may exist as deposits in the substance of the pulp itself. These are the constructive affec- tions of dentine. 5. What is the sensory function of the pulp? The pulp of a tooth is not its tactile organ; the sense of touch resides in the pericementum. The stimuli to which a pulp normally responds are ther- mal changes, applications of hot and cold provoking painful response. Mechanical and chemical irri- tants affect the pulp, and cause painful response when the dentine is deprived of enamel. 6. What is the peculiarity of pulp pain? Like all other organs in which the tactile sense is normally absent, irritation caused in it gives rise to pain which is referred to some other part. Pain arising from disorders of the dentine or pulp is rarely localized, but is reflected to some other branch of the great nerve-trunk supplying the pulp. 7. Of what special value is a knowledge of this fact? It furnishes a means of diagnosis between affec- tions of the pulp and those of the pericementum. A tooth which is sore to the touch has its peri- cementum, not its pulp, affected. Paroxysms of pain caused by the taking of cold substances in the mouth have their origin in a disorder of the pulp. DENTAL PATHOLOGY AND TPIERAPEUTICS. 6l 8. How are these dentinal deposits designated? Those obHterating- the tubules are called tubular calcification. Occupying the wall of the pulp- chamber, they are known as deDOsits of secondary dentine; if found in the substance of the pulp itself, they are called pulp-nodules. q. What is the general cause of these deposits? A mild and continued irritation of the ]n\\p trans- mitted to it through the contents of the dentinal tubuli leads to formative reaction upon the part of the pulp. 10. What are the most common causes of the irritation? The irritation produced by the invasion of caries; second, the presence of metallic fillings close to the pulp, which, owing to their high conductivity, cause irritation through thermal stimuli. 11. What is meant by irritation of the pulp? A degree of stimulus which exalts the general functions of the organ. 12. What are the two sources of irritation to the pulp? Extrinsic and intrinsic. 13. What are the chief of these classes? Intrinsic causes: secondary deposits upon the periphery or in the substance of the pulp. Extrin- sic causes : exposure of the pulp, through the prog- ress of caries, permitting the access of irritants to parts which normally are well protected. 14. How soon may pulp-irritation be said to 62 COMPEND OF As soon as the loss of enamel exposes the con- tents of the tiibuli, these being the terminals of the peripheral cells of the pulp. 15. What is the range of pulp-irritation? From mild stimulation to necrosis. 16. What are the effects? They depend upon the degree of irritation, the extent and grade of vascular disturbance. Stimu- lation is productive of secondary growth; the functions of the cells are exalted. More marked irritation probably tends to the formation of nodu- lar deposits or other formative structural changes. The higher grades of vascular excitement produce alterations in the vessels of the pulp, minute aneur- isms; general inflammation of the pulp commonly produces necrosis of the organ. Suppuration and ulceration of the pulp are later stages. 17. What usually determines the degree and ex- tent of vascular disturbance? The depth of invasion of the carious process. 18. Give a more detailed description of the con- nection between caries and functional and organic pulp disturbances. When the carious process invades the outer layers of dentine, the pulp is stimulated, and attempts the formation of a barrier to the advance of the dis- ease. Later, the source of irritation approaching the pulp, greater functional disturbance results, until irritating matters, principally micro-organisms and their waste products, gain access to the pulp. With exposure of the organ, the pyogenic cocci, DENTAL PATHOLOGY AND THERAPEUTICS. 63 always present, find an entrance, and suppuration ensues, 19. What is the symptom most frequently noted as accompanying the progress of dental caries? Pain. 20. Prior to near exposure of the pulp, what is the source of the pain? Irritation of the contents of the dentinal tubuli, called hypersensitivity of dentine. 21. How soon does this symptom appear? As soon as dentine is exposed. It occurs through exposure of dentine at the base of enamel-fissures, upon the worn surfaces of teeth, and at the necks of the teeth as soon as the cementum is lost, 22. What are the symptoms of hyperesthesia of the dentine? Reflex pain; if an upper tooth, referred to some portion of the distribution of the superior maxillary nerve ; if a lower tooth, referred along the course of the inferior maxillary nerve. 23. How is the symptom elicited? By the introduction of salt, acid, or, particularly, sweet substances to the exposed dentine; again, by the touch of an instrument, pain is produced through the contact of the instrument, and ceases when the latter is removed. 24. What is the probable mode of transmission of the pain? The impression is received through the contents of the dentinal tubuli, transmitted to the odonto- blasts, and through these cells to the terminal fila- 64 COMPEND OF merits of the plexus of non-medullated nerve-fibers which underlie the odontoblasts. 25. What is the method employed to destroy the hyperesthesia? By benumbing or destroying the contents of the dentinal tubuli. 26. What two classes of drugs are employed for the purpose? Coagulating cauterants, such as zinc chlorid, carbolic acid, creasote, trikresol, or the actual cautery. Analgesic agents, such as the oils of cloves, cinnamon, thymol; or the sedative alkaloids, cocain, morphia, aconitia, atropia, and veratria. 27. What other means are employed for the pur- pose? First, through a limited desiccation of dentine by means of blasts of warm air; next, through the ac- tion of agents which abstract water from the tis- sues, — zinc chlorid, chromic acid, solutions of tan- nin in glycerol; sodium carbonate, or sodium peroxid; or, again, by the action of the stronger mineral acids. 28. What rule should govern the application of these remedies? The more shallow the carious cavity, the more powerful may be the agent employed; and, vice versa, as the carious process approaches the pulp, the analgesics are substituted for the cauterants. 29. In what order may they be employed for obtunding hyperesthetic dentine? Beginning with exposure of the most super- DENTAL PATHOLOGY AND THERAPEUTICS. 65 ficial layers of dentine, nitric or sulfuric acid; next, chromic acid or zinc chlorid; following these, the phenyls, carbolic acid, creasote, and trikresol; next, the analgesic oils and the alkaloids. 30. Should they always be applied in the order given ? No; the milder agents are first applied, and the stronger eschewed, unless the milder are found in- effective. 31. What agent is unqualifiedly to be con- demned as an obtundent? Arsenious oxid, or cobalt (which contains ar- senic). 32. What agent and means give promise of greatest success as an obtundent? A mixture of cocain in guaiacol driven into the dentine, or, if required, into the dental pulp and beyond it, by means of a cataphoretic current. 33. What is the second cause of odontalgia af- fecting the dental pulp? Irritation of the pulp, through the deep invasion of caries. 34. What are the prominent causes of pain in this connection? Acid products of fermentation; mechanical causes, producing pressure upon the layer of den- tine covering the pulp; and thermal changes, pro- ducing irritation. 35. What is the nature of the pain? Depends upon the degree of irritation. If com- paratively mild, a steady, gnawing pain is felt. 66 COMPEND OF usually referred to the immediate region of the af- fected tooth. If active hyperemia of the pulp be present, the pain may be throbbing; this variety of pain is, however, unusual, common though it is in the succeeding grade of irritation. Applications of cold provoke pain; the pain induced by the applica- tion of heat is less pronounced. 36. What are the succeeding grades of pulp irri- tation? Hyperemia, active and passive; inflammation, suppuration, and gangrene. (See after Caries.) 1. What are the destructive affections of the dentine? Dental caries, erosion, and an extremely rare affection, resorption of the dentine. 2. What is meant by resorption of dentine? A loss of dentine, progressing from the periphery of the pulp-chamber toward the enamel. It is a resorptive process by the dental pulp. 3. What are its symptoms? None, or very vague, until the resorption has proceeded so far as to enable the operator to see the pink pulp through its translucent enamel covering. 4. What is its prognosis? Data are wanting. 5. What is its therapeutics? An alterative tonic, arsenic iodid, administered to a patient presenting this condition, resulted in a constructive process which replaced the dentine lost through the retrograde metamorphosis. (Kirk.) (Erosion is discussed later.) dental pathology and therapeutics, 6/ Dental Caries. 1. What is dental caries? A gradual decay of the tissues of a tooth, always proceeding from the periphery toward the pnlp. 2. How are its causes divided? Into predisposing and exciting. 3. What are its predisposing causes? Local, and perhaps constitutional. The local causes are faults of structure, form, and positions of the teeth, forms and positions which permit the massing and retention of food debris; faulty struc- ture permits the rapid invasion of the carious pro- cess. Constitutional states expressed by lowered vital tone appear to permit the more rapid multipli- cation of the exciting cause of caries. Areas of de- fective calcification in the dentine, known as inter- globular spaces, furnish situations which favor the rapid extension of the carious process. 4. What is this exciting cause? Micro-organisms, which produce lactic fermenta- tion ; through their action carbohydrates are decom- posed into lactic acid, which acts as a chemical sol- vent. 5. To whom are we indebted for the determina- tion of this fact? To Dr. W, D. Miller. The theory of solution through the action of acids was followed by that of fermentation as the cause of caries. It was Dr. Miller who first demonstrated the origin and mode of action of the solvent, and who first produced actual artificial caries. 68 COMPEND OF 6. What is the morbid anatomy of dental caries? A break of any extent in the continuity of enamel, exposing an area of dentine. The latter tissue is cupped out, destroyed over a greater or less area, the concavity containing fermenting masses of food debris. Beneath these masses the dentine is decal- cified, soft, and almost structureless; the under sur- face of the enamel-walls overlying the carious cav- ity is eroded. Beneath the structureless portions of dentine the latter tissue has its tubuli invaded by and filled with micro-organisms. A constant fea- ture of this invasion is a progressive widening of the dentinal tubuli. The depth of invasion of the organisms is far in advance of any perceptible softening. 7. What is the pathology of dental caries? The specific organisms of lactic fermentation gain access to the dentine, either through a solution of the overlying enamel by lactic acid, the waste product of the organisms, or by defects of the enamel permitting the ingress of the ferment to the dentine. The food of these organisms is the debris of carbohydrates. The waste product of the organisms is lactic acid. The acid attacks the den- tine, forming the lactate of calcium. The latter chemical phenomenon removes the free lactic acid from about the organisms and permits their further growth, checked or destroyed if an excess of their waste products accumulates about them. The or- ganisms advancing by way of the tubuli, their waste product decalcifies the sheaths of the dentinal DENTAL PATHOLOGY AND THERAPEUTICS. 69 tubtili, enlarging the tubuli until they merge into one another. The invasion of the transverse processes of the tnbuli is secondary. In decalcify- ing the carious dentine, lactic fermentation is suc- ceeded by fermentations of other varieties, notably butyric fermentation, this being followed by putre- factive decomposition. A usual associate of the in- vasion of caries is pigmentation, this probably due to the chromogenic (color-producing) organisms. Many varieties of organisms find a suitable soil of development in the mass of carious dentine. 8. What are the signs and symptoms of dental caries? The signs are cavities, detected either by actual observation or by means of appropriate instruments, called explorers. The symptoms are pain and usu- ally odor. The pain may be reflected along any part of the course of the fifth cranial nerve. The odor of caries is distinctive. 9. What is its clinical history? In the order of frequency caries attacks, first, pits, grooves, and fissures in the enamel; second, the ap- proximal surfaces of the teeth; third, smooth but unclean surfaces; fourth, necks of the teeth, at the enamel border. The occurrence is governed by the presence or absence of spaces in which lactic fer- mentation may proceed. Pits and depressions first exposed and attacked are those upon the articulat- ing faces of the first permanent molars. The next teeth exposed which ofifer spaces in which lactic fer- mentation may proceed are the upper incisors. 