; Digitized by the Internet Archive in 2010 with funding from Open Knowledge Commons (for the Medical Heritage Library project) http://www.archive.org/details/workonoperativ01blac ^AJT^-^-^ A WORK OPERATIVE DENTISTRY IN TWO VOLUMES. VOLUME ONE, THE PATHOLOGY OF THE HARD TISSUES OF THE TEETH. GLOSSARY AND INDEX. 187 ILLUSTRATION'S. G. V. BLACK, M.D., D.D.S., Sc.D., LL.D. DEAN AND PROFESSOR OF OPERATIVE DENTISTRY, DENTAL PATHOLOGY AND BACTERIOLOGY NORTHWESTERN UNIVERSITY DENTAL SCHOOL. THIRD EDITION CHICAGO: MEDICO-DENTAL PUBLISHING COMPANY. LONDON: CLAUDIUS ASH, SONS & CO., LTD. 1917. Entered, according to Act of Congress, in the year 1917, by the Medico-Dental Publishing Co., the Office of the Librarian of Congress, Washington, D. Entered at Stationers' Hall, London, Eng. ; HENRY 0. SIIEPARD CO., PRINTERS, CHICAGO. PREFACE. The original intention in writing this book was to confine it strictly to a consideration of dental caries and its treatment, but later atrophy and erosion of the teeth were added. Atrophy of the teeth seems now to have been completely made out both as to its causation and the principal forms of the injury to the hard tissues of the teeth, and it was thought best to place this infor- mation on record in permanent form. Much of the detail as to these injuries may, however, be discovered in the future. Our information regarding erosion is far from complete and it now seems probable that much time may elapse before its investi- gation will develop satisfactory results. Its apparent increase in frequency and the great damage it is doing, calls for the clos- est study that the profession can give. Otherwise than the presentation of these two conditions, this book will be confined strictly to the consideration of dental caries and its treatment. This comprises the main features of Oper- ative Dentistry, though in fact it is only one department of our daily work at the chair. Diseases of the dental pulp, diseases of the peridental membranes, alveolar abscess, and the whole group of pathological conditions of the soft tissues, are subjects for another volume. The time has passed for including in one book all of the subjects of dentistry. While I have not been unmindful of the needs of the general practitioner in the preparation of the book, it has been planned especially for use of students in dental schools. The subjects are introduced and carried forward step by step, from the sim- pler to the more complex, with complete explanations of the nomenclature for the beginner in the work of preparing cavities and filling teeth. In the treatment of this subject, the questions of the pathology of caries applicable to the prevention of recur- rence of decay after fillings have been made, and the conditions under which operations should or should not be done, have been repeated often in order to keep these matters constantly before the mind of the student. In the arrangement of the matter, the logical order usually observed in books has been followed. That is, the pathology has been presented first and the treatment later. This is not always IV PATHOLOGY OF THE HARD TISSUES OF THE TEETH. the best order in teaching, and especially when the subjects are presented in that detail that is necessary to completeness. In order to read most understanding^ of the pathology of typhoid fever, for instance, one must have had much practical observa- tion of the disease. The more prominent facts should be obtained first and the more intimate detail added later, when personal observation has given a wider view. In the study of dental caries and its treatment, I have usually preferred to adopt such a plan in teaching. With that view, the second volume would be given to the student first. Following this thought, an outline of the principal points of the pathology involved is usually given with or preceding the treatment of each class of dental caries. In the first study by which the student is prepared for the begin- ning of the practical observation and treatment of caries, this answers the purpose. The more serious study of the pathology of dental caries is then undertaken later. If this plan is adopted, the first parts of the second volume would be given the student in the operative technic course in the freshman year. This would be reviewed and completed in the junior year. The first volume would then belong to the senior year. The book may be used, however, in either order. In the order as arranged, the more serious study of the pathology coming first, the reminders introduced in the second volume will be of direct advantage. With but few exceptions, the illustrations are original. Those illustrating the preparation of cavities are reproductions of pictures made by my own brush, and the photographs and photomicrographs have been made by Dr. F. B. Noyes from specimens of my personal preparation from material I have gathered myself, which remained under my personal observa- tion and study during the entire process. I am under especial obligation to Dr. Noyes for the excellent assistance he has given in the photographic work, and to my son, Dr. Arthur D. Black, for very valuable assistance and suggestions in the preparation and arrangement of the manuscript. G. V. BLACK. Chicago, III., June 22, 1908. PREFACE TO SECOND EDITION. The sale of this work has now exhausted the first edition of five thousand copies. This happens to come at a time when I am unusually busy in the preparation of a work on the pathology of the dental pulp and the investing tissues of the teeth, and, as I do not feel that a revision of this work is necessary at the present time, I publish a second edition with the correction of a few errors and omissions. G. V. BLACK. Chicago, August 3, 1914. PREFACE TO THIRD EDITION. It having become necessary to print a third edition of this work, I have thought it advisable to include the essential fea- tures of the studies of Mottled Teeth, a report of which, pub- lished in the Dental Cosmos for February, 1916, was the last scientific writing by my father. It was completed but a few weeks before his death. I have also substituted in Vol. II for the chap- ter on Pulp Treatment, the chapter on the same subject as pub- lished in the Special Dental Pathology, which contains more of detail. There are also a few additional illustrations. ARTHUR D. BLACK. Chicago, August 3, 1917. CONTENTS OF VOLUME I. PATHOLOGY OF THE HARD TISSUES OF THE TEETH. PAGE Introduction xhi Dystrophies of the Teeth 1 Nomenclature 2 Histological Characteristics the Basis for Classification 3 Atrophy of the Teeth 5 Etiology 10 Histological Characteristics 13 The Deformity in the First Permanent Molars 21 Treatment 24 The Enamel Whorl 27 Wrinkled Teeth 28 White Spots in the Enamel 30 White Enamel 31 Mottled Teeth 34 Brownin 35 Histological Characteristics 35 New Prohlem in Dental Pathology 37 Sporadic Cases 38 Diagnosis 38 Tables of Results of Examinations of Mottled Teeth Opposite page 39 Susceptibility to Caries 40 Etiology 40 Erosion of the Teeth 42 Diagnosis of Erosion 43 Frequence of Erosion 44 Forms of Erosion 45 Etiology of Erosion 50 Treatment of Erosion 57 VIU PATHOLOGY OF THE HARD TISSUES OF THE TEETH. PAGE Caries op the Teeth 60 Historical 60 General Statement 65 Caries of Dentin 68 Caries of Enamel 74 Penetration of Enamel in Pits 76 Penetration of Enamel in Proximal Surfaces of Incisors 77 Superficial Spreading of Caries in Proximal Surfaces of Bicus- pids and Molars 81 A Closer Examination of the Injury to the Enamel 83 The Eelation of Occlusion to the Localization of Caries 85 Penetration of Enamel in Buccal and Labial Surfaces 90 Caries as a Whole. Its Clinical Features 91 Occlusal Surface Decays in Molars 92 Proximal Surface Decays in Molars 93 Occlusal and Proximal Surface Decays .in Bicuspids 97 Misplacement of Beginning Proximal Decays 100 Secondary Extensions Gingivally of Proximal Decays 101 Injuries by Interproximal Wear 104 Proximal Surface Decays in Incisors and Cuspids 107 Gingival Third Decays in Labial and Buccal Surfaces 109 Spreading of Decay Around the Teeth 113 Systemic Conditions 115 Physical Characters of the Teeth 118 General Summary of Results of Physical Examinations of the Teeth 120 The Hardness and Softness of the Teeth 122 Faults in the Structure of the Enamel 124 Physiological and Pathological Differences between Bone and * Dentin 126 Studies by Dr. J. Leon Williams 128 Sialo-semeiology 129 The Saliva 132 Acidity of the Saliva, Viscosity of the Saliva, Glutinous Deposits from the Saliva, Signs of Susceptibility and Immunity to Dental Caries. Microorganisms of the Mouth 138 TABLE OF CONTENTS. IX PAGE Utility of Studies of Dental Caries 142 Vital Phenomena in Caries. . . .,. .1 , 144 Sensation in Dentin 146 Obtunding Sensitive Dentin . 148 Thermal Sensitiveness 150 Management of Patients 153 Cleanliness 154 Cleaning which Patients should do for Themselves, The Tooth Brush, Mouth Washes, Tooth Powders, The Toothpick, Ligature, Tape and Rubber Bands. The Force Used in Mastication in Relation to the Strength and Health of the Peridental Membrane 161 The Force Used in Chewing Foods 161 Gnathodynamometer Records. The Force Required in the Mastication of Food 165 Phagodynamometer Records. Sensitiveness of the Peridental Membrane 168 Management of Light and Care of the Eyes 172 Examinations of the Mouth 178 Treatment of Dental Caries 188 Prophylactic Treatment of Caries by Artificial Cleaning 188 Treatment of Dental Caries by Filling 190 Curative Effect of Fillings 193 Selection of Filling Material 198 Management of Cavities by Classes ,. 203 Classification 203 Cavities of the First Class 204 Cavities of the Second, Third and Fourth Classes. 208 Limitation of Extension for Prevention 214 Thermal Sensitiveness 219 Lodgments of Food in the Interproximal Space 220 Prophylactic Value of Form in Proximal Fillings 222 Cavities of the Fifth Class 225 Caries in Cases of Recession of the Gums 230 Esthetic Considerations 232 X PATHOLOGY OF THE HARD TISSUES OF THE TEETH. PAGE Management of Children's Teeth 235 Relation of Growth and Shedding of the Deciduous Teeth to their Treatment 237 Premature Eruptions of Teeth 238 Absorption of the Roots of the Deciduous Teeth 239 Accidents During Absorption of Roots of the Deciduous Teeth 241 Treatment of Caries of the Deciduous Teeth 247 Treatment of Decays of the Deciduous Incisors and Cuspids. . . 248 Treatment of Decays in the Deciduous Molars 253 The Childhood Period of the Permanent Teeth 258 Growth of the Roots of the Permanent Teeth 258 Intercusping of the First Permanent Molars 262 Special Functions of the First Permanent Molars 263 Caries of Permanent Teeth During the Childhood Period 265 First Permanent Molars, Lingual Pits of Lateral Incisors, Proximal Cavities in the Incisor Teeth, Proximal Sur- face Decays of Lateral Incisors, Open Apical Ends of Root Canals, The Pulps of the Lateral Incisors. Glossary 279 Index 307 LIST OF ILLUSTRATIONS. NUMBER Dystrophies of the Teeth 1-47 Atrophy. Hypoplasia 1-29 Incisors and cuspids 1, 2, 3, 4, 5, 6, 7, 8, 16, 17, 22 Diagram showing positions of atrophy marks at various ages. . 9 Diagram showing lines of Retzius 10 Sections of incisors and cuspids showing zones of atrophy. .11, 12, 13, 14, 15, 18, 21, 23, 24, 25 Diagram showing zones of atrophy, Zsigmundy 15 Zone of injury from atrophy mid-length of root 19, 20 Cast showing atrophy of first permanent molar 26 Sections of first permanent molars showing zones of atrophy 27, 28, 29 Enamel whorls 30, 31 Wrinkled teeth 32, 33, 34, 35 White spots in the enamel 36, 37 White enamel 38, 39 Mottled teeth 40, 41, 42, 43, 44, 45, 46, 47 Erosion op the Teeth 48-62 Dish-shaped areas 48, 49, 61 Wedge-shaped areas 50, 51, 52 Flattened areas 53, 54, 55 Irregular areas 56 Figured areas 57, 58, 59, 60 Gold crown cut by erosion 61 Proximal surface erosion 62 Caries of the Teeth 63-145 Caries of Dentin 63-74 Dializer 63, 64 Salts dialized from saliva 65 Crystals of sugar 66 Tooth split to show area of decay 67 Occlusal surfaces of molars 68, 69, 70 Split teeth 71, 72 Dentinal tubules containing microorganisms 73, 74 Xll PATHOLOGY OF THE HABD TISSUES OF THE TEETH. NUMBER Caries of Enamel 75-103 Occlusal surfaces, pit decays, split teeth 75, 76, 77 Proximal surface decays in incisors : Proximal surface 78 Split teeth 79, 80, 81 Photomicrographs of sections 82, 83, 84, 85 Proximal surface decays in bicuspids and molars : Proximal surfaces 86, 87, 88, 89, 90, 91 Cross cuts 92, 93, 94, 95 Photomicrographs of sections showing the injury to the enamel by caries 96, 97, 98 Relation of occlusion to the localization of caries: Buccal view of bicuspids and molars 99 Occlusal view of bicuspids and molars 100 Normal occlusion, buccal view 101 Occlusal views of upper and lower teeth 102, 103 Caries as a 'Whole. Its Clinical Features 104-145 Occlusal surface decays in molars, split teeth 104, 105. 106 Proximal surface decays in molars, split teeth. .107, 108, 109, 110. Ill Occlusal and proximal surface decays in bicuspids: Split teeth 112, 113, 114, 117, 118 Photomicrographs of sections 115, 116 Misplacement of beginning decays, central incisor 119, 120 Secondary extensions gingivally of proximal decays, photomi- crographs of sections 121. 122, 123 Injuries by interproximal wear 124, 125, 126, 127, 128 Proximal surface decays in incisors and cuspids : Proximal surfaces 129, 130 Split teeth 131, 132, 133 Gingival third decays of buccal and labial surfaces. .134, 135, 136, 137, 138, 139, 140, 141 Spreading of decay around the teeth 142, 143, 144, 145 Systemic Conditions 146-158 Physical characters of the teeth, photomicrographs of sections of enamel 146, 147, 148, 149, 150 Physiological and pathological differences between bone and dentin, photomicrographs : Cross section of bone 151 Lengthwise section of bone 152 Cross section of root of tooth showing absorption 153 LIST OF ILLTJSTKATIONS. Xlll Section of bone, showing absorption 154 Section of root of tooth, showing repair of absorption by eementum 155 Plaques on the teeth, photomicrographs of sections of teeth and plaques. Williams 156, 157, 158 Vital Phenomena in Caries 159-161 Diagram illustrating sensation without nerves in dentin 159 Split incisors, showing abrasion 160, 161 Force of Mastication '. 162-166 Gnathodynamometer, for measuring strength of bite 162, 163 Dynamometer, with micrometer attachment for determining stress a substance will bear without crushing, also the com- pression under stress 164, 165 Phagodynamometer, for measuring force required to chew food . 166 Treatment of Dental Caries by Filling, Photomicrograph of Salts Dialized from Saliva 167 Caries in Cases of Recession of the Gums, Treatment by Silver Nitrate ,. .168, 169, 170, 171 Management of Children's Teeth 172-186 Diagram showing calcification of the deciduous teeth 172 Diagram showing absorption of the roots of the deciduous teeth 173 Apex of root of deciduous incisor forced through gum by per- manent tooth 174, 175, 176 Treatment of caries of the deciduous teeth : Labial view of deciduous incisors 177 Lingual view of deciduous incisors 178 Proximal decays of deciduous incisors treated by filing and silver nitrate 179, 180, 181, 182 Proximal decays of deciduous molars treated by cutting and silver nitrate 183, 184, 185, 186 Childhood Period of the Permanent Teeth. Diagram showing calcification, period of eruption, and time of completion of roots of the permanent teeth 187 Pathology of the Hard Tissues of the Teeth. INTRODUCTION. THE injuries which occur to the hard tissues of the teeth dur- ing their development, and which occur to them hy accident or disease after they have grown, are peculiar to the enamel and dentin. They have no apparent relation or natural kinship with similar developmental or acquired injuries or diseases of other tissues of the body, except some atrophic injuries to the hair and nails. This is made so hy the histological structure of these tissues, in that they have no power of repair and recovery from injuries. The hair, nails, and the continuous growing teeth of a few animals, while having no means of repair of developmental or acquired injuries, dispose of the injured parts by the pro- vision for the wearing away of the substance, and with this the defects. Growth continues to supply new material, and in this negative way may effect a repair. The soft tissue appendages of the teeth, however, as the pulps, peridental membranes, alveolar processes, gums, etc., are developed under similar histological, physiological and patho- logical laws as other soft tissues and bones ; and possess similar powers of repair. The developmental injuries are confined to failure in develop- ment of parts of the enamel and dentin because of general sys- temic conditions which interfere with nutrition at a time when some particular part of the tooth is being formed, or is growing, and the injury is confined to that part. Other tissues have the power of repair of such injuries later. Since the enamel and dentin do not have this power of self-repair, such injuries in them are permanent. There is a similar failure of self-repair in these tissues when injured by accident or disease after they have been formed, or have grown and completed their develop- ment, such as accidental breakage of parts or injuries by erosion or by caries. As these tissues are not subject to inflammation, XVI PATHOLOGY OF THE HAKD TISSUES OF THE TEETH. nor to physiological or pathological changes in the same sense in which these occur in soft tissues and the bones, and as they are amenable to treatment only by artificial repair, it seems especially fit and desirable that these be considered in a group to themselves. Those conditions that occur in the form of malformations or misbuildings, such as supernumerary teeth, odontomes, mal- formed teeth, etc., belong to a different class and require totally different treatment. The type of dystrophy, which has been commonly designated as atrophy of the teeth, is met with so frequently in the practice of operative dentistry, and the injuries of the teeth are often so severe, that it has seemed to me that the facts gathered by recent investigations should be placed in permanent form in our litera- ture. Until very recently little had been accurately known of the forms of these lesions, and many errors are being made in the treatment which may be avoided by a closer study of the condi- tions. While in many cases but little can be done to improve the appearance of affected incisors, a large proportion of the first molars which are now lost may be protected and remain useful in mastication, as well as to serve their full purpose in the development of the features. On the subject of erosion, much greater interest is being manifested in recent years than formerly ; the interest in its pathology has been increased by recent investigations and the continuance of these should be stimulated with the hope that its causation may become more definitely known and some satis- factory cure or preventive discovered. The subject of dental caries and its treatment is and must remain the most important subject in conservative dentistry. No great improvement in its treatment can be had without improvement in the understanding of its causation, the condi- tions of the beginnings of caries of the enamel and the means to be employed in the prevention of its recurrence about the mar- gins of fillings. To this end, extensive studies have been made of this particular phase of the subject with the view of placing that which is now known in systematized, usable form, for both students in dental schools and for practitioners. This feature of operative dentistry has been deemed of so much importance to the dental profession and to our people that, in writing of technical procedures in filling teeth, it has been held continuously before the mind of the student and practitioner by frequent INTEODUCTION. XV11 explanations and repetitions. This has seemed necessary because of the general disregard of the study of dental caries in its rela- tion to treatment by filling shown by most recent writers. It is intrinsically wrong to treat the subject of filling teeth simply from the mechanical standpoint; it is wrong in that it tends to produce in the minds of students the idea that filling teeth is a purely mechanical pursuit. This is far from the proper concep- tion of the facts. In filling teeth, the closest use of our knowl- edge of the pathology of dental caries and of the local conditions of its occurrence, and of its recurrence after fillings have been made, should be put to full use in every case, in order that the greatest benefit may be derived from filling operations. To state this in the fullest detail has been a special object. To this end, studies have been made of dental caries and the various forms it assumes in its beginnings in the enamel, spread- ing of colonies of microorganisms on the surface of the enamel, carrying with them the spreading of beginnings of caries into the surface of the enamel, and the manner of penetration of the enamel. These have been carefully illustrated by photographs and photomicrographs, beginning with the simplest forms, and, by careful arrangement, proceeding to the more complex through the different phases. There have been included, so far as seemed possible by this method, illustrations of the directions of this spreading and the local conditions which favor it and which hinder or prevent it. The areas of the surfaces of the teeth rela- tively most susceptible to the beginnings of caries, as differen- tiated from the immune or relatively immune areas, have also been illustrated. On account of the extreme importance in the practical operations of filling teeth of this particular phase of the subject, it has been illustrated, with two or three exceptions only, by photographs and photomicrographs reproduced by the half-tone method without any retouching or artificial modifica- tion in any way. To these a few diagrammatic illustrations have been added. The fact has been kept prominent that immunity to dental caries, which may be complete, or which will approach complete- ness, even in persons, who, as children, were very susceptible to caries, will become established in early adult life in the larger proportion of cases in which effective protection has been given by filling operations, by continuance of active mastication of food, and reasonable care as to cleanliness. This matter, which was neglected because of previous misinterpretation of observed XV111 PATHOLOGY OF THE HAKD TISSUES OF THE TEETH. facts, is, with continued observation, assuming greater impor- tance in dental practice. The systemic conditions producing the changes in the saliva on which susceptibility and immunity are based, while mating progress, has not yet assumed any such exactness of definition as to be of immediate use in practice. In the technical procedures in filling teeth, the details of the adaptation of instruments to the work of cavity preparation have been brought into close systematization through notes of practical work at the chair representing actual operative experi- ence. This has been expressed in forms of nomenclature that are simple, systematic and effective in teaching, in pointing out defi- nitely the instruments for use and the manner of use of each. Every detail of cavity form is systematized and brought under a system of nomenclature comprised under a very few efficient rules, which render it simple and effective for teaching purposes and for general use by practitioners of dentistry. All of this has been systematized and improved through many years of actual work in teaching and has proven sufficiently flexible to cover all kinds and varieties of cases presented. The careful classifica- tion of cavities and of instrument forms adapted to each make it possible to teach cavity preparation in a way that it is easily learned ; cavities may be more easily prepared, the time con- sumed is shortened, the operation is more definite in its results. Taken altogether, these mark an improvement in the effective- ness of operative dentistry. Improvements that seem to have been but little thought of heretofore have been made subjects of careful study and system- atization. Operative dentistry, particularly when closely pur- sued for years together, is extremely taxing upon the nervous system of the operator, and many men break themselves down purely through assuming positions at the chair that are unnec- essarily fatiguing. This arises from assuming wrong positions in the beginning and the failure to obtain that relief which is clearly and easily possible by change and the rest that change brings, without ceasing or slowing the work at the chair. System- atization of these matters and bringing them under forms of nomenclature in which they may be taught and discussed under- standingly should result in great good. Dentistry has its own nomenclature which has become dis- tinct from the nomenclature of comparative dental anatomy. The nomenclature of dental anatomy from the standpoint of dentistry and of operative dentistry belongs distinctively to INTRODUCTION. XIX dentistry, and should in no case be confounded with the nomen- clature of comparative dental anatomy, nor the one used in the place of the other, nor should any effort be made to harmonize them. When the human teeth are under consideration from the comparative anatomy standpoint, the nomenclature of compara- tive anatomy, which is suited to the description of the teeth of animals in general, should be used. In that nomenclature we do not speak of buccal and lingual surfaces of teeth but of inner and outer surfaces, the bicuspids in dental nomenclature become premolars in comparative dental anatomy. While there are points of coincidence in these nomenclatures, there are wide differences that could not be reconciled without positive injury to both. DYSTROPHIES OF THE TEETH. ILLUSTRATIONS: FIGURES 1-47. THE condition resulting from imperfect, defective, or bad formation of growth constitutes a dystrophy ; dys — imper- fect, defective, bad ; trophy — growth, development. Therefore, any dystrophy noted must have occurred during the growth of the tissue. A tooth that is misshapen, off color, or otherwise deformed during growth, is in the condition of dystrophy. Acquired deformities, such as erosion, abrasion of the teeth in chewing food, etc., after the teeth have formed, are excluded from dystrophies. The dystrophies of the teeth consist of imperfections in development due to some disturbance of nutrition during the time of formation or growth. In each class of cases some part of the tissue is either imperfectly developed, or some particular part has failed to develop, or has developed in an erratic man- ner. Among these dystrophies, there are certain things common to several, such as imperfection of the cementing substance between the enamel rods. In others, the enamel may be want- ing or may have an unusual arrangement, while in others defects may be present in all of hard tissues of the teeth. It is only recently that these conditions have received such histological study as to make out the scheme of each, and sep- arate them into special classes of deformity. The gross appear- ance of some of the more frequent of these deformities of the teeth has of course been well known for many years. All of these deformities thus far seen may be grouped in such a way that each one will be distinguished as a special deformity, and those that are essentially alike may be grouped together. Sections prepared for microscopic observation form the basis of this classification.* * These examinations have convinced me that the words atrophy and hypoplasia are no longer desirable. These words have been applied to a specific deformity of the teeth caused by malnutrition, and they have also been used almost continuously in describing abnormal teeth of any and all classes. This they can not properly do, and it seems actually necessary that other words be substituted. The continued use of the word atrophy has become a bar to progress, and it will be noticed that I have in this writing substituted the word dystrophy as applied to all forms of imperfect development, and have used other terms as descriptive of the several dystrophies. I have, as in previous editions of this work, used the word atrophy as applied to that form of dystrophy caused by malnutrition, only because I am unable to find a satis- factory word to replace it. PATHOLOGY OF THE HARD TISSUES OF THE TEETH. Nomenclature.* Atrophy. Hypoplasia. Contemporaneous accretional dys- trophy. A deformity occurring along the lines of accretion, con- temporaneously in all teeth in process of development during a period of malnutrition. In this the enamel rods, the cementing substance between the rods, and the dentin are all involved and part of each is either imperfectly formed or wanting. The enamel whorl. A deformity occurring within the enamel, in which there is an abnormality of direction of the enamel rods, usually associated with a pit in a surface that is normally smooth. Wrinkled or corrugated teeth. A deformity characterized by abnormal ridges and grooves of the enamel surface, with scalloping of the dento-enamel junction, and much disarrange- ment of enamel rods. In each of these scallops there is a dis- turbance of the direction of the enamel rods. They are thrown into circles and whorls and not infrequently open cavities occur in the tissue. The condition is comparatively rare. White spots in the enamel. A deformity observed as a spot which is paper white in the enamel; a form of dystrophy in which the enamel rods are normally formed, but the cementing substance which should occupy the spaces between the rods is missing. These spots are not very frequent, and many of them are passed over without observation. They are of little impor- tance. White enamel. A deformity similar to the white spots, except that all of the enamel of the teeth is composed of rods without the cementing substance, and the crowns of all of the teeth are pure white. This is a very rare condition. Mottled enamel. An endemic deformity, distinguished espe- cially by the absence of the cementing substance between the enamel rods in the outer fourth, more or less, of the enamel, and presenting great variety of color. In certain regions of comparatively few square miles, many thousands of persons have this deformitv. * Note. — Dr. Black wrote these paragraphs relative to the nomenclature of the dystrophies of the enamel only a few weeks before his death. He was not then satis- fied with the terms applied to the various dystrophies, and expressed his intention to revise them before publication. He was especially anxious to find a simple term to displace the terms atrophy and hypoplasia. In his last writing he used the term contemporaneous accretional deformity, but realized that this was too long. It seems best to retain the words atrophy and hypoplasia until a satisfactory substitute can be found. dystrophies of the teeth. 6 Histological Characteristics the Basis for Classification. To one who has made careful histological studies of the structure of the teeth, these various deformities point to the need for further investigations. Knowing, as we do, the plan on which the teeth are gradually formed from certain points of beginning, we recognize one form of dystrophy in which all of the hard structures of the various teeth that were in process of formation at a given time were imperfectly formed, due to an interruption of the normal activities of constructive cells. We note that the portions of the teeth formed both before and after the particular time are perfect. This suggests at once a gen- eral interruption in the nutritive processes during the period of malformation, and inquiry as to the health of the individual at the age indicated by the malformed part reveals the relation- ship between the two as cause and effect. We recognize another form of dystrophy in which there is a failure of the formation of the cementing substance between the enamel rods in irregular areas, notwithstanding the fact that all other structures of the same teeth, and the cementing sub- stance in other parts of these teeth, formed during the same period, are perfect. Or there may be a partial failure in the development of the enamel rods, as seen in the pits in teeth which are otherwise normal in their formation. Such conditions represent an interruption of the normal activities of certain elements of the formative cells, while cells of the same type close by have functionated properly. These .contraindicate a general systemic disturbance and speak for a purely local inter- ference. We observe another form of dystrophy in which the cement- ing substance between the enamel rods is entirely wanting in all of the teeth of an individual, while every enamel rod is per- fectly formed. In this there apparently is a disturbance or lack of activity of an entire group of formative elements, and again we must think of the cause as being more general. We may imagine the lack of a certain necessary stimulus, as a result of which the cells which should form the cementing substance have failed to do so. Although no such relationship is known, the situation is comparable to the relationship between certain duct- less glands, as the thyroid and suprarenal glands, and other organs and cellular elements, the secretion from these glands in normal quantity being necessary for the proper functional activity of the related organs or cells. Again we see in the mottled teeth an endemic type of dys- trophy, confined to persons living in certain geographic areas. 4 PATHOLOGY OP THE HARD TISSUES OF THE TEETH. In this there is a failure of the formation of the cementing sub- stance between the enamel rods in the outer third only and in very irregular patches, the cementing substance between other rods being perfect. The fact is well established that these defects occur in the teeth of more than 80 per cent of persons who live in such geographic areas during the period of enamel formation. If such individuals reside in one of these known geographic areas during the period of formation of a number of the teeth, and elsewhere during the formative period of other teeth, only those which are formed during residence in the area will show the characteristic defects. These present the most difficult problem of all in relating the histologic defect to the cause, since the formation of perfect cementing substance and the lack of formation of this substance are contemporaneous in the individual tooth or several teeth. There is a local failure of cells to functionate, which is evidently the result of some general systemic condition. These observations indicate that there are separate forma- tive cells for the enamel rods and for the cementing substance between the rods ; that under certain conditions both processes are interfered with, while in others there is a failure in the for- mation of the cementing substance, but not of the rods, and in others a failure of rod formation. Future studies may deter- mine how these things come about. In the following pages the various dystrophies will be described. To get a proper understanding of these conditions in relation to the causes, it is necessary that one have a good knowledge of the histological structure and development of the teeth. There should be in mind for each tooth the average time of beginning formation and the period required for growth to completion. This is necessary to determine the age at which the cause of the particular defect was operating. If it was a condition of malnutrition its effect should be recorded by defects in the portions of all teeth in process of formation at the time. For example, at the age of three about two-thirds of the crown from occlusal to gingival of the first permanent molar has been formed ; at the same age only about the incisal third of the central incisor has been formed, usually a little less of the lateral incisor and only the tip of the cuspid. Therefore an illness at the age of three which resulted in a defect of any one of these teeth in the position mentioned should involve all of them. The defect in the cuspid could not be as far away from the incisal edge as in the central incisor, because the central is always in advance of the cuspid in its formation. (Figure 9.) DYSTROPHIES OF THE TEETH. O Likewise one should be familiar with the lines of accretion of the enamel — the lines of Eetzius — as shown in Figure 10. Each of these lines represents a period of growth of the enamel — ■ a layer, all of which was constructed during a