70 COMPEND OF Any defects or pits in these crowns offer a fitting space for the retention of organisms, so that the bas- ilar pit, when deep, is nsnaUy attacked. The second permanent molars are next in order, the fissures forming the retaining spaces. Next the approx'mal surfaces of the upper bicuspids; and if the fissures upon their articulating faces are deep, they are in- vaded. Following these are the approximal sur- faces of the lower second bicuspid; next the upper cuspid; next the buccal surfaces of the teeth and the crowns of the third molars; next the lower bicuspid, and last the lower anterior teeth. The student will note that these situations are such that the mechanical cleansing by the movement of the tongue, cheeks, and saliva is of decreasing effective- ness; therefore the organisms of lactic fermenta- tion and their soil (food debris) are retained in con- tact with the teeth. lo. What is the diagnosis of caries? Fine explorers of various shapes are pressed into, first, the fissures and pits of the teeth, next between and over their approximal surfaces. Caries is de- tected by the edge of the explorer sinking into cavi- ties or passing over softened areas of the enamel. The approximal spaces are further tested by passing across their walls floss silk; as a rule, if it is not frayed or torn, the enamel surfaces are intact. Painful sensations following the introduction of salt, sweet, or acid substances in the mouth indicate ex- posure of the dentine, and search is made by means of explorers for minute cavities, fissures, or defective DENTAL PATHOLOGY AND THERAPEUTICS. 7I edges of fillings. Any space in which the point of a fine explorer sinks is to receive attention. Caries in teeth containing fillings is usually indicated by bluish discoloration of a tooth- wall overlying the filling. II. What is the prognosis? As a general rule, favorable; the results depend- ing largely upon the skill with which the indicated therapeutics is applied. The less extensive the process in a denture, and the less deep its invasion in individual teeth, the better is the prognosis. Therapeutics of Caries. 1. What is the therapeutics of dental caries? The general therapeutics is the removal of the infected material and the unsupported enamel walls, and their replacement by materials, insoluble in the fluids of the mouth, which shall serve to re- store the lost form of the tooth, seal the cavity her- metically, and sustain the stress of mastication. 2. Is it necessary to remove all of the infected dentine? Not ahvays; but the greater amount, at least all evidently softened portions, should be removed, and the walls subjected to contact of germicides which shall serve to sterilize the infected portions of den- tine which have not been removed. 3. Why is this invaded structure suffered to remain ? Exquisite hypersensitivity of the dentine may prevent or render inadvisable thorough excavation ; 72 COMPEND OF it is quite possible to perfectly sterilize the infected tissue, and it serves as a non-conducting protective covering- to the dental pulp. 4. What is the importance of the non-conduct- ing layer? The dental pulp is singularly intolerant of stimuli due to thermal changes. A pulp habitually receiv- ing such stimuli becomes the seat of structural changes, frequently of nodular deposits in its sub- stance, or, it may be, entire calcification about the tissues of the pulp. 5. What are the degrees of caries, and why is this distinction of degrees made? Superficial, deep-seated, and complicated; each stage requires special treatment. 6. What is the general treatment of the first grade? The thorough removal of infected and softened tissues, and their replacement by a physically perfect filling. 7. What is meant by a perfect filling? It is chemically unchangeable in the fluids of the mouth; is a non-conductor; is perfectly adaptable to the walls of prepared cavities; is susceptible of a perfectly smooth finish, and is unchangeable as to its form; possesses sufficient strength to resist the stress of mastication, and is of harmonious color. 8. Which of all the filling-materials possesses these characteristics in highest degree? Gold. 9. To what causes is the failure of gold as a filling-material attributed? DENTAL PATHOLOGY AND THERAPEUTICS. J^) The most common, and believed by some to be the universal cause, is faulty adaptation. Owing to lack of skill or care upon the part of the operator, the filling-material is not perfectly adapted to the margins of the cavity, or else these margins are improperly prepared. The next cause is such a structure of the enamel as renders the perfect adap- tation of gold to margins impossible. 10. What is the treatment of the second stage or degree of caries? The removal of infected tissues and weakened structures; thorough sterilization of the dentine; covering the walls of the dentine with a substance wTiich shall prevent irritation of the pulp through thermal changes; and perfectly filling the cavity, as in the first grade. 11. What is the treatment of the third stage of caries? This grade of caries ranges from almost to com- plete exposure of the dental pulp. If the pulp be not exposed, it is usual to remove all of the decalci- fied and infected dentine except that acting as the immediate pulp-covering. This layer is to be per- fectly sterilized by means of non-coagulating anti- septics; any undue sensitivity which exists should be subdued -by means of sedatives; a layer of a non-irritating material should be placed over the softened area; over this a non-conducting cavity- lining, over which a filling is to be placed. 12. What antiseptics are to be preferred in this connection? 74 COMPEND OF 25 per cent, pyrozone, oil of cinnamon, and solu- tions of thymol. 13. Why are the latter employed? They are both analgesic and antiseptic. 14. What pulp-protective is to be preferred? First, a film of one of the ethereal varnishes; over this a thin layer of oxysulfate. 15. What cavity-linings are employed? Zinc phosphate and the oxychlorid of zinc. 16. Why is the latter not used as a pulp- capping? When freshly mixed, and for some time succeed- ing, it is irritating to the pulp, and may produce im- mediate irritation or midesirable results in the future. 17. What effects are desired after this treat- ment? First, that a recalcification of the softened dentine shall occur; second, that the softened layer may re- main unchanged indefinitely and be perfectly neu- tral as to its efifects. 18. What results may follow the application of irritating linings? A functional activity of the pulp may be produced which shall cause dentinal deposits in or about the pulp; theoretically, it is desirable that a restoration or recalcification of the softened dentine should occur, but there is no means of limiting or gauging the extent of nutritive activity which may be pro- duced. 19. W'hat is the next grade of dental caries? That in which the pulp is exposed. DENTAL PATHOLOGY AND THERAPEUTICS. 75 20. What are the usual results in nearly-exposed pulps ? Vascular disturbances of the pulp, attended by pain. (See Hyperemia of the Pulp.) 21. What in exposed pulps? Inflammation, first simple, next purulent, affect- ing the pulp. Hyperemia of the Pulp — Grades of and Effects. 1. What is meant by hyperemia of the pulp? An excess of blood in the dilated vessels of the pulp. 2. What is its cause? Exposure of the pulp to sources of irritation, either extrinsic, through the invasion of caries, heating in finishing, etc., or intrinsic, owing to the presence of calcific deposits upon or in the pulp. 3. What is its morbid anatomy and pathology? The irritation produces a paralysis of vessel-walls, and the vessels are irregularly dilated in the form of minute aneurisms. If the irritation be continued, extravasations of blood may occur from the dilated vessels. Death of the pulp may occur from hemor- rhagic infarction. 4. What are its symptoms? Remarkable increase of response to slight ther- mal changes. Pain commonly referred to some other than the affected tooth, or along the course of the fifth nerve, the pain being frequently referred to 76 COMPEND OF the ear. Pain is paroxysmal, sharp, and lancinat- ing. 5. What is its diagnosis? The symptoms are usually elicited in a carious tooth, the pulp not being exposed. Not infre- quently it occurs in teeth not the seat of caries; diagnosis is made by isolating each suspected tooth, and testing by means of warm and cool water; the affected tooth gives abnormal response. 6. What is its prognosis? Usually depends upon the number and severity of the paroxysms. To insure continued health, the blood-vessels must resume their normal condition. They may recover their tonicity after several parox- ysms, and yet may be permanently injured by one severe paroxysm. If the pulp response subsides to the normal, recovery has occurred; an increasing response to heat is a danger-signal. 7. What is its treatment? Obtain rest from thermal changes. If a carious cavity exists, use sedatives in the cavity and fill tem- porarily with gutta-percha or temporary stopping. If the symptoms occur in a tooth without a cavity, cover it with a gutta-percha cap for a period. 8. What medicinal remedies are employed? First, sedatives in the carious cavity; oil of cloves; solutions of thymol in glycerol; cocain and glycerol. These remedies are to succeed the ster- ilization of the infected dentine. Coagulating anti- septics and sedatives are of questionable utility. Counter-irritation, either a vesicant applied but DENTAL PATHOLOGY AND THERAPEUTICS. 'J'] once or a rubefacient employed for some time, at a point distant from the affected tooth. 9. If the symptoms persist, what condition is indicated? Venous hyperemia or congestion of the pulp, with permanent alterations of the walls of the ves- sels. A condition frequently attended by the for- mation of nodular deposits. 10. What treatment is indicated? Relieving the paroxysms by means of obtundents, and subsequently devitalizing the pulp. Inflammation of the Dental Pulp. 1. What is inflammation of the pulp? The phenomena described under the head of in- flammation occurring in the dental pulp, but, being confined in unyielding walls, the tissues cannot swell. 2. What are its causes? Injuries of greater severity than productive of hyperemia. Commonly the organ is exposed to the fluids of the mouth, and pathogenic organisms gain access to it. Blows upon a tooth may give rise to pulpitis. Injuries to the vessel-trunks as they enter the apical foramen, such as rapid moving of teeth by regulating appliances, too severe wedging, or increasing looseness of teeth, subjecting the vessels to compression or torsion, are all causes of pulpitis ; pressure of fillings upon the pulp or thin laminae of dentine covering it; exposure in excavation and the employment of irritating remedies or materials are 78 COMPEND OF also causes; conductivit}^ of thermal chang-es through metallic fillings. 3. What is its morbid anatomy? The veins are distended; foci of cellular exudates are seen ; these latter may occur at but one point, or be generally distributed throughout the pulp. Ex- travasations of red corpuscles may be seen, which appear to be foci of inflammation. Owing to the confinement of the pulp, fluid exudates cannot occur, except the organ be largely exposed, when fluid exudations occur (coagulable lymph), and the pulp swells through the orifice of exposure. In some cases the pulp undergoes hypertrophic changes, as the result of chronic inflammation, and extrudes from the chamber, in some cases filling a large carious cavity. The condition is known as fungous pulp. 4. What are its symptoms? The pain is more continuous than in hyperemia; it is dull and heavy; increases markedly in the re- cumbent position. In other cases no symptoms other than a vague uneasiness may exist, and yet marked pulpitis be present. Percussion upon the afifected tooth elicits increased response. Pains may be indefinitely localized or referred entirely to distant parts, notably to the ear, the temporal or occipital region. 5. What is its prognosis? Pulps may remain vital after attacks of marked inflammation, but, as a rule, those whicli have been the seat of pulpitis are debilitated and die. 6. What is its treatment? DENTAL PATHOLOGY AND THERAPEUTICS. 79 If the inflammation has not been violent, it is a common practice to attempt the conservation of the pulp, which attempt is rarely successful. The den- tine and surface of the pulp are sterilized; the in- flammatory action is dispelled by means of seda- tives in the cavity and counter-irritants applied to the gum. Pulp-Capping. 1. What is the treatment of exposed pulp? Provided the exposure be recent and no vascular disturbances have been evident, indicated by throb- bing or gnawing pain, an attempt is made toward its conservation. 2. How is this accomplished? Through the operation of pulp-capping. 3. What is the object in saving the pulp? It prevents loss of translucency of the tooth. Teeth containing vital pulps are stronger than those from which this organ has been removed. Teeth which have lost their pulps may become the seat of pericementitis, an affection very rare in those con- taining vital pulps. 4. What are the conditions for success in this operation? The pulp itself, when sources of irritation are re- moved, must be in such condition that a return to its normal state is possible. Considering the ana- tomical changes in the vessels of the pulp, which accompany hyperemia, it is rare that a pulp may be saved which has been the seat of more than one con- tinued attack of throbbing pain. An exposed pulp 8o COMPEND OF is almost immediately invaded by pyogenic organ- isms, so that pulps which have been exposed may be invaded by the suppurative process and give but little subjective evidence of disease. The symp- toms elicited by the operator, although a guide, are by no means an absolute one. The patient's physi- cal condition and temperament must be such as will favor the recuperative process. 5. How is the exposure of the pulp diagnosed? Exposure of the pulp may not be evident; it is not always to be detected by sight. The existence of dentine fissures or malformations may subject the organ to the ingress of irritants, and there be no external evidence of exposure. A point of exposure is usually seen as a round, red area. 6. What is the prognosis of the operation? In a majority of cases, bad, the pulp either exhib- iting immediate evidence of vascular disturbance, or its painless death ensues. The ratio of success is greatest with freshly-exposed pulps, particularly with those which have been accidentally exposed by the operator in excavating. 7. What qualities should a proper pulp-capping possess? It must be non-irritating, unchangeable in bulk or form, and be applied without the exercise of the slightest pressure. If it is antiseptic and sedative, it is all the better. 8. What materials are in common use for the purpose? A paste of zinc oxid and oil of cinnamon or DENTAL PATHOLOGY AND THERAPEUTICS. 8 1 cloves; a paste of zinc oxysulfate, which hardens; layers of paper coveredi with ethereal varnishes; small disks of softened gutta-percha are also em- ployed. Oxychlorid of zinc is an unreliable mate- rial in this connection. It may produce any grade of irritation when applied as a capping. 9. How is the zinc paste applied? The tooth is placed under rubber-dam. The cav- ity and surface of the pulp are thoroughly sterilized by means of a 3 per cent, solution of pyrozone, or a 10 per cent, solution of meditrina, then dried. A concave disk of tin or lead, about twice as large as the area of exposure, is filled with the paste mixed thin. This is carried into position and placed very gently. The patient should feel no pain. The sur- plus paste is wiped from about the edges of the cap, and a film of ethereal varnish quickly applied, while the cap is held in position by an instrument ; as soon as the varnish hardens, holding the cap in position, a thin paste of zinc phosphate is flowed over the cap, covering it and the deeper portion of the cavity, and lining the latter completely. 10. How is the oxysulfate applied? A saturated solution of zinc sulfate in water is the fluid of this cement, the powder being uncalcined zinc oxid. From powder and fluid a thin paste is made. A small piece of glazed paper, large enough to fully cover the area of exposure, is dipped in the paste, and quickly and gently laid over the ex- posure, where it quickly hardens. This is covered in turn by a layer of zinc phosphate. o2 COMPEND OF 11. What are the indications of success follow- ing this operation? A slight discomfort, which gradually grows less, until the pulp merely exhibits a normal reaction to applications of heat or cold. (Flagg.) 12. What are the signs of failure? An increasing response to applications of heat or cold, particularly of the former. (Flagg.) Dr. Flagg counts from six to twelve months as the period of probation. 13. What other disposition may be made of ex- posed pulps? They may be devitalized, removed, and the space formerly occupied by them filled with a material v/hich shall hermetically seal the root at its apex. Extirpation of the Pulp. 1. What are the two methods in vogue of pre- paring the dental pulp for extirpation? Benumbing it by injections of cocain, and devital- izing it by means of preparations containing arsenic trioxid. Cocain-guaiacol may be driven into the pulp by a cataphoretic current, destroying the sen- sibility of the organ. Applications of the arsenic trioxid are in almost universal use. 2. What is the action of arsenic upon the vital pulp? Its application is followed by pain, which may be continuous or throbl^ing, usually lasting for about two hours. It is evident that hyperemia and inflam- mation are refiexly induced by the irritation of the DENTAL PATHOLOGY AND THERAPEUTICS. 83 sensory filaments. When the pam ceases, indicat- ing paralysis of the nerves, the arsenic is absorbed by the pulp and its vitality destroyed. There is no absorption during the inflammatory stage, and no absorption should the pulp be the seat of inflam- mation when the arsenical application is made. 3. What amount of arsenic is usually applied? From the i-ioo to 1-25 part of a grain. 4. How does variation of the dose influence the effect? Very minute quantities, as a rule, cause delay in the death of the pulp. Applications of larger doses may be followed by symptoms of apical pericemen- titis. 5. What agencies influence the results of appli- cation? First, the menstruum employed. Carbolic acid, by its coagulating effect, interferes with the absorp- tion of the arsenic. Pulps in a state of inflammation will not absorb the arsenic. The presence of de- posits of secondary dentine in the pulp may render the effects of an arsenical application almost nil. 6. What is the length of time usually required to effect pulp-devitalization? From twenty-four to forty-eight hours. 7. What is the usual source of great and contin- ued pain following an application of arsenic? Pressure of the application and its covering upon the pulp. 8. What is the usual formula of arsenical paste? 84 COMPEND OF R — Arsenious acid, gr. j ; Cocain hydrochlor., gr. ij; Ol. cinnamon, q.s. Ft. paste. 9. What are the offices of these constituents? The ol. cinnamon is a sedative and non-coagulat- ing antiseptic. The cocain is analgesic, and causes the contraction of the arterioles, lessening the hy- peremia, thus facilitating the absorption of the ar- senic, the devitalizing agent. 10. What is the first step preparatory to making an arsenical application? Washing the cavity with strong antiseptics, re- moving debris, and, where perfectly feasible, gain- ing full access to the pulp. Should any inflamma- tion be present, the cavity is washed out with warm electrozone, and an application of thymol and ol. cinnamon made until the symptoms have disap- peared. This is sealed in the cavity for twenty-four hours, when the arsenical application may be made. 11. What two important precautions are to be taken? First, that no arsenic come in contact with the gum, or sloughing, which may be extensive, will certainly occur; second, the avoidance of all pres- sure upon the pulp. 12. How are these accidents guarded against? First, by so shaping the cavity as to form a deep pocket for the reception of the application, and em- ploying a material for its retention which may pre- vent its escape upon the gums; to avoid pressure, the retaining medium should be a material which DENTAL PATHOLOGY AND THERAPEUTICS. 85 mav be placed Avithont the exercise of pressure and which shall hermetically seal the cavity. Zinc phos- phate is the material recommended for this purpose. 13. How is the application to be made? A disk of paper or a small ball of cotton, about I- 16 inch in diameter, is to have placed upon it a portion of the paste about the size of a pin-head. This is laid gently upon the point of exposure, and zinc phosphate, mixed thin, is flowed over it to re- tain it in position. Before the cement has set, the saliva is admitted to its surface. In about forty- eight hours the cement and paste are removed, and the pulp will be found devitalized. 14. What result occasionally follows an arsenical application, and what is its treatment? Intense pain upon contact of the arsenic with the pulp. The application is to be removed; sedatives applied; when quiet is restored, the arsenic is placed at some distance from the pulp, sealed in, and per- mitted to remain for a week. 15. How are devitalized pulps removed? By means of barbed extractors, and in some in- stances by chemical solvents. 16. What other disposition may be made of the devitalized pulp? The coronal portion may be removed, and the canal portions converted into stiff antiseptic fila- ments. 17. How is this accomplished? By means of mummifying pastes. Prepkrations which contain alum or tannin as a hardening, gly- 86 COMPEND OF cerol as a dehydrating, and thymol as an antiseptic agent. i8. When is this method employed? When, for any reason, it is impracticable or im- possible to thoroughly remove pulp-iilaments and fill the canals. 19. What is a primary essential to the removal of pulp-filaments? Familiarity with the anatomy of pulp-chambers and canals. 20. What is the usual form of the dental pulp? It represents an approximate miniature of the tooth. 21. What is the usual arrangement of pulp- canals in the several teeth? The central and lateral incisors and cuspids (upper) exhibit an almost round orifice of en- trance to the pulp-canals. The upper first bi- cuspid, commonly two canals, a round opening into the buccal and one into the palatal aspect of a root, frequently bifurcated for half its length. These openings may be connected by a fine line. The upper second bicuspid usually has a dumb-bell- shaped canal orifice. The upper molars, three canals, as a rule; the palatal canal has a large round orifice; that of the anterior buccal root, round or triangular and small; the disto-buccal root, very small. The same arrangement is found in the sec- ond molar; in the third molar, also; but here varia- tions are not uncommon. There may be but one large canal, and, again, four, or it may be five DENTAL PATHOLOGY AND THERAPEUTICS, 87 minute ones. The lower incisors, cuspids, and bi- cuspids usually have a single canal, which has an oval opening'. The lower molars have, as a rule, but two roots. The canal of the posterior root is large, and has a round orifice. Those of the anterior roots are small, and have a dumb-bell shape; the handle long and attenuated. The roots of the several teeth, when curved, usually have the apices of the roots pointing from the median line. There are, how- ever, numerous exceptions to this rule. 22. How is a pulp removed? The tooth is sterilized, placed under rubber-dam, and washed out with pyrozone. Free entrance is gained to the pulp-chamber, and the body of the pulp is burred away or cut away. Easy entrance is next obtained to each pulp-canal. A tested barbed extractor, placed in a light handle, is passed up the largest canal, if a multi-rooted tooth, the barbs being turned away from the pulp until it is as far as it can readily be passed, when the broach is rotated, the teeth engaging the length of the pulp- filament, and it is withdrawn; the operation is re- peated in the other canals. 23. Should any filaments remain, what disposi- tion is to be made of them? Sulfuric acid, 50 per cent, sol., or trichloracetic acid, full strength, is pumped into the canal by means of fine cleansers until the filaments are de- stroyed. 24. What condition is now found at the apex? A lacerated wound, if vital connection between 65 COMPEND OF pulp and pericementum existed, indicated by pain in removing the pulp; a cicatrized wound, if the connection has been destroyed completely. That is, if the arsenic has been in for more than three or four days. 25. What is the usual practice followed after complete non-septic extirpation of the pulp? Immediate root-filling. The canals are washed out with pyrozone to remove blood and to assure sterilization. Alcohol is pumped into the canal by means of broaches, and is evaporated until the den- tine appears dry. The majority of clinicians next pump a small quantity of oil of eucalyptus in each canal, and fill the canals with preferabl}' gutta- percha points packed with warmed instruments. Statistics indicate that the greatest ratio of success attends the filling of the canals with a paste of oxy- chlorid of zinc. 26. What olDJection is urged against immediate root-filling with gutta-percha or oxychlorid? Difficulty in removing these fillings in case trau- matic pericementitis should occur, which is not un- common. 27. What practice is advised in its stead? The filling of the canal for a week with aristol and well-packed crude cotton, when the wound at the apex will have healed. Suppuration of the Pulp. I. What is meant by suppuration of the pulp? The formation of pus upon the surface or within DENTAL PATHOLOGY" AND THERAPEUTICS. 89 the substance of the dental pulp. In the former case it is ulceration of the pulp; in the latter, ab- scess. 2. What are its causes? The invasion of the pulp by pyogenic organisms. In a majority of cases the pulp is exposed to the fluids of the m.outh; the organisms gaining access to the surface of the pulp, a molecular disintegration of that organ proceeds; it is destroyed progressively bv an ulcerative action. The process not infre- quently follows upon attempts at the saving of pulps which have been exposed. Cases of increased con- ductivity through metallic fillings may run the scale of hyperemia, inflammation, then suppuration. 