given time. It is without the province of this writing to go into detail in these matters, and the student is referred to the several authori- tative works on dental histology. ATROPHY OF THE TEETH. Hypoplasia of the Teeth. A contemporaneous accretional deformity — a dystrophy in which all portions of the teeth in process of formation at a par- ticular time are imperfectly formed along the lines of normal accretion or growth. As in the previous editions of this work, the term atrophy is applied to this condition, also the term hypoplasia, which has been used widely in the German writings. Because of the fact that the application of both of these terms has been too general, has included all kinds of deformities, and also because of the fact that the term atrophy represents two distinct ideas in medi- cal literature, I am of the opinion that both terms should be dropped as applied to this condition. The term atrophy has been applied to a failure of development of a local part because of a failure of nutrition ; it has also been applied to the wast- ing of a part because of a local failure of the nutritive process. The term atrophy has been used to designate this condition since it was first spoken of in the English language. The contemporaneous accretional deformities of the teeth represent an atrophy of the first mentioned type ; they have never been fully formed. They come through the gums in the condition of deformity in which they are afterward seen, and do not, as some seem to suppose, waste away after having taken their places in the arch. The deformity is a result of incomplete formation. In the human teeth there is no process of repair and the deformity is permanent. Similar phenomena occur in the finger nails and the hair. During an illness that interferes seriously with nutrition, the portion of the finger nail then forming will be dwarfed, which will appear later as a groove across the nail. This, like the marking of the teeth, is not remedied by any repar- ative process. But the nail is continuously growing and the groove moves on over the length of the nail and disappears. During a severe illness that interferes with nutrition, a sec- 6 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. tion of hair is imperfectly formed, and when in the process of growth this section arrives at the surface of the skin and is sub- jected to bending, it breaks and the hair suddenly falls away These are common phenomena following severe cases of typhoid fever. The hair follicles are not injured and the hair is replaced by the regular process of growth. In the continuously growing teeth of the rodents such an injury would be finally removed and remedied in the same way as the grooving seen upon the finger nails, but this can not occur in the human teeth. The deformity, though much varied in different cases, is, when closely analyzed, always similar in character. It always consists in a failure of the formation or an imperfect formation of some specific portion of the tooth and of several teeth together. The portion of the several teeth affected is always that portion of each that was in process of formation or growth at the same period in the person's existence. To understand this well one should study closely the calcification of the crowns of the teeth and the contemporaneous lines of calcification of the different teeth. This will be more fully explained in considering the histo- logical changes occurring in atrophy. In the incisors the de- formity is oftenest seen in the form of a groove, smooth or pitted, running across the labial surface from mesial to distal, and close inspection will generally show that it encircles the tooth com- pletely, though it is most prominent upon the labial surfaces where the enamel is thickest. It is seen more often on the incisal half of the length of the crown. It may be near the cutting edge of the tooth or anywhere from that point toward the gingival line. It is also found occasionally in the roots of extracted teeth. There may be a single groove or pitted line, or there may be two or even three or more of these. The teeth affected are the inci- sors, cuspids and first molars of the permanent set, and very rarely the first bicuspids. If it is very close to the cutting edge on the central incisors it may not appear on the laterals, but the occlusal surfaces of the first molars will be atrophied. This is because these parts of these teeth are in process of formation at the same time. If the groove is a little further removed from the incisal edge of the centrals, the lateral incisors will also be similarly affected. If it is a little higher still, the four incisors, upper and lower, the cuspids and the first molars will be affected, but the bicuspids will be free from injury. It is exceedingly rare that the bicuspids or the second or third molars are affected by atrophy, for the reason that the enamel and dentin of these teeth generally have not begun to form until after the age at which these effects are most liable to occur. But few cases occur in DYSTROPHIES OF THE TEETH. / which the first bicuspids are marked. The time of the occurrence of these injuries seems to be confined mostly to the first five years of a child's life, but some cases occur later. In the engravings the endeavor has been to illustrate some of the more severe types of these deformities and to explain by illustration the histological defects. Figure 1 represents what is known as the typical Hutchinson tooth, from the claims of Mr. Hutchinson, a specialist in venereal diseases in London, England, who insisted that this deformity was the result of inherited syph- ilis. In such cases, it has formerly been supposed that the middle lobe has failed of formation, resulting in this peculiar scar, but more recent investigation seems to show that the whole incisal edge has failed in most of these cases, and that the angles of the tooth have been drawn together over the injury, giving the out- line of the tooth this rounded appearance. Certainly many of these teeth are much shorter than normal. Generally an ugly deformity of the occlusal surfaces of the first molars accompanies this type. In the molars little spiculae of cusps are likely to be sticking up much too close together, while the rest of the occlusal surfaces are much too small, crumpled together and sunken into the crown, which, other than this, will be of full size and form. These teeth decay quickly in case there is a tendency to caries in the individual. Of the incisors shown in this illustration, only the centrals are affected. The calcification of the cutting edges of these is occasionally just begun at birth, and if not begun then, is usually begun within one year. The injury, therefore, occurs soon after the birth of the child from some cause which interferes with nutrition. A very curious fact in pathology is rendered promi- nent in this form of defect. It is this : when the nutrition of any single part of the enamel organ is so impaired that its func- tion is stopped or very seriously disturbed, that particular part does not recover, and no additional enamel is formed by that part. This will appear more prominently in the histological specimens. It is for this reason that these teeth have the peculiar rounded appearance of the cutting edge. The enamel organ of that part is arrested in its work at the very beginning of the calcification, and therefore the immediate incisal edge fails entirely. The rest of the organ goes on with its work after the recovery and the tooth is drawn in over the scar. In the incisors this form of defect is apt to be attacked by decay in this incisal pit very soon after the teeth have taken their places in the arch. They should be filled at once if decay is discovered. This par- ticular form of atrophy is seen less frequently than others. The occlusal surfaces of the first molars are occasionally 8 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. badly deformed when the incisors have escaped. Usually these have just begun their calcification at birth, and occasionally the calcification of the central incisors does not begin for one year after birth. In such cases a severe illness may injure the molars and not injure the incisors. Much the more common forms are those illustrated in Fig- ures 2 and 3, the illustrations showing rather bad cases. In Figure 2 the deformity is confined to the cutting edges, appar- ently, of the central and lateral incisors above and below, and the four first molars. In the case here illustrated the whole of the incisal edge of each of the incisors above and below is dwarfed and shortened. This dwarfed portion ends abruptly toward the gingival. This is common in these cases. In many there is more or less rounding down of the well-formed part of the crown to the deformed part, but often it is so abrupt as to form a square shoulder along which there is apt to be a series of sharp, deep pits. In the case from which Figure 2 is taken there are no pits whatever, and the deformity consists purely in the dwarfing of the incisal edges. But the entire occlusal surfaces of the molars were in very bad condition because of dwarfing that presented many abrupt fissures in which decay began almost immediately after they had come through the gums. In such cases as this the appearance of the incisor teeth may be much improved by grind- ing away the dwarfed portion and shortening the cuspids a little to correspond with them. The teeth may appear a little short, but that is sometimes much less noticeable than the blemish. In other cases, occurring in the same locality and affecting the same teeth, there may be but little dwarfing of the incisal edges of the incisors. The effect may be but a slight groove that may be smooth or more or less pitted, or in cases of a still milder type the distinct groove may be lacking and a row of fine pits in the enamel will be the only deformity. Generally, the effect is more marked in the occlusal surfaces of the first molars than in the incisors. In the case illustrated in Figure 3 the injury has occurred later, when the child was between three and four years old. The incisal portion of the incisors had been formed, and, therefore, there is no dwarfing of this portion of these teeth. But there is a very marked groove encircling the crowns of the incisors and cuspids, marked with pits, with smoothly rounded bottoms. Both the groove and the pits in the groove are abrupt toward the gingi- val and thin away toward the incisal. This is a constant charac- teristic of these deformities, which will be readily understood by a study of the histological sections and the calcification lines of Ketzius. The circular form of this deformity, as it passes DYSTEOPHIES OP THE TEETH. y from tooth to tooth across the front of the mouth, is well marked in Figure 3 ; indeed, it presents rather more of the circular form than usual, indicating especially that the cuspids were a little later than usual in their calcification, and for that reason the mark is nearer the incisal edge in proportion to the position on the incisors than it would otherwise have been. It is not frequent that we see so severe a mark as here shown so high upon the labial surfaces of the incisors. It seems to be a general rule that the higher upon the teeth the less marked is the deformity. Pretty generally, in this position on the cen- trals, the mark is a shallow groove, more or less pitted, or a row of pits without a distinct groove. In all of these cases the lower teeth bear marks similar to those in the upper. In Figure 4 a case is illustrated that is somewhat out of the usual form in several particulars. When the impression for the cast from which the illustration was made was taken, the cuspids had not come through the gums, but one of the first bicuspids had erupted, and, to my surprise, showed a deep mark encircling the point of the buccal cusp. Also the history of the case shows that the lateral incisors did not erupt for two years after the centrals had taken their places. In the centrals the incisal edges are fully formed, but there is a deep groove with rounded pits encircling the crowns at nearly mid-length, while nearly the whole incisal half of the laterals is badly deformed. This indicates that the beginning of the calcification of these teeth was late, as compared with that of the centrals. This particular form of deformity of the lateral incisors is not very frequent, but yet a considerable number have been seen, quite enough to indicate a tendency to this particular deformity. In the common vernacular this has been called the inverted finger nail deformity. If we imagine the finger nail taken up and turned with the convex side down and set back in the end of the finger, we would have something very like this deformity. The whole appearance of this case at the time of my observation of it, indicated unusual irregularity of the time of calcification and eruption of the different teeth. The first molars, both above and below, had already been destroyed by decay, beginning in the deformity of the occlusal surfaces. Figures 5 and 6 show a lower incisor with a double deform- ity. Figure 5 is a view of the labial surface, and Figure 6 of the mesial surface. The dotted lines show the normal tooth form. The two, taken together, show the extent of the dwarfing of the crown of the tooth. In this case the surface of the enamel was smooth and without pits. Figure 7 shows an upper central very badly deformed. This is also a double deformity and was further injured by decay 10 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. starting in pits in the abrupt portion of the groove nearest the incisal. The sharp, deep pits shown along the line of the second groove have not been caused by decay, but were there when the tooth came through the gums. These teeth are from different persons, and in both cases were extracted in order to remedy the defect with artificial teeth. This seems to have been done under the mistaken notion that the roots of the teeth would not be good for artificial crowns. Extended observation shows that the roots of such teeth are as apt to be well developed and as good for crowning as those of any other teeth. When the crowns are so badly deformed that it is out of the question to employ filling operations and preserve the pulps, artificial crowns should be resorted to, rather than to remove the teeth. In case the crowning involves the removal of the pulp, this should be delayed as long as possible in order that the roots may be fully formed and the apical foramen reduced to a small size. One should wait until the patient is sixteen to eighteen years old, and twenty would be still better. In many cases of considerable actual deformity of the teeth the color remains very perfect, and in this case, if the incisal edges of the incisors are fairly complete, the deformity is not prominently noticeable, as is shown in Fig- ure 8, from a photograph taken directly from the mouth. Etiology. This deformity of the teeth is always caused by illness that has interfered with nutrition at the time the particular parts of the teeth affected were in process of calcification. My attention was strongly called to this through a controversy between Mr. Hutchinson of London, and Dr. Magitot, of Paris, who took opposite views some thirty or forty years ago. From Mr. Hutch- inson 's observations he was led to believe at first that all of these cases were caused by inherited syphilis, while Dr. Magitot had come to the conclusion that they were due to eclampsia. This controversy led to a closer study of this whole subject, and finally Mr. Hutchinson yielded the point so far as to say that inherited syphilis was a frequent cause, and for many years beld that the type shown in Figure 1 was always caused by inherited syphilis. That form, therefore, has been called the Hutchinson tooth. As showing how errors are liable to be per- petuated, most of the books on general medicine, surgery and venereal diseases, which mention these deformities at all, ascribe them to inherited syphilis, following the first writings of Mr. Hutchinson without further investigation. They are continually accusing innocent persons of crime. The author has followed this subject pretty carefully ever fill J^'^ if& iHijitfi Fig. 1. Atrophy of the cutting: edge of the central incisors, forming ; ually called " Hutchinson's tooth.' surfaces of the first molars are also badly marked. FIG. 2. Atrophy of the cutting edge of the C€ some portions of the occlusal surfaces of the first Fig. 3. Atrophy marks on the incisors and c around the crown of each tooth atrophied. The axial surfaces. Fig. 4. Atrophy marks on the incisors, showi incisors. lection with this for: rid lateral incisors. When this occurs, will also be injured. In this case there is a pitted groove lolars have a similar groove on their inverted fingernail scar on the lateral Figs. 5. 6 and 7. Single Each of these show two zones lines of the crowns. Figures teeth, the crowns of v of injury. The dotted 5 and 6 ar i different v , have been badly dwarfed by atrophy. 3 are intended to show the normal out- of the same tooth. ££ * Fig. 8. Atrophy of incisors and cuspids showing no discoloration. Photographed direct fro mouth of girl eighteen years of age. Fig. 9. Outlines of the incisors and cuspids and of the first molars, somewhat over which lines are drawn representing average positions at which atrophy marks will the ages named in years by the numerals attached. In these represents birth. 1 ont two years of age, etc. The rule is that in atrophies occurring before the sixth year the and second molars are not marked. nd cuspids and of the first molars, somewhat enlarged, occur at year. ■ bicuspids DYSTROPHIES OF THE TEETH. 11 since Mr. Hutchinson wrote, adding observation after observa- tion, and has arrived at the conclusion that there is no special form of disease that is especially blamable for this affliction, but that any form of disease that seriously interferes with nutrition is liable to bring about this result, i e., that it is not the partic- ular form of disease, but that it is the condition of malnutrition that is the cause, no matter what the disease which has induced that condition. I have seen cases of typical Hutchinson teeth which were certainly in no way connected with a syphilitic taint of any kind. Some of these observations may be of interest. Mr. and Mrs. B., known by the author intimately from childhood, had a child which seemed healthy at birth, but soon afterward became anemic and did very badly for two years. Growth was a failure during that time, and it was with great difficulty that the child was kept alive. In its third year, however, the child recovered and became strong and healthy and developed well. When the permanent teeth came through the gums, almost the incisal third of the cen- trals and laterals was badly dwarfed, the points of the cuspids had failed and the occlusal surfaces of all of the first molars were badly deformed. I attended a child two and a half years old through a severe case of typhoid fever. When the permanent teeth came through they were marked with a deep groove, irregularly pitted, similar to Figure 3, but not so high up on the crowns. An English woman brought her child to me on account of a very ugly marking of the incisors which had just come through the gums. In reply to my inquiries she could not remember that the child had had an illness of any kind. The boy had always been healthy and had escaped all of the infantile diseases. Being convinced that something had occurred that would have been noted, I asked her if the child had had any kind of an injury. This quickly brought out the statement that the child had had a severe burn, a scald, on the side and back, that had healed slowly after much suppuration. Indeed, the child had been very ill with septicemia for a month or six weeks. The time corresponded with the marks upon the teeth. Cases like these, but every one different in detail, could be multiplied almost indefinitely. Scarlet fever, measles and whooping-cough come in for a large share in producing these marks. My observations for some time led me to believe that ' scarlet fever and measles are most often to blame for the rows of fine pits, but of late I have found so many of these following other forms of disease that I am led to doubt the distinguishing 12 PATHOLOGY OF THE HAKD TISSUES OF THE TEETH. features of these marks. Certainly, hereditary syphilis comes in for its full share of these cases. On the other hand we can not say, at least I can not, that marked teeth will result from this or that illness. If the hair falls out or the finger nails show a groove after an illness we are apt to find the teeth marked also. Very many of the cases that I have noted and watched for the coming of the permanent teeth have presented teeth without a blemish. Indeed, among all of the cases that I have noted and watched, the marked teeth have been the exception rather than the rule. Still, it remains true that when I have been able to obtain a satisfactory history, the marked teeth have coincided in time with some form of disease that might well have interfered seriously with the nutritive proc- esses. The history is not always easy to get, even among intel- ligent people. I once remarked to a lady in my chair that she had been very sick with scarlet fever when she was about two years old. She was very sure she had not, for she had never been told of such an occurrence. When I explained that accurate knowledge of the facts was of considerable scientific value she said she would question her mother regarding it. The next day I received a note saying her mother's story agreed with my sup- position, both as to the particular disease and the date of the illness. I have seen many of these cases, however, in which I could find no history of the illness causing them. To assist in searching for the cause that has led to this deformity in cases coming before us, I introduce a diagrammatic chart, or index, indicating by lines across the incisors, cuspids and first molars, the positions the grooves across the teeth assume because of disease occurring at different ages of the child. Figure 9. These lines have been varied a little from the true contemporaneous calcification lines to suit better the appar- ent positions upon teeth that are shortened by severe atrophy. This chart will point out the age at which any injury occurred as well, perhaps, as it can be done in a chart of this character, which, of course, is founded upon averages. Pretty wide varia- tions will occur in the time of the calcification of the teeth of individuals, and also between the several teeth of the same indi- vidual. There is certainly as much variation as eighteen months in the time of the beginning of the calcification of the central incisors, and a greater range possibly with all of the other teeth, except the first molars. These latter are perhaps the most con- stant. But these certainly vary from the twenty-fifth week of uterine life to something near six months after birth. The chart is intended to give only a general average as to the time of the illness that has caused these injuries. dystrophies of the teeth. 13 Histological Chaeacteeistics. In presenting the histological characteristics in this form of dystrophy, it may he stated that all of the cases thus far examined by myself, no matter how different their outward appearance, present one plan of departure from the normal arrangement of tissues. The differences are due only to posi- tion, the number of zones of injury and in the details of severity. This plan is inseparably linked with the plan of development of the dental tissues. Except in the pits that often accompany it, the zones of injury always follow the lines of Eetzius very rigidly. In the dia- gram, Figure 10, the lines of Retzius are made especially prom- inent to recall distinctly their direction on different parts of the enamel cap of the crown of the tooth. In microscopic observa- tion these are usually clearly seen in some parts of the enamel cap, particularly in central labio-lingual sections. They vary, however, indefinitely in prominence in different sections, and in different parts of the same section. Generally, they do not show clearly in all parts of a section, and those who have not studied them carefully should refresh their memory as to the course of these lines in different positions on the crown of the tooth. These lines are the index to the growth of the enamel cap. They are the real lines of accretion and show distinctly the order in which the enamel cap is built up, layer after layer, in its growth. This growth begins at the dento-enamel junction, in positions which represent the cutting edge (or points of the cusps in molars and bicuspids) and grows from within outward, while the dentin begins its growth at the same point and progresses from without inward. The growth of dentin is always a little in advance of the enamel as it grows from the incisal edge of the front teeth (or the points of the cusps of other teeth) toward the gingival line. This contemporaneous accretional deformity, in all cases, consists of an arrest, or partial arrest, of growth of both enamel and dentin in the particular zone being developed at the particu- lar time. In the milder cases growth is imperfect, leaving certain definite markings outlining the particular parts of the tissue then being formed. In all the severe cases the growth of both enamel and dentin is arrested. There seems to be no recovery of the part of the enamel organ that was at the time in active function. No more enamel whatever is formed over the area affected after recovery from the condition of malnutrition, except as the new formation is telescoped over the area of the old. The dentin pulp, however, rebegins its growth function 14 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. apparently immediately the condition of malnutrition has passed. But the parts of the tooth which should have been formed during that period are not formed at all. A certain part of the tissue which should have constituted the perfect tooth has been left out, and the distortion of form which we so often see results from patching the second growth onto the first and the total failure of particular portions of the enamel. This total failure of the enamel is not in the direction of the thickness, but is always on the lines of Retzius. Therefore, as we shall see later, there is not a failure of the total thickness of the enamel at any point, except in a few cases in which the injury occurs at a time when calcification was just about to begin, as sometimes occurs in the so-called Hutchinson tooth, and may, rarely, occur in others. For instance, in the diagram, Figure 10, there are four layers of enamel represented over the incisal edge. If total arrest of growth should occur at the time the first two layers are completed, the third and fourth layers will never be formed. The enamel will remain over the incisal edge with only these two layers. Then perhaps the fifth and sixth layers shown, more or less, will also fail, and the seventh and eighth layers will overlap the first and second somewhere near half their length, because the formed part of the incisal edge sinks into the dentin pulp. The dentin pulp has also stopped its growth at the same time and the part that failed of growth is left out of the final tooth form. These are the fundamental propositions presented in the explanation of the histological groupings of tissue and the short- ening of the tooth crown found in these cases. Figure 11 is a photomicrograph* of a little more than the incisal half of a crown of a central incisor, showing two zones of injury. Figure 12 shows an entire crown with a single zone of severe injury. In each of these the malnutrition was so severe as to arrest the growth of both enamel and dentin. In each an injury has occurred, affecting the incisal edge of the tooth. By comparing these with the diagram it is easily seen that when a certain thickness of growth of enamel had formed over this part, development was arrested and no more enamel was formed. In each case the enamel is thickest at the incisal edge and thins away to the groove which encircles the tooth crown, which is here presented in section. A band of very dark growth is seen under the new after-growth of enamel following the lines of Retzius on down to the dento-enamel junction. A comparison * Note. — In this work any photographic illustration made by reflected light will be called a photograph, even when moderately magnified. But when transmitted light through a thin section has been used, it will be called a photomicrograph. It has not been thought necessary to mention these terms in every instance. DYSTROPHIES OF THE TEETH. 15 now with the diagram shows that the growth has been arrested on the lines of accretion or lines of Eetzius, as you may please to call these lines, Figure 10, in both cases. Also, it is seen that the second injury in Figure 11 is similar in plan to the first, differing in detail only because of the changed direction of the lines of accretion. In Figure 11 the incisal edge is broken, as usually occurs in these thin edges, but Figure 12 is from a tooth extracted soon after it came through the gums and all of the tis- sue formed is present. Figure 13 is an illustration with a much higher power of the labial side of the first zone of injury shown in Figures 11 and 12. Figure 14 is from the second zone of injury on the labial side. In these, the tissues and the lines of Eetzius are fairly well shown, and by studying the photomicrographs carefully, the relations of the tissues formed before and after the injury may be made out. It will be noted in Figure 13 that the one particu- larly dark band, which represents the surface of the enamel formed over the incisal edge, is continued under the enamel of second formation to the dento-enamel junction. Beginning a little farther from the incisal, a line of interglobular spaces appears in the dentin, and running almost parallel with the dento-enamel junction, continues on toward the incisal edge. Faint traces of these appear even in the small picture, Figure 11. "With sufficient amplification, this line of interglobular spaces is found to continue to the incisal edge and join with the similar line from the opposite or lingual side ; that is, in the whole tooth it is a sheet or zone of interglobular spaces passing throughout the full extent of the dentin, of which this is a section. This line represents the injury in the dentin. It also represents more. It marks the boundaries of the old and the new formation of dentin and is the line on which these have been patched together. On the other hand, the one dark line in the enamel marks the line on which the new formation of enamel is patched onto the old. After a very careful study of sections from many of these teeth, it becomes clear that the part of the tooth which should have formed during the stoppage of growth was not formed at all. The enamel organ was destroyed through its whole thickness to the point where the dark line limiting the first enamel forma- tion reaches the dento-enamel junction, and when the second formation began it was telescoped over the old and laid down upon it, as shown in the illustration. The crown of the tooth was shortened that much, certainly, and may have been shortened very much more. When we study carefully Figure 12, with its single line of injury, and note how the little part of the incisal edge formed before the injury is literally sunken into that por- 16 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. tion formed later, we must conclude that the shortening is much greater than that shown by the apparent telescoping of the parts. In the dentin the same thing occurs, only that it is expressed dif- ferently because of the different character of the tissue. The line of interglobular spaces shows where the second growth was telescoped into the first. A study of Figure 14 shows exactly the same plan in the arrangement of the tissue in the second zone of injury, including the overlapping of the new enamel onto the old and the accom- panying line of interglobular spaces in the dentin. The shorter overlapping of the enamel at the point of injury is due to the changed direction of the lines of growth. The actual shortening of the tooth may have been much greater. When we study the short and stumpy forms of many of the crowns of these mal- formed teeth, we must conclude that the shortening is often very much greater than this overlapping. It is this shortening and telescoping together 'of the different parts that is responsible for the greater part of the distortion of form so often observed in these teeth. It appears certain that the tendency is to form each of the parts on the lines that each would have had at the specified time of growth if there had been no interruption of the growth. We may gain another view of this by studying the lines of the labial dento-enamel junction. In the study of sections of many human incisor and cuspid teeth, this line is found to form a continuous curve from the incisal edge to the gingival line, as seen in the diagram, Figure 10. The amount of curve may vary indefinitely, but it is always a continuous curve in every normal tooth. In sections of these malformed teeth, this curve is found broken by a recurve at the zone of injury in every case, even in the lighter forms in which the growth seems not to have been completely arrested. This disturbance of the direction of this line seems to be due to the effort to form the second part on the lines that would have been laid down at that time if the growth had been going on regularly, and the larger and smaller are patched together. In the dentin the growth has been in abey- ance and the growth begins on the lines on which it was left off. But immediately the tendency is to enlarge to the greater out- line of the tooth as it would have been at the time had the growth not been interrupted. This causes a recurve in the line of the dento-enamel junction. In the enamel, the telescoping seems to be actual. That part of the enamel organ that had not arrived at the period of enamel building is uninjured and is pushed for- ward over the previously formed enamel and lays down its layers of the second growth of enamel thus far over the old. No other --^ SXSn^tr^ &2ff& t ^X"^ FIG. 11. Section of an incisor showing two zones of injur Fig. 12. Section of a cuspid showing groove in section. Magnified eight diameters, into the body of the crown of the tooth. of atrophy, sinking of the single al edge Fig. 13. Atrophy. A photomicrograph of a portion including the zone of injury nearest the incisal edge on the labial from the same section shown in Figure 11. In this the lines of Retzius may be seen in the enamel, also the dark line of junction between the enamel of first formation and enamel of second formation, reaching from the dento-enamel junction, with the enamel of second formation overlapping that of the first. The line of interglobular spaces in the dentin, running almost parallel with the line of the dento-enamel junction, is well shown. Fig. 14. Atrophy. A portion including the second zone of injury seen in Figure 11. In this position the lines of Retzius diverge more sharply from the direction of the line of the dento-enamel junction, and the overlapping of the third growth of enamel onto the second is shorter. The discoloration is greater. The line of interglobular spaces is broader, and in this position diverges more sharply from the line of the dento-enamel junction. Otherwise it is similar in plan with the first zone of injury shown in Figure 13. ^mp Fig. 15. Lengthwise section through portion of crown of an atrophied tooth. a. Direc- tion toward the crown. b. Direction toward the root. z. Dentin. c. Interglobular spaces. E. Enamel. s. Wedge-shaped piece separated by line of injury. x. Line of injury. s 1 Full thickness of enamel. Zsigmundy. ** Fig 16 Labial surface of a centi-al incisor, photographed to show the appearan groove. The dark color in parts of the groove makes it appear deeper than it really is of a section cut from this tooth is shown in Figure 18. Fig. 17. Photograph of the lingual surface of the same tooth shown in Figure 16. Fig. 18. A photomicrograph of a portion of a section from labial incisor. Figures 16, 17. showing a milder sort of inj interrupted but not permanently stopped. The 1 dentin of first formation from that of the second ortion of the central .. hich the growth of the enamel was nterglobular spaces literally divides the The section was broken and the parts placed position. A scrap of enamel preparation, as represented by the dotted lii Figs. 19, 20. Root of tooth parted on lines of growth. Photographed from the specimen extracted by the author. Photographs of a bicuspid tooth which had a zone of injury mid-length of the root, and which was pulled apart in telescope form along the line of injury, i. e., the line of interglobular spaces. In Figure 19 the parts are photographed in normal position. In Figure 20 the two parts are separated, showing how they are telescoped together. Fig. 21. A portion of a section through a central incisor, sort. The plan of the injury, and the telescoping together of tV as in Figures 13, 14, but the discoloration is much less. The th away before extraction in an effort to improve the appearance. ing atrophy of the se\ rts, is seen to be the s cisal edge had been gr< DYSTROPHIES OF THE TEETH. 