3. What is the pathology and morbid anatomy of suppuration of the pulp? There are two classes of cases, the ulcerative and the abscess. The former may also be subdivided into two classes: First, those in unfilled teeth; sec- ond, those occurring in teeth which have been filled. In the first class, occurring after pulp-exposure, the carious cavities being unfilled, the blood-vessels are irregularly dilated; there is an irregular loss of tissue from the surface of the pulp; beyond the sup- purating surface the vessels are surrounded by a profuse inflammatory exudation (cellular) ; the ul- cerative process undermines the layer of odonto- blasts, which retain their forms longer than the other tissue-cells of the pulp; the ulceration may involve the organ to any extent. Second, cases occurring under fillings; immediately upon the removal of 13 QO COM PEN D OF the filling and pulp-capping, pus is seen to escape from the surface of the pulp. Examination of such pulps may exhibit the effects of ulceration or those of class two, or abscess of the pulp. This process may occur without the destruction of the layer of odontoblasts covering the pulp, for upon puncturing the pulp, an escape of pus follows. An examination reveals one or several abscess-cavities, some filled, others unfilled with pus. There may be one large cavity occupying the center of the pulp. The pro- cess of suppuration follows the veins. In some cases the abscess may involve the entire organ, giv- ing it a white appearance. 4. What are the symptoms? Those of inflammation of the pulp, but intensi- fied. There is a greater exhibition of reflex pains. Perhaps the most constant symptom is increased response to hot applications, which subsequent cold applications relieve. In the last stages, symptoms of pericementitis supervene, which usually csase for a variable period after sloughing of the pulp. 5. What is the prognosis? Fatal to the pulp. If the pulp-canals be not per- fectly cleansed and sterilized, pericementitis and al- veolar abscess may occur in from a week to years. 6. What is the treatment? In the last stages, the remnants of the pulp, as a rule, may be removed painlessly by means of a barl^ed broach. In the earlier stages, the insensitive portions of the pulp-tissue are scraped away. If the suppurative process be very superficial, an applica- DENTAL PATHOLOGY AND THERAPEUTICS. 9I tioii of arsenic is made. As soon as the pulp-cham- ber is opened it is to be filled with powerful antisep- tics, such as 25 per cent, pyrozone, or a 25 per cent. sol. of sodium peroxid. If the root portions of the pulp be still sensitive, progressive broaching with a 50 per cent. sol. sulfuric acid will usually enable the operator to destroy and remove them. Ten per cent. sol. of formalin may be applied and sealed in the tooth for a week. This penetrating antiseptic devitalizes and hardens the remaining tissue, and it may then be removed. Subsequent to the removal of the pulp, the pulp-canals and dentine must be rendered aseptic. 7. How is this accomplished? As a rule, by applications of 50 per cent. sol. of sodium peroxid. The solution NaoOs is pumped into the canals and perm.itted to remain for a few minutes, when an application of hydrochloric acid (10 per cent, sol.) is made. Sodium hydrate and sodium chlorid are formed, and nascent oxygen dis- engaged. (Na/J.-f HCl = NaOH+NaCl+O.) The sodium hydroxid saponifies the fatty matters, dissolves albuminous matters; the disengaged oxy- gen acts as a sterilizer, and, being liberated in deep parts, drives out the solutions. 8. What is the usual practice in such cases? Immediate root-filling as soon as sterilization is assured. 9. What material as a root-filling has met with the greatest measure of success, according to sta- tistics? 92 COMPEND OF Zinc oxychlorid; although many or most op- erators prefer gutta-percha. Diseases of the Periceaientum. 1. What are the morbid conditions to which the pericementum is subject? A series of nutritive disturbances, ranging from sHght and continued hyperemia to molecular necro- sis of its entire substance. 2. What is meant by pericementitis? An inflammation of the meml^rane covering the roots of teeth. It is also called dental periostitis and periodontitis. 3. Into what classes may these inflammations be divided? Into three: first, those beginning at the gum mar- gin; second, those beginning at the apex of the root; third, those beginning at some lateral aspect. 4. What are the causes of the first variety? First, salivary calculi; second, serumal calculi; third, the local effects of drugs being eliminated at the gum margin, notably mercury, i:)Otassium iodid, and pilocarpin. 5. What is the usual cause of the second variety? The entrance of septic matter from the pulp- canals of pulpless teeth to the tissues of the apical space. 6. What are the causes of the third class, those producing phagedenic pericementitis? Gouty pericementitis and inflanuuations follow- ing plantation. DENTAL PATHOLOGY AND THERAPEUTICS. 93 7. How is pericementitis classified as to dura- tion of existence? Into acute and chronic. 8. What is its range of severity? That of any periostitis; it may range from a mild stimulation, leading to a localized thickening of the cementum, to a general periostitis, involving the bodies of the maxillary bones. 9. What is the general symptom of the mild cases? Slight hypersensitivity upon percussion. 10. What of severe cases? General inflammatory symptoms about the parts ; fever, with all of its attendant symptoms; the tem- perature, in extreme cases, may rise to 105° F. Subsequently, septicemia, or even pyemia and death, may occur. 11. What is the common cause of the severe cases? Entrance of pyogenic organisms from the pulp- canals of teeth into the tissues of the apical space and into the lymphatics. 12. How may pericementitis be classified ac- cording to its effects? Into constructive and destructive. 13. What are meant by these? Constructive pericementitis is the form causing hypertrophy of the cementum. A destructive peri- cementitis is one causing a degeneration and necro- sis of the pericementum. 14. What is hypercementosis? 94 COMPEND OF A localized or general hypertrophy of the ccmen- tnm of a tooth. 15. What is its cause (general)? A slight and continued irritation of the perice- mentum, — a constructive pericementitis. 16. Specify some of its particular causes. Faulty occlusion, thread-biting, biting hard sub- stances, are causes affecting the apical and lateral aspects of the teeth. Other sources of irritation may be found in irritation of the gingival portion of the pericementum, by invasion of caries; protrud- ing fillings irritating the soft tissues; perforated roots, or the presence of foreign bodies at the edge of the pericementum; beyond the inflammatory focus, about the source of irritation, the pericemen- tum may be stimulated to constructive activity. Cases are found for which there is no discoverable cause. 17. What is the morbid anatomy of hyper- ccmentosis? The pericementum is slightly liyperemic. Pro- jecting from the general surface of the cementum are secondary masses. These may be isolated nod- ules; bulbous masses about the apices of the teeth; or, again, the thickening may be general, a distinct line marking near the neck of the tooth the junction of the secondary with the original cementum. Sec- tions exhibit the union of the growth with its base. The deposits have the appearance of exostosis. They may be soft or hard, and in some cases re- markably smooth. DENTAL PATHOLOGY AND THERAPEUTICS. 95 18. What are its symptoms? Those of a very mild pericementitis, occurring in a tooth at irregular intervals; as the deposit increases, painful sensations become more severe, until the tooth becomes the seat of intractable pain. These symptoms may extend over a period of years. Its occurrence is unusual before the age of thirty- five. 19. What are the more remote effects of hyper- cementosis? Dr. Flagg {Dental Cosmos, March, 1878) presents a list of reflex nervous disturbances, involving not only the several branches of the fifth cranial nerve, but the second, eighth (sight and hearing), and also some of the cervical nerves, all of which he has found associated with dental exostosis. 20. What is its diagnosis? It is made by exclusion, the patient usually com- plaining of pain about the teeth: each probable source of pain is sotrght out, until, if no other ex- planation be found, exostosis is suspected. Many of the diagnoses of the cases giving rise to wide reflex pain are post-mortem, extraction revealing the presence of hypertrophied cementum. In ob- stinate ocular or aural disorders, for which the aid of specialists has been unavailing, an examination of the teeth may reveal a dental disorder as the possible source of the reflex pain. 21. What is the prognosis of hypercementosis? Many cases of hypercementosis give rise to no symptoms; those which are the source of pain fur- 96 COMPEND OF nish a bad prognosis as to the preservation of the tooth. 22. What is its treatment? In its earher stages, when mere passing discom- fort is the complaint, local massage may be em- ployed. Any evident sources of irritation, such as malocclusion, caries invading the cementum, or foreign bodies, are to be corrected, remedied, or re- moved. In persistent cases extraction is the only remedy; the extraction must be carefully and com- pletely made. In event of a reflex neuralgia being ascribed to the hypercementosis, extraction is to be guarded. As it is next to impossible to positively locate the affected tooth, • the most probable of- fender is removed first and the effect noted; more than one extraction may be required. 23. What is meant by traumatic pericementitis? Pericementitis arising as the result of mechan- ical violence. 24. What is its common cause? Blows, falls, thread-biting, excessive use of the mallet in building down teeth; severe wedging, and too severe occlusion. 25. WHiat are its grades of severity? It ranges from a mild and temporary irritation to abscess, or even necrosis. 26. What is a frequent accompaniment in se- vere cases? Death of the puli); probably due to thrombosis of the apical vessels. 2"]. What are its symptoms? DENTAL PATHOLOGY AND THERAPEUTICS. 9/ In mild cases, tenderness upon percussion ; if more severe, slig^ht protrusion of the tooth and greater tenderness; in very severe cases the tooth may be forcibly displaced. 28. What is the morbid anatomy? The case is surgically one of bruise. If a very severe blow has been received upon the tooth, suf- fusion of the dentine may occur; the red blood-cor- puscles are disorganized, and their coloring-matter invades the dentine. If the pulp has been killed, the fact may not become evident for years, and only then through an increasing opacity of the tooth. 20. A'NHiat is the treatment? That of a bruise; surgical rest being indicated, the affected tooth is to be immovably held by a suit- able appliance. Remove all existing sources of ir- ritation, and apply antiphlogistics. such as frequent washing with ext. hamamelis. 30. AA^hat is the most common cause of acute pericementitis? The entrance of micro-organisms and their prod- ucts into the tissues of the apical spaces, following upon the putrefactive decomposition of the dental pulp. 31. AYhat are the symptoms and clinical his- tory of acute apical pericementitis? In the last stages of purulent pulpitis a tooth re- sponds to hot applications, the pain being relieved by cold. The tooth exhibits a slight sensitiveness to pressure and percussion. A period of quiet su- pervenes, of some weeks or months, when the in- •4 98 COAIPEND OF duction of pain upon pressure reappears. The gum overlying the tooth becomes injected. The effu- sion into the pericementum causes extrusion of the tooth, so that it is longer than its neighbors. The pain becomes throbbing, increasing in severity. In mild cases the symptoms are not severe; in the sec- ond grade the inflammatory phenomena are more pronounced, and so on until the fifth, the most se- vere grade, when the contiguous tissues participate, and there is great oedema, symptoms of more or less diffused periostitis of the maxillary bone. There may be rigors (chills) and fever, the temperature in some instances as high as 104°. The pulse, full and bounding in the early stages, may become quick and soft, and evidences of septic intoxication occur. Cases are recorded where the disorder unchecked has been followed by metastatic abscesses (pyemia) and death. 32. What is its diagnosis? A tooth containing a very deep cavity, or a crownless root, becomes sore to pressure, and ex- truded from its socket; the gum overlying shows evidences of any degree of inflammation. Increas- ing tenderness to pressure, and general inflamma- tory symptoms. 33. What is the prognosis? Usually depends upon the readiness and com- pleteness with which the exciting causes may be re- moved; second, upon the severity of the inflamma- tory symptoms. If the conditions are favorable, the comfortable retention of the tooth for years is DENTAL PATHOLOGY AND THERAPEUTICS. 99 probable. If symptoms of maxillary periostitis are pronounced, the affected tooth is usually doomed. In more severe cases adjoining teeth may be affected and lost. If septic intoxication occur, the retention of the tooth will depend upon the readiness with which the symptoms disappear after sterilization of the center of infection. 