17 explanation of the phenomena is presented after the study of numerous cases. The discoloration that occurs in these teeth would seem to be an essential characteristic, if it were judged entirely by the teeth obtained for making sections. This material is very diffi- cult to find. Only extracted teeth can be used, of course, and few of them are extracted until so badly decayed that they are use- less, except those that are so badly discolored that patients and their friends urge their removal on that account. Examinations in the mouth reveal many cases of very considerable deformity without notable discoloration, as the photograph, Figure 8, taken from the mouth, attests. Many of the zones of injury show no discoloration. Numerous writers have given short descriptions of these teeth, scattering back for a hundred years. Most of these have dealt with the outward appearance only. Very few have pub- lished any studies of the histological characters, and most of these have been very brief and imperfect. Among the better should be mentioned Wedl, 1870 ; Baume, 1882 ; Walkoff , 1885. But by far the most important of the studies that have appeared is that by Dr. Otto Zsigmondy, of Vienna, Austria, in a paper pre- sented at the World's Columbian Dental Congress in Chicago in 1893. Unfortunately for Americans, no translation into English has been published. I personally examined many of Dr. Zsig- mondy 's sections and learned further of his conclusions in con- versation. The one thing that impressed me then, and impresses me now, as I reread his paper, is his conviction that the tissue distortion has been produced by a condition that has been of very short duration, because the apparent zones of injury in the dentin were often — ■ nearly always, indeed — so very narrow when con- sidered in their relation to the developmental lines. He could not, therefore, account for the marked deformity of these teeth. At the time he wrote he did not have the advantage of photo- micrographic reproductions, and his illustrations were very meager and insufficient. One of the best of them is reproduced in Figure 15. Figure 18 is a photomicrograph of a section of the labial portion of a zone of injury of the milder sort apparently, occur- ring in a central incisor. In this there was considerable discolor- ation of the enamel occurring irregularly along the line of injury in the labial surface, as shown in the photograph of the tooth, Figures 16 and 17. The discoloration in the line of the groove has the effect of a shadow in the photograph and makes the groove appear deeper in the discolored portions, which is not the fact. The particular section from which Figure 18 was made 18 PATHOLOGY OF THE HABD TISSUES OF THE TEETH. was chosen from a part showing the least discoloration. In this case the only distortion of the crown apparent in a superficial view of the tooth is the groove encircling the tooth and the dis- coloration. Also, the section shows that there was not a com- plete arrest of growth of the enamel. With a good light the enamel rods may be traced with the microscope through the darkest lines of the section, and they are seen to be well formed. There is no appearance of the telescoping process. The groove in the enamel appears much less pronounced in the section when highly magnified as shown, than it does in the photographs of the tooth. In the dentin, however, the injury is very severe, as shown by the clean-cut continuous line of interglobular spaces, which literally cut the dentin first formed from that formed later, and in the examination of the labial line of the dento-enamel junction in the full section, it is found to be distorted by a recurve, showing the interference with growth to have been pro- found and that some real shortening of the tooth must have occurred. As a further illustration of the possibilities in this class of injuries, I present two photographs, Figures 19 and 20, of a bicuspid tooth showing the separation of the telescoped parts in an injury of this kind occurring mid-length of the root. I extracted this tooth myself. The patient, a stranger, applied for relief from caries of bone of the upper jaw, and this tooth was situated on the border of the carious area in such position that it seemed to be best to remove it, though the tooth and its individual alveolar process were otherwise in good condition. At the moment of removing the tooth, it was noticed ihat the apical portion of the root did not come away, but was pulled from its place and remained loose in the alveolus. Laying the tooth on the bracket with the forceps, this apical portion was picked out with the foil pliers and laid with the tooth for after examination, because it seemed to be a very curious break. The operation was completed and the patient dismissed with an appointment to return later for further treatment. On exam- ination, this tooth and root were found to have pulled apart like a telescope tube, and the telescoping was on the lines of growth of the dentin. Figure 19 shows the tooth and root placed together in the normal form, in which a marks the line of break. In Figure 20 the two parts are separated, showing how the apical portion telescopes into the body of the root. I suppose there was some severe illness of short duration at the time this part of the root was developing, which prevented the deposit of cal- cium salts, and a sharp, distinct and continuous line of inter- globular spaces occurred. At the time, the root was developed DYSTROPHIES OF THE TEETH. 19 only as far as shown in the lower section of Figure 20, and had the broad conical opening shown at b. The internal diameter at the point to which the end of the apical portion reaches was of the size shown by the end of that piece. The result was that the solid dentin formed at that time represented only the lower square end of the upper piece. This was broken in the effort to extract and the root pulled apart on the line of the area of interglobular spaces, the line representing the lines of the proc- ess of growth. The patient failed to keep his appointment for further treat- ment and was not seen again. The opportunity to inquire into the nature of the nutritional disturbance that had caused this rare form of injury was lost. The specimen, however, tells its own story clearly. This case shows that the root of a tooth may also be injured by a condition of malnutrition, though such an extreme occurrence as this must be rare. I have noted a considerable number of cases in which a zone of injury occurred in the dentin beginning below the gingival line, as in the case shown in Figures 19, 20, though they are far more rare than those occurring in the crown of the tooth. Figure 21 represents another case of injury of the graver sort, occurring in a central incisor, in which but little discolor- ation is apparent. The wide overlapping of the new onto the older enamel, the complete breakage of the enamel rods along the line of junction of the two, the change in the course of the enamel rods in the two formations of enamel and the profound disturb- ance of and recurving of the labial dento-enamel junction, all point to a long suspension of nutrition and account for the grave distortion of the form of the tooth. This is much like that shown in Figure 12. The line of interglobular spaces is sharp and severe, but very narrow, and the dentin is normal immediately on either side. The incisal edge had been ground away in the endeavor to improve tbe appearance before the tooth, with the other incisors, was extracted. About one-third of the normal length of the crown had been missing. The next case is very curious in several respects. It is a bicuspid tooth that showed a very slight groove in the enamel not far from the gingival line. It was covered by the overlap- ping gum margin, except on the buccal surface. The whole tooth was, perhaps, as white as any normal tooth and was without any discoloration along the line of the groove, except that caused by a deposit of dark, closely adherent serumal calculus at several points. A photograph of this groove was but a partial success, as is shown in Figure 22. The tooth was then divided mesio- distally, preparatory to grinding sections. In examining the 20 PATHOLOGY OF THE HAKD TISSUES OF THE TEETH. halves with a pocket lens, a curious zone of injury in the dentin was discovered, which was photographed at once as an opaque object, which is represented in Figure 23. Two sections, two thousandths of an inch thick, were prepared and mounted with- out removing them from the cover glass on which they were ground. The sections were beautiful. No one would suspect that there was any zone of injury in either dentin or enamel. The disturbance of the line of the dento-enamel junction and in the one section a clinging bit of serumal calculus were the only abnormalities discoverable by microscopic examination. The only way I could explain this was that the something that had been seen and photographed had become obscured by the balsam. The balsam was dissolved out and the section dried. A zone of fine interglobular spaces was then found with another singular appearance in the form of a broad line of demarkation, that could not be explained. The section was remounted in a very stiff balsam without using anything to clear the dentin, with the expectation of making a photomicrograph the same evening. Something prevented, and by the next evening, the day having been unusually warm, the interglobular spaces were again filled with balsam. The shadow, however, remained, and is presented in Figure 24. It has since been found that the condition pre- sented is common to a considerable number of the slighter injuries of this type. Figure 25 is a photomicrograph of a labio-lingual section cut from near the mesial, side of a malformed tooth so that the line of interglobular spaces is cut through diagonally. This gives an exaggerated view of the zone of injury to the dentin, but will serve to impress the fact that these injuries are very severe. This presents this subject from its gravest to its slightest degree, in sufficient variety of cases to render the conditions intelligible. The Deformity in the Fiest Permanent Molars. The deformity of the first permanent molars should receive special consideration because of its greater frequence and because it so generally leads to early and rapid caries beginning in the malformed portion. The plan of injury does not differ from similar deformities in the front teeth, but the details of the injury are different because of the wide difference in the form of the tooth. Greater frequence of the occurrence of the condition in these teeth is due to the earlier beginning of calcification. In dissections of the jaws of the fetus at term, I have usually found the calcification of this tooth just begun on the points of the cusps. Sometimes there are only small spicuke, in other cases Fig. 22. Photograph of a bicuspid, showing imperfectly a slight groove from atrophy near the junction of the middle and gingival thirds of the crown. See Figures 23, 24. Fig. 23. The bicuspid shown in Figure 22 split mesio-distally and the cut surface photo- graphed as an opaque object. Note a broad zone of shadow in the dentin, extending in a semi- circular form from the groove on the mesial to the groove on the distal side. See also Figure 25. 12 FiC. 24. A photomicrograph from a portion of a seel 22. 23, showing zone of shadow in the dentin as a result < ings of this character are found in the mildest forms of atrophy marks. >n of the bic uspid shown in Figure interference with nutrition. Mark- iterference w ith nutrition th at show This g ives a stronger rlp'Satlon'ofThe'^ SuryTa E.™^^ ^^ '" ^ denti »- Fig. 26. Photograph of cast shov tion of the tooth is much reduced it second molar. Normally the occlusal \g atrophy of a first mo size. This is best appr rface of the first molar : Note that the occlusal por- ated by comparison with the ;he larger of the two. X J) c 6f J 3 §• S J^-o g.S '5 «£•".-£"< 8 o a ' I §.! 5^3 ox £x >j Fig. 28. A photomicrograph with a much higher power from another tooth with a similar atrophy to that shown in Figure 27, in which the section was cut horizontally or crosswise. The section through the interglobular spaces is, therefore, through that portion of the line showing in Figure 27. which dips toward the gingival at the buccal and lingual portions of the section. E. Enamel. d. Dentin. s. s. Line of interglobular spaces appearing as irregular dark blotches connecting the one with the other in every direction. DYSTROPHIES OP THE TEETH. 21 a more considerable part of the cusps is calcified, but I have never seen the calcification so advanced at birth that the cusps were united by calcified tissue, and evidently they are not so united, until much later. On the other hand, it was only occa- sionally that the least bit of calcification had occurred on the central incisors. More often calcification does not begin on these until about the end of the first year. Therefore, an illness that brings about serious malnutrition during the first year of the child's life is liable to wreck the occlusal surfaces of the first molars, while all of the other teeth escape injury. The injury to these teeth occurring so early is very charac- teristic if seen soon after the eruption of the teeth and before further injury has occurred by breaking away the sharp spiculae representing the malformed cusps or by caries. But it is exceed- ingly difficult to obtain specimens from which to make illustra- tions. If the injury has occurred very early, or before the enamel plates forming the lobes of the teeth have joined together, the spiculae of cusps will stand much closer together than the cusps of the normal tooth. The whole of the occlusal surface of the tooth is dwarfed, often discolored and sunken into the tooth crown. The pulp chamber will be nearer to the occlusal surface than in the normally developed tooth in proportion to the sinking of this part into the body of the crown. Figure 26. All around this the enamel of second formation wells out in the form of a broad collar to the normal size of the tooth crown at or about the base of what would have been the normally devel- oped cusps. The whole of the injured area is apt to be rough and pitted, and the pits and grooves are very apt to be wide open. This condition gives unusual opportunity for the beginning of caries and the early exposure of the pulp. It is for this reason particularly that they are so often destroyed very early. In cases occurring a little later, but before the completion of the occlusal surface, the conditions inviting the beginning of caries are equally bad. The cusps will stand further apart, are stronger, but the central part of the occlusal surface and the outer slopes of the cusps are in very bad shape. At a still later date, after the completion of the occlusal surface, the injury appears as a groove around the crown of the tooth and is gen- erally of less consequence. In all of these cases the zone of injury in the dentin is one of the very grave features, for the reason that caries reaching this zone of interglobular spaces spreads through it quickly. It has been exceedingly difficult to get material for the illustration of this for the reason that very generally the occlusal surfaces of these teeth are destroyed by caries before their removal, 22 PATHOLOGY OF THE HARD TISSUES OP THE TEETH. rendering thern useless for this purpose. Figures 27, 28 and 29, with their descriptions, serve, however, to illustrate the condi- tion of the tissue injuries fairly well, though neither of them are of the severer forms of atrophy. Figure 27 particularly shows the line of interglobular spaces in the dentin extending across the occlusal surface and dipping down gingivally along the axial portions of the dento-enamel junction. This figure also shows well the shortening of the crown between the pulp of the tooth and the occlusal surface. From the position of these zones of injury, it will be realized, from a careful study of the lines of the injury to the dentin, that the total shortening of the crown of the tooth is between the pulp and the occlusal surface in the molars. It is also between the pulp and the incisal edge, where it occurs in the incisors and cuspids. This is the reason that pulps are so frequently exposed in the preparation of cavities in these teeth. Dentists generally have not understood that the pulps were so close to the surface. When it is realized that these sheets of interglobular spaces, of which the zone of injury in the dentin showing in Figure 27 and in Figure 29 is a section spread through the entire area of the crown of the tooth, form- ing openings through which microorganisms may readily grow, it will be understood why it is so difficult to prevent the destruc- tion of these teeth by caries. It will also be understood how decay may quickly undermine the entire enamel cap, allowing it to fall away, exposing a blackened stump of dentin in all of the central portion with jagged enamel upon its margins, with decay persisting around the circumference where the line, or sheet, of interglobular spaces dips to the gingival near the dento- enamel junction. In the child, one is prohibited from forming a cavity of such depth as required to hold such a broad filling because of the nearness of the pulp of the tooth. The grave significance of this lies in the fact that caries beginning in the imperfections of the occlusal surface quickly reaches this zone of interglobular spaces and spreads rapidly through it, undermining and destroying the whole occlusal por- tion of the tooth. It often happens that the whole of this has been swept away so quickly that the area is uncovered before decay has proceeded further toward the pulp. The decaying area is then fully exposed to the fluids of the mouth, and the progress of the caries is arrested. In this case, the tooth remains as a blackened stump that soon rises in its alveolus and occludes with its fellow, which is generally in a similar condition, and both do good service. More often, however, decay continues in that portion of the zone of injury referred to, that dips under the strong enamel around the margins of the crown. Being thus DYSTROPHIES OF THE TEETH. 23 protected, it continues to burrow, finally reaching the pulp and completing the destruction. This is the general fate of these mal- formed first permanent molars. Many cases come before me in the great clinic of Northwestern University Dental School, show- ing involvement of the anterior teeth in young people. The rule is that the first molars have already been lost. Children from eight to twelve years old are coming often to have these teeth extracted. Treatment. First molars. Treatment of these malformed first molars to prevent the results detailed above, is exceedingly desirable. The treatment is required as early as the eighth year, often in the seventh. A few cases may be successfully filled. Cases which promise good results and in which the child can be con- trolled to do this work, the fissures should be properly prepared and filled with gold at once when discovered. Generally, how- ever, it will be found impracticable to make the proper prepara- tion and the fillings at so early an age because of failure to con- trol the child. As the rule, it would be necessary to do this dur- ing the seventh or eighth year. A large proportion of these cases are too badly decayed before the ninth year for filling, and many of them are decayed to exposure of the pulp, or the occlusal surface is lost during the seventh or eighth year. Ordinarily they will be seen first by the dentist when the child is brought for consultation regarding the deformity of the incisor teeth, the parents not having noticed the deformity of the first molars. Even at that time, in many cases, the first molars will be found badly decayed. This very early appearance of caries in these cases, and the fact that the pulp of the tooth is so often exposed by a decay that seems not to be very deep, greatly increases the difficulty of treatment. When the teeth can be seen very early, or as soon as they have come through the gums, and the occlusal surfaces are found badly deformed, showing many wrinkles and deep fissures, it is generally best to grind away any small, sharp spiculse of cusps that are liable to be broken in chewing food. Then, if decay has not actually begun in the fissures, these may be dried out and filled at once with oxyphosphate of copper cement with- out further preparation. Often such a course will be necessary in order to do anything that will be of service to the child. In the deeper fissures in which decay starts earliest, it will do excel- lent temporary service. When decay has made some progress the softened material should be removed, after breaking away 24 PATHOLOGY OF THE HAED TISSUES OF THE TEETH. any undermined enamel, and the cavity thus formed filled with oxyphosphate of copper. In any case, oxyphosphate fillings should be examined as often as once in three months to see that they are doing well and to mend up any failures. In this way these teeth can often be tided along and serious decay prevented until such time as permanent operations can be made. Those cases in which the condition of the occlusal surface is still worse and in which decay seems to start in spite of the effort to prevent it in this way, a gold cap may be made to cover in the entire exposed part of the crown. After grinding down the more prominent points that will cause the cap to interfere with the occlusion, an impression should be taken in modeling com- pound. This may be taken in the little impression cups used in crown work. Often these may be cut down considerably to decrease their bulk, which, in the mouth of the little child, is a serious objection. The arrangement should be made to obtain a very sharp impression very quickly. To this end, the softened modeling compound should be placed in the cold cup and allowed to partially stiffen. Then the surface should be warmed quickly over a Bunsen or alcohol flame and quickly conveyed into the mouth and pressed over the tooth. It should be held in position for several minutes, if practicable, so that the mass may become hard enough not to be drawn or marred in its removal. By this plan a very sharp impression can be obtained. From this a gold cap can be formed to cover in the occlusal surface of the tooth and may be cemented in place. There should be no attempt to make a full gold shell crown. It should only overlap the axial surfaces sufficiently to hold it in place. A renewal later, when it can be slipped further over the tooth, should be expected in many of the cases. The gum will cover much of the crown at the age of seven or eight years, and the child will be very sensi- tive about any pushing away of the soft tissues. Sometimes it will be impossible to place these without some interference with the occlusion. This will not be of much impor- tance if the interference is not very considerable, for the occlu- sion is quickly accommodated by movement of the teeth in early childhood. Special attention should be given to the intercusp- ing of these caps that the teeth may not be caused to slide out of position during the process of shedding the deciduous teeth. (See article on the intercusping of the first molars in Manage- ment of Children's Teeth.) These caps can often be improved by filling in deep grooves and by some broadening of the occlusal surfaces of the models before they are swedged; and, in doing this, the intercusping can be studied and arranged. Generally the crowns will have to be made rather flat and the cusps short DYSTROPHIES OF THE TEETH. 25 in order to prevent raising the bite excessively, especially if this must be done after the teeth have come into full occlusion. These caps should be regarded as a temporary expedient. When the child is older the time will come when the teeth may be permanently Med with gold and the repair made permanent. In the bad cases, requiring considerable gold building, this should not be attempted before the person is eighteen or twenty years old. The pulp is so near the occlusal surface that it will be much endangered if this building of gold with sufficient anchorage be undertaken earlier. In the meantime a careful guard must be kept to see that decay does not begin on the axial surfaces along the gingival margins of these caps and cause trouble. Caps put on in this way at from seven to ten years of age, even if they reach fully under the free margin of the gum at the time they are placed, will be some distance from the free margin of the gum after a few years. If decay occurs, a new cap may be made to cover it. It is the duty of every dentist having families in his charge to see to it carefully that these malformed molars are taken care of in this way, or some similar way, very early. After the patient has grown older and the teeth have come further through the gum, other devices may be used if thought necessary. Some cases may be successfully treated by grinding away a considerable part of the injured enamel and thus gain a smooth surface that will be kept clean by the excursions of food in masti- cation. This may often be employed advantageously after con- siderable decay has occurred. For little children it should be done little by little, having them come to the office frequently for this purpose. Particularly this should be the case if any sensi- tiveness has developed. Incisoes and cuspids. The treatment of incisors and cuspids should be along different lines. In a very large proportion of these cases, no treatment whatever is necessary, for these teeth are not much inclined to decay because of the injury. Some- times decay does occur, and if the injury is confined pretty closely to the incisal edge, it may usually be treated by grinding away. Often the injured portion may be ground away so that the tooth will look fairly well. It will be a little bit short, but the inclination will be to protrude further through the gums and increase its length in that way. If necessary, other teeth in the neighborhood may be ground also, shortening them a little, and in this way the esthetic in appearance may be satisfied, removing much, sometimes all, of the injured portion. Often teeth that are marked by grooves may be made to look very well by grinding the enamel smooth and level, making in this 26 PATHOLOGY OF THE HAED TISSUES OF THE TEETH. way a fairly good tooth form, being careful, however, not to expose the dentin on the labial surface. Exposure of the dentin on the cutting edge is not very objectionable. Frequently much harm is done to these malformed teeth by attempting to fill blackened pits. At the points where these occur, the teeth are often very thin and an injudicious effort to excavate results in cutting through to the lingual surface, and after removing perhaps considerable material to gain the proper anchorage, the operator finds the incisal portion of the tooth too weak to stand. No filling should be made for the pur- pose of closing up blackened pits, unless it is first found that there is abundant tooth material for strength after the excava- tion has been made. Also it must be remembered that the pulps of these malformed incisors are very near the incisal edge as a rule, and exposure of this organ in the excavation is very liable to occur. Incisor teeth that are so malformed as to be very unsightly in appearance, should not be treated hurriedly. They should be tided along until such time as the pulps may be removed, not only with safety, but that the roots may be filled in such a manner that they may do service for the lifetime. If they can be kept in position without other treatment than that intended as tem- porary, until the patient is eighteen to twenty years old, it is very much better that it should be done. Then the crowns can be cut away and artificial crowns put on with the best prospect for future service. Certainly no crowning operations should be undertaken in these teeth before the patient is sixteen years old, and eighteen to twenty is very much better. Long observation of the removal of the pulps and filling roots for young people shows that these teeth do not do well. It is true that we can remove the pulps and fill the roots of the central incisors at twelve years old in very many cases with results that, within the first year or two, seem perfect, but it is also true that these teeth tend to break down, the roots to split, or some catastrophe is very likely to happen to them before the patient is twenty-five years old, and the teeth are lost. Many of them suppurate after they have been apparently in perfect health for several years after the root filling has been made. All of these considerations unite to advise that the removal of crowns for the purpose of placing artificial crowns be delayed as long as possible. The roots of these teeth are just as good for the purpose of artificial crowns as the roots of fully developed teeth ; in fact, all of that portion of the tooth root-wise of the injured part is normally developed as a rule. DYSTROPHIES OF THE TEETH. 27 The Enamel Whorl. Pits are a common accompaniment of the contemporaneous accretional deformity, but in no way a necessary part of it, as is shown by the many cases of even the severer injuries in which they are absent. Indeed, in reckoning up the cases coming under my notice, enamel pits seem not to have been present in more than one-fourth of them. Further, these enamel pits occur in teeth that are otherwise normal. It is not very rare to find a single pit in the enamel of some one tooth of an otherwise per- fect set of teeth. In microscopic sections, the same histological characters are found as in pits accompanying the contempora- neous accretional deformity. They mark an imperfection, or partial failure, in the development of the enamel rods, confined to a small area, usually round, and evidently are most apt to occur in cases where there has been some marked difficulty in enamel development. Hence, they are a very common accompani- ment of the accretional deformity. Not infrequently, the rows of pits in the enamel are the only signs of injury to the teeth as a result of an illness. In this case the rows of pits form zones on the parts of the teeth contemporaneous in development, as one of the expressions of the accretional deformity. Aside from conditions of general malnutrition, pits may occur in any part of the enamel, showing no especial preference as to teeth or locality on any tooth. The pit marks the failure of development of the enamel rods at a point, leaving a hole of more or less depth. This is generally filled, or partly filled, with an amorphous material, dark in color, varying from a yellowish hue to a deep black. I have never yet made a section of one of these in which the dentin was exposed, though some are as deep or deeper than the normal thickness of the enamel. In all of these cases of very deep pits there is a depression in the dento-enamel junction, as shown in Figure 30, and a lining of enamel, in which the enamel rods are arranged in a segment of a whorl, all pointing to the center like the spokes of a wheel, in the bottom of the pit. When the enamel rods forming these whorls have grown about a certain length, growth ceases, and an opening is left, and this may extend as an open pit to the outer surface of the enamel, leaving an opening the full depth. Or this may be filled in part by a dark material not resembling enamel. Or, again, the surrounding enamel rods may close over it, partially or completely obscuring the pit, so as to form a smooth enamel surface over it. In Dr. Callow's case, described later, the deformity consists mostly in numerous whorls, many of them extending deeply into the dentin. These 28 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. definite whorls are at the dento-enamel junction, or actually partly within the dentin. But many pits are formed within the usual thickness of the enamel without disturbance of the line of the dento-enamel junction, as shown in Figure 31. In most of these cases there is much disturbance of the direction of the enamel rods in the immediate neighborhood as the rule. In some there seems to be a failure of the enamel organ to perform its function of rod formation at the particular spot. In and about many of these pits there is deep discoloration. Many times the dark color is confined to the pit itself, which is partially filled with a substance strongly resembling the chittinous covering of insects in appearance and in which no enamel rods can be made out. In other cases the dark color extends broadly in, or among, the enamel rods about the pit. In these pits the disturbance follows the general direction of the enamel rods in the locality. This is as true of the pits that accompany the accretional deformity as those that occur as isolated defects. In this the pit is distinctly different from the other injuries to the enamel in the accretional deformity, for these as uniformly follow the lines of Eetzius. I have been unable to form any idea of the pathology con- cerned in the formation of these pits. Their prevalence in cases of accretional deformity indicates that they are due to disturb- ances of nutrition. They consist essentially in a failure in the formation of enamel rods. But such remarkable disturbances as those shown in Dr. Callow's case indicate that there may be some other pathological element not yet understood. His- tologically, they seem to be a very distinct form of dystrophy. The rule is that these pits need no treatment. They rarely decay, but as there is a slight opening and the tissue is often black or dark colored for a little bit around it, dentists frequently cut them out and make fillings. There is no reason for doing this unless softening has occurred, or in other words, unless decay has actually begun. Of course in that case the filling is the proper procedure, but not otherwise. Wrinkled or Corel t gated Teeth. Teeth presenting an unusual dystrophy, to which I have applied the term wrinkled teeth, are characterized by an irregu- larity in the surface of the enamel, and of the line of the dento- enamel junction. The most typical form is shown in Figure 32, in which all of the teeth of the denture presented an enamel surface of alternate ridges and furrows. This is a photograph of a skull found in the anatomical laboratory of the Dental Fig. 29. A photomicrograph from a portion of a mesio-distal section of a first molar show- ing in the section two zones of interglobular spaces. It shows only a part of the mesial half of the section Note that the line of interglobular spaces nearest the enamel, the first line, follows closely the dento-enamel junction. This follows the prominence of the mesial marginal ridge of dentin (on the left in the picture) and then dips down to the gingival. The line of injury to tne enamel also rounds over this prominence and again touches the dentin just above the point of ending of the injury to the dentin. The second, and more marked zone of injury to the dentin, swings out quickly from the dento-enamel junction, on the left in the picture, and runs across much deeper in the tooth, showing the amount of dentin formed before this occurred. Fie. 30. An enamel whorl in the enamel near the dento-enamel junction, the surface of the enamel presenting a pit over the whorl. Normal enamel is marked A, A : dentin. B. B ; the pit in the surface. C ; the whorl. D. It will be observed that there is a heavy deposit of brownin in the deformed enamel, which lies next to the dentin. In fact, there is a recurve of the dento- enamel junction to partially accommodate the whorl. A little different direction in the cutting of the section, so that the pit in the surface would be missed, would show only the dark spot in the enamel and the whorl in the direction of the enamel rods, which would appear if the spot was not so black as to interfere with seeing: the enamel rods. Fig. 31. A photomicrograph of an enamel whorl beginning in the midst of enamel tissues, showing a failure of the development of enamel rods. The pit is nearly filled with amorphous material, very dark in color, and much of the enamel in the neighborhood is discolored. Fig. 32. — This photograph is from a skull found in the anatomical laboratory of the dental department of Creighton University by Dr. E. H. Bruening. All of the teeth of this individual presented the same deformity as those shown in the illustration. A section prepared from this skull was lost by accident. The scalloping was very regular. In this case the teeth presented an irregular wrinkling upon their surfaces, the wrinkles passing horizontally around the teeth. These wrinkled teeth have always a scalloping of the dento-enamel junction. Fig. 33. resentati- sections were cut. A cuspid, a bicuspid and a molar tooth from Doctor Callow's case. These are fair representatives of the appearance of the other teeth from the same mouth, from several of which An extreme case of wrinkled teeth. F.G. 34. Portion of enamel from near the gingival line on the buccal surface of a second molar from Doctor Callow's case. DYSTROPHIES OF THE TEETH. 