34. What is its treatment? First, that of all inflammatory diseases — remove the cause. As this latter is the septic matter (pyo- genic and other organisms) contained in canals, the mouth is first freely lavaged with powerful antisep- tics, solutions of phenol sodique, 3 per cent, pyro- zone, or 20. per cent. sol. of meditrina. Entrance to the pulp-chamber is secured through the filling, or, if the inflammatory action be high, by the shortest and most direct path through the tooth by means of a spear-pointed drill. The affected tooth is to re- ceive mechanical support during this operation. Powerful antiseptics are worked into the canals by means of broaches, and the vent-hole left open. Counter-irritation is induced over the healthy gum adjoining the inflamed area. 35. What is the treatment of more severe cases? Even though the inflammatory symptoms be marked, accompanied by fever, a full, bounding pulse, an attempt may be made to abort the inflam- mation. The antiseptic measures are vigorously applied, local blood-letting is employed, a couple of leeches applied to the gum, and hot water held in the mouth after their removal. Dry cups are ap- 100 COMPEND OF plied to the neck. Quinine snlph., gr. viii, to which morphia snlph. gr. ^ has been added, are adminis- tered; the patient placed in bed with the head ele- vated. If the pulse be full and bounding, ten drops tr. aconiti rad. are placed in water oz. i, and a tea- spoonful of the mixture administered every hour until the pulse is normal. If in five hours the in- flammatory symptoms are not relieved, the patient is to have the feet placed in hot water, to be well wrapped in blankets, and Dover's powder, gr. x in hot lemonade, administered until there is free dia- phoresis. The succeeding morning a tablespoonful of magnesise sulph. is given in a gobletful of water. 36. What is the rationale of this treatment? The local blood-letting and dry cups are for the purpose of unloading the blood-vessels of the af- fected area. The quinine and morphia are given to reduce the extent of corpuscular exudation and to quiet the irritability of the nervous system. The maximum of quinine effect is in five hours, so that if at the expiration of that time the desired effect be not gained, the quiet of the nervous system is ob- tained by the action of the opium in the Dover's powder. Both opium and ipecacuanha act as dia- phoretics ; by increasing the volume of blood in the cutaneous circulation, blood is drawn from the in- flamed area. The administration of the Epsom salts is for the purpose of derivation and lessening of the general volume of the blood. The aconite, by reducing the pulse, lessens the vascular phenomena in the inflamed area. The continued use of anti- DENTAL PATHOLOGY AND THERAPEUTICS. lOI septics by destroying- the bacteria lessens the symp- toms. 37. If, despite all measures, severe inflammatory symptoms are not reduced, what is to be done? Immediate extraction of the offending tooth. 38. What is the common result of acute perice- mentitis? The formation of pus in the tissues of the apical space. 39. What is this called? Alveolar abscess. 40. What are the symptoms? After the inflammatory symptoms of pericemen- titis have been present for from twenty-four to sev- enty-two hours, there is a marked lessening of their severity; the swelling of the gum, which has been tense and hard, becomes soft and easily pitted; the summit of the swelling becomes yellow, bursts, and there is a discharge of pus. (This will be discussed later.) 41. Wliat is another common variety of apical pericementitis? The chronic. 42. What are its causes? A persistent source of irritation of less severity than necessary for the production of acute apical pericementitis. Septic infection of mild grade, in teeth having open canals through which effusions may drain from partially cleansed and imperfectly sterilized canals, protruding root-fillings, mal- occlusion from any cause. I02 COMPEND OF 43. "What are its symptoms? The tooth is tender to pressure, shghtly loosened, and elongated. There is more or less vascular in- jection of the overlying gum. 44. \Miat is its treatment? Removal of the causes. Determine by means of articulating (carbon) paper the points of excessive contact: if there be malocclusion, grind away the portions marked by the paper until the tooth is free of contact with its antagonist; this gives rest. Should the tooth contain a large open cavity, it is to be sterilized. Each root-canal is to be entered and thoroughly cleansed by means of broaches and anti- septics. Be careful that no decomposing matter is thrust through the end of the root. If the tooth contain a dead, but not disintegrated pulp, endeavor is made to extract it en ))iasse. If the symptoms are found with a tooth containing a large filling, free in- gress to the roots is to be secured for their cleansing and sterilization. If the pulp has died after the insertion of a filling, it is removed, the roots steril- ized and filled. If a pulpless tooth, careful search is made for uncleansed or imperfectly cleansed canals; these, when found, are thoroughly cleansed, steril- ized, and filled. Minute or tortuous canals are cleansed by fine Donaldson's cleansers and sulfuric acid. A drop of 50 per cent, acid is applied to the entrance of the canal, and the cleansing instrument is introduced progressively by a combination of careful rotary and pumping movements. Addi- tional applications of acid are made until the canals DENTAL PATHOLOGY AND THERAPEUTICS. I03 are freely open. The snlfiiric acid also acts as a sterilizing agent in this procedure. 45. How is a dead pulp in an apparently sound tooth diagnosed as a cause of pericementitis? Fiy an increasing opacity. A light, preferably that of the electric mouth-mirror, is placed behind the tooth, and its loss of translucency determined. Without marked malocclusion the tooth is found to be loosened and the overlying gum injected. 46. How are such Cases treated? By the exercise of the utmost antiseptic precau- tions. The mouth and the teeth are to be perfectly sterilized, every instrument employed to be soaked in powerful antiseptics. After gaining direct access to the pulp-chamber, the stronger antiseptics are applied to the decomposing material. The contents of the chamber are syringed and drawn away until the canal is cleansed. Applications of strong solu- tions of sodium peroxid are made, which dissolve the pulp remnants and sterilize the canal and the dentine. The canal is then filled tentatively. Un- less the greatest care and rigid antisepsis be fol- lowed in these cases, intractable inflammation of the pericementum may arise. 47. What is the patholog}' and morbid anatomy of alveolar abscess? The pyogenic organisms are present in the pulp- canals of teeth containing putrescent pulps. Their waste products are a source of irritation to the tis- sues of the apical space. These tissues become a suitable soil for the development of the organisms. I04 COMPEND OF Pericementitis occurs, as above described, and pus is formed. If the pus finds egress through the canal of the tooth, the acute inflammatory symp- toms subside, and the formation of pus continues, owing to the presence of the organisms ; but so long as the canal remains open there are no acute symp- toms. If the pus be unable to make exit through the natural channel, it may find exit in one of sev- eral paths. The most direct path is to the external alveolar wall, except in the palatal root of superior molars, where its path is toward the palatal process. In the former case, the wall of the alveolus is at- tacked and perforated; the suppurative process in- volves next the cancellated tissue of the alveolar process; next, its outer plate. Before finding exit, the external periosteum is attacked, and it may be raised from the outer wall of the process, and pus accumulate between the periosteum and the bone. Usually the pus penetrates the periosteum; next, the gum, finding exit immediately over the apex of the affected root. 48. What result may follow the stripping of the periosteum? Necrosis of the uncovered bone. 49. In what other situations may the pus find exit? In abscess affecting the lower teeth the pus may penetrate the body of the bone itself and overlying tissues, and escape externally upon the face, as, for example, under the chin, in abscess from lower incisors. Under the lateral aspect of the maxilla, DENTAL PATHOLOGY AND THERAPEUTICS. I05 from abscess upon posterior teeth, the pus may meet a plane of tissue and follow the course of that tissue. A case has been recorded of pus burrowing along the fibers of the platysma myoides, opening upon the shoulder. In upper teeth, the'pus from an abscess over the centrals or laterals may perforate the floor of the nasal cavity; from bicuspids and molars, perforation of the floor of the maxillary sinus may occur. Others of these cases may have opening upon the cheek. Not infrequently pus from the apical abscess finds exit at the neck of the tooth. 50. What is the diagnosis of alveolar abscess? Any fistula found about the jaws or alveolar process is to be referred primarily to the teeth. As a rule, a fistula overlies an abscessed root. Ab- scess is diagnosed in any tooth which has been the seat of an acute pericementitis lasting more than forty-eight hours. A soft silver probe may be bent to follow the direction of the sinus, and thus detect the afTected tooth. This procedure should be fol- lowed with all fistulas about the jaws or face. 51. What is the diagnosis of alveolar abscess without fistulous opening? As a rule, the pulp-chamber will be found com- municating with the exterior through a large cari- ous cavity. The pulp-chamber and canals are filled with a decomposing mass; the gum over the roots is injected, the tooth more or less loose. Attempts at sealing the carious cavity by closing the drain- age from the abscess provoke inflammatory disturb- ance. 15 106 COMPEND OF 52. What is the prognosis of alveolar abscess? Depends upon the amount of destruction of peri- cementum. As a rule, the prognosis is good. Alveolar abscesses may persist for years, and ap- parently gain but little headway, destroying but a limited amount of tissue. They are, however, al- ways a menace to the tooth's retention. Although productive of but slight local disturbance after a fistula is established, they are at all times to be viewed as possible centers of septic infection. 53. What is the treatment of alveolar abscess? Thorough removal of the cause and dead ma- terial, and establishing such conditions as will per- mit the regenerative process. The cause being the pyogenic organisms and the decomposing organic matter in the pulp-canal, dentine, and apical ce- mentum, the first step is thorough evacuation of the contents of the abscess-cavity and the destruction of the micro-organisms. If a fistula be established, the entire tract, from carious cavity, through the pulp-canal into the abscess-cavity, and out of the fistula, is to be freed of dead and septic matter. Pyrozone is injected through the tract, driving the dead material from all recesses out through the fis- tula. Sodium peroxid, 25 per cent, sol., may be employed, or pyrozone, 25 per cent, ethereal solu- tion. The application should be thorough, to in- sure the sterilization of the dentine of the root. The application of a powerful and persistent anti- septic follows. Carbolic acid alone is not now used with the same freedom as it was formerly, for it is DENTAL PATHOLOGY AND THERAPEUTICS. 10/ productive of unnecessary tissue-destruction. Dr. Black's I, 2, 3 mixture is to be preferred. The pulp-canal is solidly filled with a cotton stopping which has been saturated in the same mixture or with campho-phenique, and the crown-cavity sealed temporarily. The case is examined every few days to note the condition of the fistula. In two or three weeks the abscess-cavity should be filled with organized tissue, when the fillings of crown and canal are removed and replaced with permanent fillings. 54, What is the treatment of abscess without fistnla? Abscesses without fistula are evacuated by means of pyrozone, after a thorough cleansing and scrap- ing of the pulp-canal. The campho-phenique, or I, 2, 3 mixture, is pumped into the sac. A loose cotton dressing is placed in the pulp-chamber and the cavity sealed. The dressings are removed every second day, the cavity washed with pyrozone, and, if any pus is found, subsequently dressed with the permanent antiseptic; the cavity and canals are dried, and the cotton and temporary stopping re- placed. After a week or ten days, the cotton should exhibit no evidences of exudation; then canal fill- ings of cotton are placed, each succeeding filling being tighter, until a perfect stopping of this ma- terial is borne. The gum over the root should now have returned to its nomial color. 55. How and when are artificial fistulse to be established? I08 COMPEND OF Blind abscesses, which exhibit a persistent forma- tion of pus despite the rise of antiseptics tlirough the pulp-canal, are to be opened from the exterior. A soft, smooth, fine broach, over which a small disk of rubber-dam is thrust, is carried up the pulp-canal until it penetrates the abscess-cavity. The length of the tooth will be indicated by the rubber-dam. This distance is measured upon the gums to indi- cate the outer wall of the abscess-cavity. A drop of a lo per cent. sol. of cocain is injected, and in a few minutes a crucial incision is made through the gum to the process. A spear-pointed drill is then driven through the wall into the cavity. The case is now treated as an abscess having a fistula. After each dressing a strand of floss silk is passed into the ab- scess-cavity from the gum, its end protruding, to serve as a drain. 56. When and why is the apex of a root ampu- tated? In cases of persistently-open fistulse discharging serum, a probe passed through the fistula detects an absence of pericementum from the apex of the root ; the cementum is found to be rough. The apical portion of the cementum is saturated with septic material and is necrosed. The root-canal is to be thoroughly sterilized and filled, usually with gutta- percha. The fistula is enlarged and free access gained to the abscess-cavity, enlarging by means of antiseptic tents frequently changed. When a clear view of the root-apex is gained, a small fissure- bur is employed to cut ofi that portion of the root DENTAL PATHOLOGY AND THERAPEUTICS. IO9 projecting into the abscess-cavity. The cut surface is then smoothed and rounded. 57. What is a common effect of tlie operation? Faihire of the regenerative process to fill the cav- ity, the cut end of the root becoming exposed. 58. What treatment has been suggested to pre- vent this, and why is it not usually successful? Placing in the cavity a sterilized sponge-graft. The difficulty of attaining the necessary asepsis usually causes failure. Calcic Inflammation and Calculi. 1. What is calcic inflammation? An inflammation of gum or pericementum, or of both, caused by the deposits of calculi upon the teeth. 2. Into what two classes is it divided? Into those caused by salivary and those caused by serumal calculi. 3. What is meant by salivary calculi? A deposit of the calcium salts, which have been held in solution in the saliva, about the necks of the teeth. 4. What is their composition? Mainly calcium phosphate and carbonate (over 75 per cent.), water, and organic matter (22 per cent.}, the organic matter being largely mucin. 5. How are they formed? Their starting points are usually at the linguo- cervical portion of the lower incisors, and the bucco-cervical aspects of the upper molars, the lie COMPEND OF calculi about the lower incisors being more dense than those about the upper molars. From these points they extend over the crowns of the teeth, be- tween them, and insinuate themselves between gum and tooth. 6. What effects are caused by them? At the points of contact with the gum the latter is seen to become hypereinic, then oedematous; in swelling, the space between the necks of the teeth and gum is enlarged. The calculus encroaches upon this space; the soft tissues are kept in a con- stant state of irritation, next inflammation. The inflammation affects the pericementum and alveolar process, and there is an absorption of these tissues, until finally the tooth is deprived of support, and its increasing looseness is followed by its loss. Each particle of calculus acts as a destructive irritant to the soft tissues with which it is in contact. 7. What is the prognosis of this disorder? It depends entirely upon the extent to which the calculus has caused resorption of the process and destruction of the pericementum, and the thorough- ness with which the deposits may be and are re- moved, 8. What is the treatment? Removal by mechanical means, and smoothing the surfaces from which the calculi have been re- moved. Large scalers, formed to draw-cut, are first employed to remove the larger masses. Next, fine scaling blades, formed to push-cut, are applied over the teeth, removing the finer particles and the DENTAL PATHOLOGY AND THERAPEUTICS. Ill closely adherent scales. No hope of cure is to be entertained until the last vestige of deposit has been removed. Pyorrhea Alveolaris. 1. What is pyorrhea alveolaris? It is a term applied to a condition characterized by a gradual loss of the pericementum of teeth, an atrophy of alveolar walls, and attended by the de- posit of calculi upon the roots of the teeth and by a flow of pus. The term is faulty in that it actually describes but one, the last, symptom. 2. What varieties of the disease are met with clinically? First, those beginning beneath the gum-margin and progressing toward the apices of the roots, at- tended by the deposit of flat, smooth, hard, dark calculi. Second, those beginning upon a lateral aspect of a root, the gum-margin at first unaffected, the destruction of pericementum radiating from the first point attacked. Third, cases described by Dr. Black as phagedenic pericementitis, the clinical his- tories of Avhich are intimately associated with those of the second class. 3. What name is given to salivary calculi and those appearing just beneath the gingival margin? Ptyalogenic calculi. (Peirce.) 4. What other name has been applied to the second-named variety of calculi? Sanguinary calculi (Ingersoll); serumal calculi (Black). 112 COMPEND OF 5. What distinctive name has been given the de- posits occurring- upon the lateral surfaces of the roots ? Hematogenic calculi (Peirce). 6. Are all of these diseases alike? No; they differ in causes, clinical history, prog- nosis, and treatment. Class One. 1. What are the causes of the first variety of pyorrhea alveolaris? Predisposing and exciting. The direct predis- posing cause is a catarrhal condition of the gums, produced by many causes, both constitutional and local. The usual local causes are overcrowding of the teeth, their malocclusion, non-occlusion, or mal- positions. Lack of oral hygiene is the most pro- lific source of the disturbance, leading to the most extensive destructions. The direct local cause is a sub-acute inflammation of the margins of the gum. 2. What is the morbid anatomy and pathology? At the earliest stages the gum-margins are seen to be swollen, and loosened from their attachments to the necks of the teeth. A fine instrument passed into the space detects the presence of a foreign body adherent to the tooth. There is evidence of re- sorption of the alveolar process next to the calculus. If the disease progresses very slowly, the outer peri- osteum is the seat of a constructive periostitis, lead- ing to a thickening of the process, while the inner portion of the alveolar wall is undergoing atrophic DENTAL PATHOLOGY AND THERAPEUTICS. II3 change. Pyogenic cocci gain entrance to the pocket formed about the parts by the detachment of the gum, and a progressive degeneration of the peri- cementum occurs. At the termination of the dis- ease, when the surface of the root is incrusted by many small deposits, the alveolar walls absorbed, the pericementum is destroyed everywhere except at the apex, the tooth still being retained by a small Cjuantity of fibrous tissue. 3. What is the probable source of the deposits? The irritated glands of the inflamed gingivae pro- duce an altered secretion, which is coagulated by the acid of the lactic fermentation of food debris; lime-salts from the saliva are entangled in the coag- ulum, the form of the calculus being due to the pressure of the overlying gum. The deposits act as irritants, which cause inflammatory and, as soon as organisms proliferg,te, suppurative degeneration of the pericementum. Coincident with this degenera- tion is a melting dow^n of the alveolar walls. 4. What is the clinical history of the disease? A swelling and loosening of the gum from the tooth, increasing deposits upon the root, a flow of pus from beneath the gum-margins, and a pro- gressive loosening of the tooth in its socket. Fre- quently an early symptom is a growing malposition of a tooth. 5. What is the diagnosis? The onlv disease with which it might be con- founded is an alveolar abscess discharging at the gum-margin. In the latter cases there has usually 16 114 COMPEND OF been a history of acute apical pericementitis, and when the discharge of pus occurs a probe may be passed to the apex of the root without resistance. Deposits of calcuh near the apex are common when these cases are of long- standing. In pyorrhea the probe will meet with the resistance of the still at- tached pericementum, and by careful examination deposits toward the gingival side may be found, even if minute. 6. What is the prognosis? The disease may be arrested at almost any stage, provided every source of irritation be perfectly re- moved. 7. What is its treatment? It is directed toward removing every source of irritation, and curing the morbid conditions caused by the irritation. The first step is a general sterili- zation of the mouth, so that pathogenic organisms will not be introduced into deep parts during the scaling operation. The next stage is sterilization of the pockets, syringing with 3 per cent, pyrozone in both instances. Next, a removal of the deposits by fine scalers, used with a push-cut; heavy scalers should never be employed. If the teeth are loose, they are to be immovably lashed together, or re- tained in position by means of mechanical appli- ances (swaged plates, etc.). Faults of occlusion are corrected by grinding off redundant tooth-structure. An antiseptic and astringent mouth-wash is to be employed very frequently, until the gums appear to be reattached to the teeth. DENTAL PATHOLOGY AND THERAPEUTICS. II5 Second Class. 1. What is phagedenic pericementitis? A molecular disintegration of the pericementum of the teeth; beginning near, but not at the apex of, the root, it travels rapidly toward the gingival mar- gin. In its early stages no deposits of calculi are to be detected, but later they are usually found. Pus-formation, although usually present, does not always occur. 2. What are its causes? Undetermined. 3. What is its clinical history? Usually a history of a pericementitis may be elic- ited, the pain being obscure and indefinitely located. An examination may reveal a loosening of the gum from the neck of the tooth, and a flat blade may be passed for a considerable distance toward, in some cases quite to, the apex of the root. Testing the tooth by applications of cold will show the pulp to be still alive. Melting down of the alveolar wall is a secondary factor in the history. The destruction of pericementum is apparently, first, of the root, not the alveolar portion. In the last stages, if a single- rooted tooth, the tooth may drop from the shrink- ing socket and show an entire destruction of the pericementum. 4. What is the pathology and morbid anatomy? The morbid anatomy corresponds with that of the occlusion of a pericemental artery, followed by a death of cellular elanents, and next a degeneration of the remainder of the pericementum* and more Il6 COMPEND OF slowly of the alveolar walls. The death of a lateral portion of the membrane and absorption of a portion of the alveolar wall may occur before there is evidence of disease at the gum-margin. 5. What is the diagnosis? A loosening of a tooth without evident cause, such as mechanical irritation, death of the pulp, or deposits of subgingival calculi. An attempt is made to pass an instrument up into the alveolus from the gum-margin. If this be firmly adherent and the margins of the alveolus intact, a sharp probe may be passed through the gum to detect an absence of alveolar wall. 6. What is the prognosis? Usually unfavorable. 7. What is its treatment? The principle of treatment is the removal of dead and foreign materials and the inducing of tissue- regeneration to restore lost parts. Third Class. Gouty Pericementitis. 1. What is the third variety of pyorrhea alve- olaris? Hematogenic calcic pericementitis. 2. Into what are its causes divided? Predisposing and exciting, and into immediate and remote. The remote causes are any which ren- der the pericementum a weakened articulative tis- sue; they are the predisposing causes. The great majority of cases observed have affected the teeth DENTAL PATHOLOGY AND THERAPEUTICS. II7 of persons who are the victims of the gouty dia- thesis, wliicli diathesis is regarded as the predis- posing cause. The exciting cause, in the majority of cases, is the deposit of calcuH upon or in some portion of the pericementum lying between the apex of the root and tlie gum-margin, although a degeneration of the membrane does and may occur without the presence of perceptible calculi. 3. What is the clinical history of the disease? Very frequently that described under the head of phagedenic pericementitis. The history of a typical case may extend over a period of years. There is a personal or a family history of gout. Obscure neu- ralgic pains have been felt in and about the jaws for some time, particularly at night. One or more teeth may be seen to shift position without evident local cause. The teeth are but little, if any, affected by dental caries. The teeth, one or more, will give evidence of pericemental inflammation, as though an alveolar abscess were forming, as frequently it is. Thermal test shows the afifected tooth to contain a vital pulp. The discharge from the focus of in- flammation may make its way directly through the gum, or burrow along the pericementum and dis- charge at the neck of the tooth. The acute in- flammatory symptoms in other cases may subside. In either event the tooth loosens progressively, and an instrument passed through the gum reveals, at times, a loss of alveolar wall over a portion of the root, and usually the presence of a calculus. Should the discharge be at the neck of the tooth, Il8 COMPEND OF the calculus may be detected by passing a probe by that way. If these deposits be removed, washed, and tested, they will be found to respond, at times, very faintly to the murexid test, showing the pres- ence of urates. 4. What is the morbid anatomy and pathology? If teeth are extracted soon after inflammatory symptoms present themselves, it is usual to find the cervical portion of the pericementum intact; at some point of the apical half a calculus may be noted at times, evidently attached to the cementum ; in other cases the deposit may be in the pericemen- tum; surrounding the deposit is an area of necrotic tissue. It is presumed that, as a feature of the gouty process, an arterial twig or twigs have be- come occluded, and a death of cellular elements en- sues; the necrotic area acquires an acid reaction, which causes the precipitation of urates in the area. These deposits and the necrotic tissues act as irri- tants, and an inflammation is induced which is fol- lowed by a degeneration and necrosis of the peri- cementum and a degeneration or melting down of the alveolar walls. Pyogenic organisms gain en- trance to the disease area, and the tissue loss is hastened by the suppurative process. Accretions to the primary calculus occur, which are, as a rule, composed of calcium phosphate, combined with the morbid secretions of the part, forming adherent cal- culi. 5. What is the diagnosis? A patient from whom a clear gouty history may DENTAL PATHOLOGY AND THERAPEUTICS. II9 be elicited presents with one or more teeth exhibit- ing looseness. The gum-marg-ins are apparently unaffected, although in some cases pus may be ex- uding from the alveoli; in other cases, a serous fluid. An absence of caries is usually noted, no local causes existing which would explain the disease process. 