29 Department of Creighton University by Dr. E. H. Bruening. This defect has no relationship whatever to a definite period of malnutrition, because it does not follow the lines of accre- tion, and is present in all of the teeth. In such cases the dento- enamel junction also shows much variation from the normal continuous curve, being wavy and in some cases very irregular. In the case illustrated in Figure 32 the dento-enamel junction was a series of quite uniform scallops. I show several illustrations of another case of this type of dystrophy, Figures 33, 34 and 35. I received from Dr. J. E. Callow, of Antigo, Wisconsin, sixteen teeth removed by him for a young woman who applied to him for treatment. They included incisors, cuspids, bicuspids and molars. The condition of these teeth, as indicated by their outward appearance, is very fairly shown in the photograph, Figure 33, of a cuspid, bicuspid and molar. All of the others were similar. Examination of these teeth showed that the injury to, or the deformity of, the enamel had no relation to contemporaneous lines of calcifica- tion. Histologically, although there were scattered interglobular spaces, there were no markings in the dentin that bore any rela- tion to those that occur in the accretional deformity. Either of these were sufficient to distinguish it as something different. In all of the teeth, from incisors to third molars, the deformity was greatest on the axial surfaces and least on the cutting edges and cusps. The surfaces were extremely rough and uneven, presenting sharp spiculse or knobs and deep pits in the utmost irregularity of form. Over some of the cusps the enamel seemed to be normally thick, but did not have the smooth glazed sur- face of normal enamel. Only occasionally a small area would show the normal smoothness. In most of the teeth the enamel assumed a normal appearance suddenly near the gingival line, and this normal part generally encircled the tooth, joining the cementum in a normal gingival line. Figures 34 and 35 are photomicrographs showing the pecu- liar histological characteristics of the enamel. In most of its parts the dento-enamel junction is lost in a wild jumble of cir- cular whorls or protrusions of enamel into the dentin. Quite a number of these whorls are hollow and empty, while some are filled with amorphous material, but all of these, without excep- tion, are lined with enamel, usually in the form of segments of whorls, as these are found in the bottom of other enamel pits. In some this lining is very thin. Some of these hollows commu- nicate with the surface by very small tubelike openings, while others seem to be closed on all sides. In occasional patches, even where the enamel began in these whorls along the dento-enamel 30 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. junction, the rods to either side straightened up and closed over them into a fairly well formed enamel. Still, most of the formed enamel is a wild, twisting, curving and bundling of enamel rods. With all of this the enamel formed seemed to be of normal hard- ness in every part. In a considerable number of places the enamel is plunged deeply into the dentin in long prolongations that were too large and long to permit photographing with any lens with sufficient amplification to enable the structure to be distinguished. The illustrations show the characters of the departure from normal very much better than it can be por- trayed in words. In this case I could get no indication of any other abnormal condition of the patient. She seems to have been otherwise a normal and healthy girl. Many of the teeth were badly decayed and it is represented that all of them, whether decayed or not, were abnormally sensi- tive to sweets, heat and cold, and to acid fruits. Also, that this condition of sensitiveness had been persistent since the eruption of the teeth. This sensitiveness was so continuous and severe that it led finally to the removal of all of the teeth for relief. In all of my observation this unique case stands alone. I have, how- ever, observed in the mouth a number of cases that may have, been of this character. The definiteness of the deformity and the perfectness with which this definite histological character was repeated in each tooth examined, indicates that it is a deformity to which the teeth are liable. This is emphasized by the frequent observation of the tendency seen along the line of the dento-enamel junction to form scallops and whorls in teeth otherwise normal. But I know nothing of the conditions leading to this kind of deformity. Dr. M. C. Smith, of Lynn, Massachusetts, presented casts of a case at Buffalo, at the meeting of the National Dental Asso- ciation, 1905, which seemed to me to be of the same character. When I examined these models, no teeth had been extracted and no opportunity presented for a histological study. Dr. Smith's case presented the same difficulty as to sensitiveness. White Spots in the Enamel. White enamel is seen in occasional white or ashy gray spots occurring in the enamel of teeth otherwise normal in color and form. These white spots are usually small and are covered with the ordinary glazed surface of the enamel, so that an exploring tine will glide over them the same as over the perfect enamel. If, however, the spots are large, this glazed surface fails to cover the central portion, being projected but part way from the mar- gin toward the center. In that case, the central area is rough, ***f the incisal edge joining at a right angl ; outlined upon the opposite «*»«+***» i •""•='" ntral incisor. £' X Figs. 58, 59, 60. Pattern form more advanced. The cut across the root of the tooth was made with the file for the examination of the condition of the pulp chamber as to calcification. Notice that a second groove was starting on the distal portion of the crown. Figure 59 shows the depth of the perpendicular groove at the incisal edge, and Figure 60 the depth of the horizontal groove. ill Fig. 61. Dish shape placed because of the ex is the third shell crown seen through the hole in Fig. 62. Proximal When first observed the holes through between t years later. The lower bicuspids and first mo ne sensitiveness of the eroded ar ch has been worn through by th crown. Man, forty years of age lar are gold shell crowns, which were eas. The crown on the first bicuspid e erosion. The white cement may be ; a dentist. ? man, about nineteen years of age. =d in this illustration, snowing round id the teeth broke away about seven EKOSION OF THE TJIETH. 49 ting that is much more extensive. In this case there was no grooving of the incisal edge, or along the incisal edge, only a slight broadening of the groove on the mesial side, and it will be noted that a similar groove is being cut upon the distal portion of the labial surface, while there is a curious half dish-shaped form on the distal end of the groove running mesio-distally. In this cutting, the angles with the surface of the tooth are very sharp, but the bottoms of the grooves are well rounded. The depth of the cut from the transverse groove to the incisal is shown in Figure 59, while the depth of the cut across the labial surface is shown in Figure 60. It was clearly apparent in examination of the tooth, that the groove running mesio-distally had cut through the calcified pulp. The incisal edge of the tooth had been much worn by ordinary abrasion. The V-shaped cut in the root of the tooth was made with a file for the examination of the pulp canal. In all my examinations of erosion I have never seen a metal- lic filling that seemed to have been cut away by erosion. Years ago I made much trial of gold fillings with a view of arresting erosion, and generally found the erosion progressing beside the filling as though no filling had been placed. The margins of the fillings stood up sharp and definite, showing no rounding. Dr. W. D. Miller, in his recent articles on erosion, claimed to have seen fillings of various sorts cut away by this process. Eecently I have met with a case which is presented in Figure 61, in which a gold crown, which had been placed' over the first bicuspid, seems to have been cut through. The patient is a dentist, and he tells me that this is the third gold crown that has been cut through at the same point. It was placed over the tooth because it had become quite deeply eroded and was extremely sensitive. The second bicuspid below also is a gold crown, placed for a similar reason. It has shown no signs of injury. It will be noted that erosion is in progress in other teeth in the neigh- borhood. In Figure 62 is presented an illustration of a case of erosion of proximal surfaces observed a number of years ago. The pic- ture is reproduced from pencil sketches made during the progress of the case. I had the privilege of observing the progress of this over a period of about seven years, nothing being done or attempted in the way of treatment. The picture represents the case as I first observed it. It appeared as if holes had been bored between the teeth, cutting about equally from either tooth. These grew larger and larger and the interproximal gum tissue receded slightly until the teeth were cut away so much that they 50 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. broke, leaving the roots in position. During all of this time, the margins of the cut at their junction with the enamel surface were sharp, presenting no observable rounding. I have observed this in the molars and bicuspids in several cases, and usually the teeth have been extremely sensitive. One gentleman had all of his molars removed from the upper jaw because of the pain they gave him in chewing food and in any effort to clean his teeth. The selection of cases for illustration has been confined to a few which seem to represent the more typical varieties of form. Variations from these, however, are constantly coming up, almost every new case presenting characters peculiar to itself. Many of them, even when the teeth are badly cut and deformed, are so clean and white that the deformity is scarcely noticeable a few feet away. But occasionally we see cases that give a very bad appearance. Etiology of Erosion. The cause of erosion is involved in the utmost obscurity. Most observers seem to have drawn their opinions of its caus- ation from the observation of the circumstances attending a comparatively small number of cases coming under their per- sonal observation. As the cases differ very materially in form of affected areas and surroundings, these views differ with the groups of cases observed. These opinions may be found in the literature reaching back some two hundred years. I may, perhaps, give a better and more condensed idea of this by group- ing these opinions into classes, than by extensive quotations. I will follow in some degree the order in which they have been prominent in the literature. They may be thus summarized : (1.) Erosion is a result of faults in the formation of the tissues during the growth of the teeth; conditions in after life have little or nothing to do with it. (2.) Erosion is caused by friction, most generally of the tooth brush carrying some abrasive tooth powder. (3.) Erosion is the result of the action of an acid in some way, as yet unknown to us. (4.) Erosion is the direct result of the action of a secretion of certain diseased glands in the mucous membranes that lie directly upon the areas being eroded. This secretion is gen- erally claimed to be acid in its reaction. (5.) Erosion is a process of absorption similar to that of the removal of the roots of deciduous teeth or the occasional absorption of the roots of the permanent teeth. The absorbing EROSION OF THE TEETH. - 51 tissue is the diseased portion of mucous membrane found lying in the eroded areas. (6.) Erosion is in some way the action of an acid, the devel- opment of which is associated with the gouty diathesis. (7.) Erosion is effected by alkaline fluids acting upon the basic substance and setting the calcium salts free, which waste away with a polished surface. (8.) "While dental caries is the result of the action of an acid developed by microorganisms, erosion is effected by the enzyme of the same or similar microorganisms. In discussing briefly the principal points in these views, we will find some overlapping more or less with each other, or separated only by the introduction of certain factors supposed important by one party, but not considered so by another. The first supposition mentioned seems to have been the older view. It was clearly expressed by John Hunter in 1778. by Fox in 1806, by Bell in 1825, and by a number of others fol- lowing these, and finally by Garretson as late as 1890. Hunter supposes that erosion is due to some certain imper- fection in the formation of the tissues of the tooth, because of which the substance gradually wastes away, continually leaving a smooth surface. His supposition seems to have been that conditions in after life had nothing especially to do in the matter. Fox and Bell do not differ materially from this view, but Bell adds the supposition that in the case of the dish-shaped areas of erosion, the tissues of the tooth have been deposited in whorls or such forms as favored this kind of wasting. To-day such views seem very strange; but we should remember that when these men wrote nothing was known of the histology of the teeth, and their view did no violence to facts known in their time. We now know that such faults in the formation of the tissues do not occur as the basis of these cases. The second supposition, i. e., that erosion is caused by fric- tion, and generally by the tooth brush loaded with abrasive powders, was held by John Tomes and many others in England, America and Germany, and is still held by many observers. According to this view erosion is no disease at all, but is purely a mechanical injury. Conditions present in quite a number of the cases seen, if grouped together and considered alone, would give strong support to this view. These cases nearly all belong to the more indefinite shapes of the wedge-like forms, and the cases which occur in the cementum after, or with, recession of the gum. A number of persons who hold this view describe and 52 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. illustrate these forms only. This has led me to suspect that in some regions, particular forms are more frequently met than others. It seems certain that in the central part of the United States one would not observe many cases of the wedge-shaped areas without finding varieties of form that would be very difficult to explain as resulting from abrasion by the tooth brush. "When Charles Tomes edited another edition of his father's work, he had seen cases that he believed could not have been made with the tooth brush, and he rewrote the chapter entire. Dr. C. R. E. Koch (Dental Cosmos, Volume 15, 1873, page 463) tried by every device he could think of to produce the conditions seen in erosion by the use of brushes and brush wheels, aided by acids in some cases and by alkalies in others. His conclusion was that it could not be done in any of these ways. He did not have the modern electric motor to run his brushes, however. Dr. W. D. Miller, of Berlin. Germany, recently published (Dental Cosmos of January and February, 1907) the results of two years' work on the etiology of erosion. He announced his belief that it is caused by weak acids or gritty tooth powders, or by both, assisted by the tooth brush. He seemed to be convinced that the tooth brush is the main factor, and that what we have designated as erosion is nothing more nor less than abrasion brought about by these agencies. During several weeks that the author was in Berlin during the summer of 1906, he was frequently in Dr. Miller's laboratory while he was engaged in these studies. Through his kindness much was seen of his plans of work in the effort to produce erosion by artificial means. Having placed a number of teeth in wax, gutta percha. or similar substance, somewhat in the form they would be in the mouth, he saturated a cloth with a weak acid solution (different solutions being used in various experi- ments) and laid it lightly over the teeth so that it would touch only on the most prominent part of their crowns. After this had remained in a moist chamber intended to prevent too much evaporation, for a predetermined length of time, the cloth was removed and the preparation placed on a machine run by an electric motor, and the teeth were vigorously brushed for a given number of minutes or hours, as determined for the par- ticular case. The cloth was then resaturated with the acid solu- tion, placed again upon the teeth, and the preparation returned