6. What is the prognosis? As a rule, not good, although patients who have suffered from nocturnal maxillary neuralgia, loose- ness of teeth, and in some cases even morbid dis- charge from about the necks of the teeth, have had the symptoms disappear through an observance of an anti-gout regimen and the administration of anti- gout remedies, without any local measures being employed. The prognosis is governed, as in any other disease, by the extent to which causes predis- posing and exciting, remote and immediate, may be removed and the effects of their action remedied. The more advanced the case, the worse the prog- nosis. As a. rule, the process eventually causes the loss of every affected tooth. 7. What is the treatment? It is divided into general and local. The general therapeutics is directed toward the elimination or washing out of waste products through bowels and kidneys, and increasing the alkalinity of the blood. In acute cases colchicum may be prescribed; in the chronic cases, potassium iodid. The administra- tion (continued) of lithia waters is recommended. The bitartrate of lithium, gr. v ter die, serves as I20 COMPEND OF an eliminant and increases the alkalinity of the blood. What is described in the text-books upon general therapeutics as an anti-gout regimen should be rigidly followed. White meats and fish are sub- stituted for beef. Alcoholic liquors are to be es- chewed. Open-air exercises are advised to increase the oxidizing function. Succulent vegetables are substituted for starchy vegetables, as the latter un- dergo fermentative changes in the stomach and perpetuate a common feature of gouty maladies and gastric disorders. The local therapeutics is di- rected to the surgical conditions present. First, any faulty or excessive occlusion should be cor- rected. Second, loose teeth should be placed in splints (ligatures, plates, or other devices). Third, the thorough removal of all deposits. This opera- tion is in some cases impossible; the deposits are too firmly adherent for removal by instrumental means, and solvents are inefificient. Fourth, pus and organisms are to be destroyed. Pyrozone, small amounts of 25 per cent, on wisps of cotton, is most eflfective. Fifth, the loose tissues are con- tracted and the congestion lessened by means of the continued use of an astringent and antiseptic — zinc chlorid or iodid, gr. iii, water oz. i. Erosion of the Teeth, 1. What is dental erosion? A progressive chemical solution of the faces of the teeth, not due to caries or mechanical abrasion. 2. What is its cause? Patients are usually the victims of the gouty dia- DENTAL PATHOLOGY AND THERAPEUTICS. 121 thesis. An altered secretion of the labial follicular glands, acid in reaction, is probably the solvent. 3. What is its morbid anatomy? -The labial faces of the teeth are commonly at- tacked; an area becomes denuded of enamel; during solution its surfaces remain polished; the invasion of the dentine is less rapid than is the surface loss of enamel, so that cup-shaped excavations are formed. The morbid anatomy is distinctive from that of dental caries. Occasionally the denuded surfaces become hypersensitive; its progress may expose the pulp, or a constructive action may oblit- erate the pulp as the disease advances. The ero- sion may proceed until the teeth-crowns are ampu- tated. In other cases the process appears to be self-limited. When the worn areas are restored by means of filling-materials, the erosion persists about the edges of the fillings. 4. What is its diagnosis? This peculiar tooth-loss occurring in dentures in- susceptible to dental caries. 5. What is its treatment? The persistent, continued use of alkaline appli- cations and alkaline mouth-washes. Phillips's milk of magnesia. The destruction, by electrical cautery, of the aiTected glands has been suggested. Cavities may be filled to protect the dentine, but the solution of enamel proceeds around their margins. Dental Pharmacology and Materia Medica. I, Into what two great classes may all remedial agents be placed? 17 122 COMPEND OF Stimulants and sedatives. Stimulants are agents which increase the activity of some one or more of the vital functions. Sedatives are those which depress functions. 2. Under what three heads may nearly all dental medicaments be placed? Antiseptics, anesthetics, and astringents. Antiseptics. 1. What is an antiseptic? It is an agent which prevents the action of path- ogenic organisms and their products upon living tissues. 2. What is a germicide? It is an agent which prevents sepsis by destroying the organisms. All germicides are antiseptics, but all antiseptics are not necessarily germicides. Iodo- form is an antiseptic, but not a germicide. 3. What antiseptics are commonly employed in dental practice? Salts of metals: the chlorids of zinc, mercury, and aluminum; sulfate of copper; nitrate of sil- ver. Alcohols and their derivatives: ethyl, or com- mon alcohol, phenylic alcohol (carbolic acid, crea- sote, trikresol, and lysol). Formic aldehyde (for- maldehyde). The -essential oils — of cloves, cajuput, cassia, cinnamon (cassia being the oil from the Chinese, the latter the oil of the Ceylon cinnamon), eucalyptus, eugenol, and myrtol. Solutions from which nascent oxygen is evolved : hydrogen dioxid, pyrozone in 3 per cent., 5 per cent., and 25 per cent. DENTAL PATHOLOGY AND THERAPEUTICS. I23 solutions, the latter two in ether. Solutions of sodium peroxid. Strong alkalies: the alloy of sodium and potassium (kalium natrium), sodium carbonate, potassium carbonate, and sodium hy- drate, produced from sodium peroxid. The mineral acids, hydrochloric, chromic, nitric, and sulfuric. Organic acids, acetic (glacial) and the trichlor- acetic. Solutions containing hypochlorites (Labar- raque's) and solutions of hyposulfites. Iodoform, iodol, and kindred substances have limited appli- cation. 4. How do the salts of metals act as germicides? By forming albuminates of the several metals when the latter are brought in contact with proto- plasm. 5. In what form and strength are they em- ployed? Usually in watery solution, and in strength sufifi- cient to destroy micro-organisms, but insufficient to kill the cells of tissues. Mercuric chlorid, in 1-2000 to 1-500 sol., to which is added ammonium chlorid to hold the mercury salt in solution. Zinc chlorid is employed in 1-40 sol. 6. How do the alcohols act? They coagulate albuminous matter. 7. In what strengths are they employed? Ethylic (commercial) alcohol is used in 95 per cent, strength. Phenylic alcohol is used in from 5 ])er cent, to 95 per cent, strength. The kresols the same; also lysol. Campho-phenique, a substance formed by the addition of carbolic acid to gum cam- phor, is used full strength. 124 COMPEND OF 8. How do the essential oils act? As protoplasmic poisons, without coagulatinq- albuminous matter. They differ in germicidal power. The oils of cinnamon and myrtol appear to possess the greatest measure of power. Thymol has marked germicidal power. The oils of cloves and eugenol, of eucalyptus, of gaultheria, have less action. 9. How does nascent oxygen act? It chemically destroys septic matter. 10. How is hydrogen peroxid used, and in what strength? The commercial forms: 15 vol. sol. is contained in an aqueous solution, usually more or less acid in reaction; 3 per cent, pyrozone is a neutral solution. In these strengths preparations may be used undi- luted. The 5 per cent. sol. of pyrozone in ether is slightly caustic. The 25 per cent. sol. in ether is promptly but superficially caustic; it is used in small quantities undiluted. 11. What other marked and desirable effect has nascent oxygen? It is a bleacher. Bleaching is evidence of perfect sterilization. 12. How is it prepared for this purpose? It is placed in the dried cavity of a tooth in 25 per cent, ethereal solution, or the latter is mixed with an equal bulk of water and evaporated one-half, giv- ing a 25 per cent, acjueous sol. of pyrozone. 13. What is the action of sodium peroxid, how employed, and in what strengths? DENTAL PATHOLOGY AND THERAPEUTICS. I25 It is used in from 25 per cent, solution to full strength, or in dry powder. The powder is slowly sifted in distilled water at 32° F. until a saturated solution is made, which is then diluted as required. In the presence of organic matter the sodium per- oxid is decomposed, forming nascent oxygen and sodium hydrate. The oxygen acts as a germicide and bleacher; the sodium hydrate saponifies fatty and dissolves albuminous matters. 14. How does the alloy of sodium and potassium act? In contact with organic matter it seizes upon the hydrogen and oxygen of such matter, forming sodium and potassium hydrate. 15. How do the mineral acids act? How are they employed, and in what strength? Hydrochloric acid is used but little. In 10 per cent, solution it may be employed to neutralize powerful alkalies. Used after applications of sodium peroxid, it forms sodium chlorid, setting free the oxygen. Sulfuric acid chemically decomposes organic matter, dehydrating it. It is used in 50 per cent, solution (Callahan) for opening and en- larging the fine and tortuous pulp-canals of teeth. Nitric acid is used in rare instances to cauterize hypersensitive dentine. Its usual office is for the cauterization of sluggish ulcers. In both cases it is employed full strength. Chromic acid (deli- quesced) is used for the same purpose, but seldom. Acetic (glacial), lactic, and trichloracetic acid de- stroy organic matter, and are almost painlessly caustic. 126 COMPEND OF 1 6. What is aromatic sulfuric acid? A solution of alcohol, sulfuric acid, and several aromatics. The alcohol is transformed into sul- furic ether. Anesthetics. 1. What are anesthetics? Agents which diminish the reception, transmis- sion, or perception of impressions which would cause pain. 2. How are they divided? Into general and local. 3. What are general anesthetics? Those which prevent pain by temporarily abolish- ing consciousness. 4. What are local anesthetics? Those which prevent pain by the benumbing of chosen areas of the body. 5. What are most common of the general anes- thetics? Chloroform, sulfuric ether, and nitrous oxid. 6. What local anesthetics are employed in den- tistry? Refrigerants, such as a spray of rhigolene, ethyl or methyl chlorid, or pental, which, by their ra])id evaporation, cause analgesia by freezing; cocain, which acts as a paralyzant of nerve terminals with which it is brought in contact; tropacocain, and eucaine. 7. How is cocain employed? ' Epidermically, applied to a mucous surface; or DENTAL PATHOLOGY AND THERAPEUTICS. 1 27 hypodermically, injected beneath the skin, and pro- ducing anesthesia over a greater or less area. 8. AA^hat precautions are to be taken in using cocain or its preparations? To inject not more than the minimum physiolog- ical dose, never more than gr. -}; to make the in- jection under the strictest antiseptic precautions, and to combine in the prescription agents which will neutralize the ill effects of the cocain, its paralyzant action upon heart and respiration, and also an antiseptic. 9. What are these agents? A I per cent, solution of nitroglycerin and mor- phia. R — Cocain, gr. 1-3; Sol. nitroglycerin, gtt. j of i per cent. sol. ; Morphinse sulph., gr. i-io; Listerine, Aquge, aa dr. i. — M. ID. AVhat other effective method is there for in- troducing cocain into the tissues? Cataphoresis. 11. What is cataphoresis? It is the introduction of drugs into tissues by means of the electric current. A drug in solution is driven by the current from the positive toward the negative pole. 12. How is cataphoresis to be distinguished from electrolysis? In the latter the drug is decomposed into its chemical elements, which, according to their electric 125 COMPEND OF relations, are attracted to either positive or negative poles. In the former process the drug is driven bodily from the positive to the negative pole with- out decomposition. 13. What are obtundents? Agents which relieve existing pain; they are local anesthetics or analgesics, and have various modes of action. 14. Give examples. Zinc chlorid and silver nitrate, both powerful cauterants, obtund the sensitivity of dentine. They chemically destroy the sensitive terminals through which pain is received. The oils of cloves, gaul- theria, cinnamon, or cassia benumb the same fibers. The mild alkalies obtund by neutralizing irritating acids. Carbolic acid and kindred substances are specific obtundents, but destroy the obtunded tissue. 15. What are anodynes? Another class of anesthetics, to which morphia, atropia, aconitia, veratria, and gelsemium belong. The first of the group is the true anodyne; it lessens pain v/ithout necessarily destroying consciousness. The abolishment of pain is a secondary factor with the other alkaloids named. 16. Name other true general anodynes. The coal-tar derivatives, phenacetin and acetan- ilid, with its preparations, antikamnia, ammonol, etc. xj. When arc anodynes employed? To lessen or abolish neuralgic pain, the exact ori- gin of which is unknoAvn, or being known cannot be removed by means of local applications. DENTAL PATHOLOGY AND THERAPEUTICS. I29 18. What objection is there to the use of the powerful alkaloids? Disagreeable and undesirable constitutional ef- fects. 19. A¥hat is the danger in using the coal-tar derivatives ? They depress the heart's action. For that reason, animonol, which contains a cardiac stimulant, is usually preferable. The dose is about ten grains. 20. What is the most common use of these agents? To relieve attacks of hemicrania (sick-headache). 21. What is their mode of action? It is unknown. A'stringents. 1. What are astringents? Agents which cause contraction of tissues to which they are applied. 2. How are they divided? Into vegetable and mineral. 3. To what do the vegetable astringents owe their efficacy? To the presence of tannic acid. 4. For what purpose are they usually em- ployed? As styptics, to arrest minor hemorrhage. 5. For what other purpose are they nstdl As constituents of mouth-washes for flabby con- ditions of the mucous membrane. 6. What preparations are employed? 18 130 COMPEND OF Ext. hamaraelis Virginica; solutions of tannic or gallic acid; infusions of white oak (Quercus alba); tinctures of kino, krameria, and of myrrh. 7. Why are infusions preferable to tinctures? Tinctures contain gums insoluble in water, which, when employed as mouth-washes, are precipitated about the necks of the teeth. 8. What metallic astringents are employed in dentistry? Solutions of zinc chlorid, gr. ii-oz. j ; solutions of alum; solution of the subsulfate of iron (Mon- sel's solution), the tincture of the chlorid of iron; alum, and the subacetate of lead. 9. W^hat are their uses? With the exception of the first and last, they are used as styptics in the arrest of alveolar hemor- rhage. The zinc chlorid solution is used as an astringent and antiseptic; the lead salt, dissolved in water dr. j-Oj, is used as an antiphlogistic exter- nally. The salts mentioned as styptics contain more or less free acid, which is destructive to the teeth. Dental Medicine Cabinet. Mark all poisons POISON. Acetanilid, combined with sodium bicarb, and cafifein citrate fantikamnia), in 5 gr. tablets. For the relief of neuralgic pain, one pellet every three hours up to five pellets. Acid Acetic. In dentistry the trichloracetic acid is used. Full strength to destroy tissue (caustic), DENTAL PATHOLOGY AND THERAPEUTICS. I3I to remove fungous gum, destroy fungous pulp, to destroy gum flaps overlying iitiprisoned lower third molars^ to destroy small remnants of vital pulps. In 25 per cent, solution it is used to soften the deposits of serumal calculi, to check oozing, and permit a better view of the pockets. Acid Boric. A mild antiseptic powder; in solu- tion an ingredient of antiseptic mouth-washes. Acid Carbolic (Phenylic Alcohol). In crystals or fluid it is a caustic, used principally in dentistry to cauterize canker sores. They are dried, and the acid (a crystal) pressed against the sore until it is white. As an antiseptic it is employed full strength to sterilize the dentine, as an antiseptic canal-dress- ing, an application to abscess-cavities. (It is com- bined for this purpose with oil of cinnamon i part, carbolic acid 2 parts, ol. gaultheria 3 parts — Black's T, 2, 3 mixture). As an obtundent of hypersensi- tive dentine it is used full strength. In 5 per cent, watery solution it is in common use for antiseptic irrigation. Acid Chromic. A powerful caustic, rarely used in dentistry, although at one time the deliquesced acid was used as an obtundent and caustic. Acid Hydrochloric (10 per cent.). Used with sodium peroxid to suddenly disengage oxygen. Acid Nitric (fuming). As a caustic for canker sores, for which purpose it has been replaced by carbolic acid; to obtund the hypersensitivity of the abraded dentine upon the articulating faces of teeth previous to excavation. 132 COMPEND OF Acid Oxalic. Used to liberate chlorin from chlorinated lime in the bleaching of teeth. Mark poison, as it closely resembles Epsom salts. Acid Phosphoric. A solution of the ortho-phos- phoric acid is the fluid of zinc phosphate cement. Acid Salicylic. An antiseptic largely fallen into disuse except as a constituent of mouth-washes. Acid Sulfuric. In 50 per cent, solution used to effect an entrance to minute and tortuous pulp- canals; it is pumped into the canal by means of Donaldson's cleansers. It is also an efficient anti- septic in the same connection. Acid Sulfuric, Aromatic. It is in part an ether. It is formed by the combination of sulfuric acid, alcohol, and aromatics. It is used full strength to dissolve carious bone, and diluted as a stimulating wash. Acid Tannic (in powder). Applied to bleeding alveoli to arrest hemorrhage. Aconite. The tincture of the root is used in com- bination with tine, iodin to relieve pericementitis. Evaporated to one-fourth its volume, it forms the dental tincture of aconite (hlagg), a powerful local paralyzant. One-drop doses of the officinal tinc- ture are given in water every hour to depress the action of the heart in the constitutional treatment of inflammation. Alcohol. Used as a solvent of gums to form varnishes; to alDStract water from parts and ]iroduce desiccation, particularly a sui)erficial desiccation of the dentine prior to root-fllling. It is evaporated DENTAL PATHOLOGY AND THERAPEUTICS. I33 rapidly by means of a hot blast. Alcohol is a pow- erful astringent. Methyl alcohol is employed to dissolve di-nitro cellulose to form a non-conducting varnish. Ammonii Carbonate. In the form of smelling- salts, as a quick cardiac stimulant in cases of faint- ness. Amyl Nitrite. Keep in glass pearls of np, iii each. In cases of pale face, cold extremities, and cardiac spasm one of the pearls is crushed in a handkerchief and the nitrite inhaled. It is the antidote for the evidence of chloroform-poisoning. Argenti Nitras (Nitrate of Silver). In crystals, used as an obtundent upon the abraded faces of teeth; as an antiseptic canal application for chil- dren's temporary teeth; as a caustic for canker sores. In from 4 to lo per cent, solution it is used as a stimulant and antiseptic application to mucous surfaces. Aristol (di-thymol iodid). A powerful antiseptic, containing iodin and thymol ; it has largely replaced iodoform, being odorless and a more powerful anti- septic. The powder is soluble in ether and oils. As a canal dressing it is dissolved in oil of cin- namon. Arsenic. The trioxid (arsenious acid) is com- bined with an equal quantity of cocain hydro- chlorate and sufhcient oil of cinnamon to make a paste. The paste is used in minute quantities to devitalize the pulps of teeth. Arsenic has a power- ful paralyzing action upon the pulp; the liquor 134 COMPEND OF potassii arsenitis (Fowler's solution) will paralyze the sensory filaments in the dentine, and presum ably destroy a pulp. The formula — R — Acid, arseniosi, Cocain hydrochlor., oa; Ol. cinnamon, q. s. Ft. paste, has largely superseded the old formula — R- — Acid, arseniosi, Morph. acet, aa; Acid, carbolic, q. s. Ft. paste. Capsicum. Is used as a stimulant and counter- irritant. As a stimulant, a few drops of the tinc- ture are placed in sterilized water or a solution of listerine, and used as a mouth-wash or a stimulating injection where tissue-regeneration is in progress, but is sluggish. As a counter-irritant, the pow- dered capsicum is mixed with powdered ginger and made into pepper-bags. These are at present most commonly used in cases of chronic or transient pericementitis. Campho-phenique. A preparation made by mix- ing- Gum camphor, Carbolic acid, It possesses the properties of carbolic acid with- out being cauterant. It is a stimulating antiseptic, — stimulating to tissue-growth, but sedative as to sensory function. Chloral Hydrate. In 20 per cent, watery solu- DENTAL PATHOLOGY AND THERAPEUTICS. I35 tion, a powerful counter-irritant; in i per cent, solu- tion, a stimulating injection. As a hypnotic, gr. x camphor and chloral, aa, is a useful local appli- cation for the relief of neuralgia. It is applied ex- ternally for the relief of pains attendant upon diffi- cult eruption of the lower third molar. Chloroform. Excluded from use as an anes- thetic in dental operations on account of the at- tendant dangers. Applied upon cotton it will fre- quently relieve the pain of pulpitis. Cocain Hydrochlorate. Maximimi dose for use in dentistry, gr. |; used in 4 per cent, aqueous solution as a local anesthetic for mucous surfaces. Combined in the following prescription it is used as an injection for the painless extraction of teeth: R — Cocain hydrochl., gr. i~6; Morph. sulph., gr. 1-16; Sol. nitroglyc, i per cent., gtt. j; Listerine, q. s. Ft. ^j. — M. The injection is made over the roots of the teeth. Cocain is an ingredient of arsenical paste. A spray of 2 per cent, solution is used to benumb the soft palate prior to taking impressions in cases of irri- table palate. Creasote. Same uses as carbolic acid. Ethyl Chlorid. In sealed tubes. A spra}^ is used as a refrigerant anesthetic for tooth-extraction and to benumb hypersensitive dentine. Iodoform. In powder and in 5 per cent, ethereal solution as an antiseptic, but not a germicide. It 136 COMPEND OF is believed that in contact with the tissues iodin is Hberated from iodoform and acts as an antiseptic. Iodoform is sedative. Its odor may be disguised by mixing- with oil of cinnamon. lodol. Properties and uses similar to those of iodoform. Iodin. In tincture is a counter-irritant, astrin- gent, and antiseptic, in the latter office particularly useful in the last stages of putrefactive decomposi- tion. In strong tincture, combined with tr. aconite, it is applied to the gums in chronic pericementitis as a counter-irritant. In diluted tincture it is ap- plied as an antiseptic and astringent in cases of con- gestion of the gums and pyorrhea alveolaris. Magnesium Hydrate, MgH^O^. Used as an antacid mouth-wash, particularly in cases of ero- sion; a film of magnesium hydrate being deposited upon the eroded areas protects them from the ac- tion of the eroding acid. Menthol. Crystals, as an obtundent in cases of pulpitis; made into pencils with cerates, to relieve neuralgia by painting over the painful tract. Oil Cajuput. It is obtundent and antiseptic. Placed in root-canals, it acts in the latter capacity, and facilitates the introduction of gutta-percha cones, of which it is a solvent. Oil Cloves (Caryophylli). Used to relieve the pains of pid])itis; in ]iaste, with zinc oxid, as a pul])- capping. Its antiseptic principle, eugenol, is used as a canal-dressing in septic cases. Oil Cinnamon. Powerfully antiseptic, and an ob- DENTAL PATHOLOGY AND THERAPEUTICS. I37 ttindent. Used as a canal-dressing in septic canals, it diffuses rapidly through the dentine. It has largely displaced other essential oils in dentistry. Penta.l. A general anesthetic; used as a local anesthetic after the same method as ethyl chlorid. Peroxid of Hydrogen, H2O2. An antiseptic. In the presence of decomposing organic matter, nas- cent oxygen is liberated, which acts as a powerful germicide, antiseptic, and disinfectant. Pyrozone. Solutions of hydrogen peroxid, 3 per cent, in water, 5 per cent, in ether, 25 per cent, in ether (caustic pyrozone). The latter is largely em- ployed as a germicide and as a bleacher of discol- ored dentine. Potassium and Sodium. An alloy of these metals is used to introduce into purulent pulps. Sodium and potassium hydrates are immediately formed, which chemically destroy all organic matter present. Potassium Bromid. A general sedative, used particularly in excitement due to cerebral conges- tion. Used as a rectal injection, gr. v-x in starch, for cases of convulsions in teething children. It is usual in these cases to combine with it gr. iij of chloral hydrate. Potassium Chlorate. Used in solution or pow- der in cases of stomatitis, tonsillitis, etc. Potassium lodid. Used in massive doses where evidences of tertiary syphilis are present. In oint- ment — Potassium iodid, gr. xx; Cerate simp., 3j. — M. it is used to rub over indurations. >9 138 DENTAL PATHOLOGY AND THERAPEUTICS. Potassium Permanganate. A powerful oxidizing antiseptic; a most efficient deodorant. Fresli claret-colored solutions are to be emplo3^ed. Sodium Peroxid, Na^O.. An invaluable agent in the treatment of septic root-canals which contain the body or remnants of the decomposing pulp. May be used dry or in solution. Thymol. A derivative of the oil of thyme. A very powerful, persistent, and penetrating anti- septic ; used as a canal-dressing, and as an obtun- dent and antiseptic applied to the dental pulp at any stage or grade of irritation or inflammation. Tropacocain. A local anesthetic of equal or greater power than cocain, without its dangers. ■ Zinc Chlorid. Deliquesced, it is used as an ob- tundent of persistentl}' hypersensitive dentine. Di- luted, it is the fluid of oxychlorid of zinc cement. In solutions 4-10 grs. — oz. j, it is an antiseptic, astringent, and stimulating injection. Zinc lodid. In 20 per cent, solution it is an anti- septic and astringent application to pyorrhea pockets. Zinc Sulfate. In saturated solution it is mixed with zinc oxid to form zinc oxvsulfate, a pulp- capping cement. :it3 ?#' RK301 Burchard Qompend of dental pathology. 389 Copy 1 RK SOlB Cl'^^ LIBRARIES (hsl,stxj 2002342456 ^^S^^ItV' 1 Bs^^ 4