to the moist chamber for the predetermined number of hours for that experiment. This was kept up day after day for weeks or for months, the experiments being much varied as to acid solutions, time, and brushing; also, certain experiments were EBOSION OP THE TEETH. - 53 being carried on without the acid solutions, and others by the use of tooth powders in use by the people. In some of the experi- ments the brushing was done by hand, as by this method more variety of motion could be used. In these ways he had certainly produced results that looked very much like many cases of erosion as seen in the mouth, especially those of the partially dish-shaped, the wedge-shaped, and the flattened varieties. I saw none of his artificial produc- tion, however, that had the sharp, clean-cut margins so often present in the real thing as it occurs in the mouth. Yet I feel certain that if these specimens had been presented to me as erosions that had occurred in the mouth in the ordinary way, I should not have questioned their genuineness. Certainly Dr. Miller has demonstrated the possibility and the probability that teeth are often injured by vigorous brushing with gritty powders, persisted in several times per day for many years together. I am not yet convinced, however, that all erosions are produced in this way, even admitting that they may be assisted in part by an acid that may be present in the fluids of the mouth. One thing particularly Dr. Miller seems to have ignored, and that is the extreme sensitiveness that is so often present in cases of erosion. I know, however, that Dr. Miller had not fin- ished his investigation of the subject at the time of his death, and that the peculiar sensitiveness occurring in erosion would have been considered by him later if he had had the opportunity. This I have regarded as peculiar to erosion, admitting, however, that cases occur in which there is no history of this symptom. It is my belief, based on the examination of many cases, that frequently sensitiveness is soon annuled by the rapid calcifi- cation of the pulps of the teeth. This has the effect of cutting off the connection of the dentinal fibrils of the crown of the tooth with the remaining pulp tissue. Then sensitiveness is ended. Therefore, many of the bad cases of erosion have not been sensi- tive for several years. This calcification has been a result of the condition of irritation communicated through the dentinal fibrils. During the time of this irritable condition there is generally a history of the cessation of brushing, for the reason that the friction of the brush can not be borne. In the case illustrated in Figure 55, the young man said he had used a brush before his teeth became so sensitive, but most of the loss of substance had occurred afterward. This is but a repetition of the history I have had from many persons. The thied supposition — that it is the action of an acid — 54 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. lias been held by many persons, and in one form or otber prob- ably has more adherents to-day than any other. How it is that an acid can so act to cut away the substance of the tooth, leaving a hard, polished surface which is a constant characteristic of erosion, while in all laboratory experiment and in caries as it occurs in the mouth the effect is a gradual softening by the solution of the calcium salts, is left unexplained, unless Dr. Miller's work noted above may be so regarded. As yet no acid has been found that will remove the whole of the tissue, calcium salts and basic substance, without previous softening. I have made some experiments on a different plan (reported with illustrations in the "American System of Dentistry," Vol- ume I, page 1003). Having noticed in some experimental work on the metals that the action of very dilute acids was different in the still condition as compared with the action in currents, I tried this upon teeth. Here I also found a difference. In a rapid current of a solution of one part of hydrochloric acid to four hundred parts of water, maintained for five days contin- uously, teeth were cut away in forms quite similar to erosion, the cut surfaces remaining hard and smooth, while other portions of the teeth were not softened. I found the loss of substance to occur only where the current broke around the teeth in a certain way. While this experiment is impossible of comparison with anything that can occur in the human mouth, it demonstrates the possibility that the action of acid solutions may be modified in some degree by conditions under which they are placed. Thus far, however, no modification has been discovered that will in any degree account for effects like those seen in erosion under conditions that seem possible in the human mouth. The fourth supposition — that erosion is caused by the secretion of certain glands in the mucous membrane of the lips and cheeks, that these glands become inflamed, or hypertrophied, from some unexplained cause, and emit an abnormal secretion which acts upon the teeth in this peculiar manner. It is certainly true in many of the dish-shaped eroded areas in incisors par- ticularly, that a certain part of the mucous membrane is found to be raised in a form that fits into the excavations in the teeth. If we touch these with blue litmus, it is instantly reddened, show- ing the fluids in the region to be acid. Several have remarked that this was especially true when the test is made early in the morning, or when rising from bed. I have personally examined many of these cases and have found the facts as stated. I have also found in these cases the prints of teeth not eroded clearly outlined in the mucous mem- EROSION OF THE TEETH. 55 branes, and these parts of the membrane showed also the same acidity when tested with litmus. After a careful and somewhat protracted study of these phenomena, my conclusion is that the little swellings on the mucous membranes are caused by the erosion, rather than the erosion by a secretion which they emit. In a considerable number of persons we will find prints of the teeth — the upper incisors particularly, and sometimes the bicuspids and molars also — in the lips or buccal membranes, and these are formed in the same manner. This explanation is strongly emphasized by the fact that erosions occur in cases in which the mucous membranes never touch the teeth, as in the somewhat rare cases of erosion of proximal surfaces, and in one case coming under my observa- tion in a girl sixteen years old, in which the bicuspids were deeply eroded in dish-shaped forms, where the tissues of the cheek had been destroyed before the teeth came through the gums, so that no mucous membrane could have touched them. The fifth supposition has certain points of similarity with the fourth in that the same raised points of the mucous mem- brane are described as fitting into the eroded areas. But instead of the erosion being caused by an acid, the supposition is that this tissue acts as an absorbing organ, and that the result is really an absorption similar to that by which the roots of the teeth are cut away. Several writers speak of having seen the usual lacuna? of absorbed areas in roots of teeth and in areas of bone undergoing absorption, in these eroded areas. This supposition necessarily carries with it the idea that certain actively functioning cells become fixed against the tooth tissue and keep that position long enough or steadily enough to effect this result. The same objection to this theory applies as to the previous one, namely, that cases of erosion occur in positions in which no mucous membrane, or other tissue, is in contact with the areas being eroded. The sixth supposition is that it is caused by an acid that is developed in association with the gouty diathesis. This is a more recent supposition. Perhaps the most notable article upon this supposition is that by Dr. Darby, of Philadelphia (Dental Cosmos, Volume 34, 1892, page 629) . Dr. E. C. Kirk, of the same city, has expressed somewhat similar views. This supposition has rapidly attained pretty wide credence. On this point my own observation is negative. Very little gout has come under my observation, and the few well-marked cases that I have had opportunity to study have shown no erosion. Yet we must now expect that the cause of erosion will eventually be found to 56 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. depend upon some change in the body fluids giving oral secre- tions favoring these results ; but how, by what, and how local- ized, are the questions. For the present it seems that we have no certain data in support of the theory connecting it with the gouty diathesis. The seventh supposition — that erosion is caused by alka- line fluids acting upon the basic substance of the tooth, setting the calcium salts free, which waste away leaving a polished sur- face — is one of the more recent. It has an individuality of its own. The supposition that an alkaline condition as affecting litmus is maintained in these localities for any considerable part of the time is certainly contrary to my personal obser- vations, and to much the larger number of recorded observa- tions in the literature. Further, in Dr. Koch's experimental work mentioned above, he found that he could not dissolve either enamel or dentin in alkalies until the calcium salts had been removed, or partially removed by acids. The enamel partic- ularly contains so little organic matter that it would seem impos- sible — first, that its organic matter could be removed in that way, and second, that if it could be accomplished it would not effect the disintegration of the tissue. The dentin has a much larger proportion of organic matter, but direct experiment seems to show that it has sufficient calcium salts to protect its organic matter from solution by alkalies. Therefore, until it can be shown experimentally that in some possible form alkalies will act to disintegrate these tissues, this supposition must be set aside. The eighth supposition, the most recent of all, is set forth by Preiswerk in his "Zahnheilkunde" ("Operative Dentistry"), 1903, page 200. It is the supposition that erosion is caused by the same or similar microorganisms as those which cause caries, but by the action of their enzyme, not by the action of their acid products. It is well known that a number of the microorgan- isms of the mouth which form acids in the presence of the carbo- hydrates, such as sugar or starch, will grow well in nutrient material devoid of these substances, but in that case will form no acid products. Preiswerk contends that the human saliva is normally alkaline, and that it is a mistake to suppose that the enzyme of these microorganisms is necessarily a peptonoid sub- stance, as these act in an acid medium. He claims to have found evidence that in alkaline or neutral conditions their enzyme is a trypsin similar to the trypsin of the pancreas which acts in the presence of an alkaline reaction. Under these conditions this enzyme acts upon the basic substance of the dental tissues, EROSION OF THE TEETH. 57 dissolving the basic substance, setting the calcium salts free, which are washed away during the chewing of food, the motions of the lips, fluids of the mouth, and in the artificial cleaning of the teeth. He claims to have in some degree proven this propo- sition by experiment with trypsin derived from the pancreas, which he found to act upon the basic substance of the teeth. It seems quite possible that trypsin might act upon bone in this manner, possibly upon dentin, but that it should so act upon enamel, which has no more than three per cent of basic substance, seems out of the question. Erosion always begins in the enamel, except in those cases in which it begins in the cementum after the recession of the gum tissue, and practically always cuts the enamel as smoothly with the dentin as if the two were one and the same tissue. In the absorption of the roots of the deciduous teeth, and not very rarely of the permanent teeth as well, all of the parts, basic substance and calcium salts, are cut away as one tissue. In the absorption of bone by the normal physiological process, the same thing occurs, and in my studies of these processes it has often been observed that the noncalcified bone corpuscles suf- fered the same fate. But even this process balks at enamel. I have often met with enamel in position to be acted upon by absorption, but this had failed. We often see almost the last trace of dentin removed from the crowns of deciduous teeth by physiological absorption, but never any part of the enamel. It appears at the present time that these facts place this process out of the question, even if the far more general observation — that the condition is acid in erosion — should be shown to be an error. Finally, I can not at present find any theory proposed, nor have I any to propose, that has not features that seem to render it impossible. I therefore feel compelled to leave the subject in this very unsatisfactory condition, hoping that an early solu- tion of the difficulty may be discovered. It seems highly probable that this will be found connected with some systemic dyscrasia, but if so, the conditions leading to its strict localization will require explanation. Treatment or Erosion. At present no treatment with the view of cure or of stopping the progress of erosion, is known, that gives promise of success in any considerable variety of the cases. There should be strict inquiry as to the patient's habits of cleaning the teeth in every case, and the use of any tooth powders whatever prohibited. 58 PATHOLOGY OF THE HAKD TISSUES OF THE TEETH. A sufficient use of clear water and the brush will, I believe, do no harm. In what I learned of Dr. Miller's work in the production of erosion it seemed to me that he was not very successful in producing erosion with the brush and water, even when much brushing was done with the electric motor. With the powders, however, the teeth were worn away. He also found sharp grit in many of the tooth powders in use. The brush used with water regularly and sufficiently, but with moderation, will certainly keep the teeth in good condition as to cleanliness. If many dentists will do this and report the results carefully as to the effect on the progress of the erosion, we will soon gain valuable clinical evidence as to the possible effect of the brush with and without abrasive powders. Those who have connected erosion with the gouty diathesis have made some effort for the relief of the general condition with the hope that the progress of the erosion might be controlled, but thus far no very considerable benfits have been reported. I have made considerable effort to reduce the evil results by inserting fillings, but can report but few successes, and am now of the opinion that some of these apparent successes were due to a coincident spontaneous stoppage of progress of the erosion, rather than from the influence of the fillings. In the case illustrated in Figure 48, 1 filled all of the eroded areas with gold, removing all that remained of the labial and buccal surfaces. This was effective for the teeth so treated, and fortunately the erosion did not spread to other teeth. I saw the case occasionally until the patient died, about fifteen years later. This was done before the modern process of porcelain crowns had become suc- cessful. The treatment was simply horrible from the esthetic standpoint, but it gave the patient the full use of her teeth with perfect comfort for the remainder of her life. In my efforts filling has been of no other value except to limit sensitiveness and depth of cutting, unless all of the surface being eroded was removed, except possibly in some of the nar- row cross cuttings and a few of the wedge-shaped areas. The erosion will go on beside the fillings and continue spreading, leaving the margins of the fillings standing as they were placed. One who has had a wide observation of erosion and of its progress from year to year may do much good by filling in certain selected cases. These should be those deep cuts across the teeth that show little or no disposition to lateral spreading. In a number of cases of this character I have cut the groove fully to the mesial and distal surfaces, and filled them with gold without other preparation. These have generally been success- EEOSIOKT OF THE TEETH. 59 ful. Early in my work I filled two of these without the exten- sion mentioned. The erosion soon made the extension, and refilling became necessary. These include very few of the cases. The wedge-shaped forms have in a few instances done well with fillings, and certainly the depth of the cutting can be materially limited. Most of my efforts with these, however, have failed to stop the spreading. "With the dish forms I have seen no suc- cess short of cutting away the remainder of the labial surface and replacing it. The artificial crown is the better treatment. In other forms of cutting, filling seems to be of no use except to limit the sensitiveness for a considerable time, and to prevent depth. The filling may be done with porcelain inlays when that seems desirable. In the great majority of cases, however, it will be better not to make fillings of any kind. I am therefore of the opinion that, as a general rule, fillings should not be made in the treatment of erosion. That which now promises the best results is to keep watch of the cases, and at the proper time cut away the remaining parts of the crowns and place artificial crowns. The sensitiveness when very annoying may be relieved, temporarily at least, by severe burnishing. The best way to do this is with the burnisher cut in ridges, something like a coarse cut bur, with the edges rounded and polished. Some use has been made of these for burnishing fillings. Place the bur on the eroded and sensitive surface while rapidly rotating, and go over its surface quickly with strong pressure. Repeat this several times and then leave it alone. The first application will cause sharp pain momentarily, but afterward there will be less, or no pain. This will generally relieve the sensitiveness for some time. This may be repeated when necessary. When erosion has progressed so far that the teeth have become much disfigured, the crowns should be cut away and por- celain crowns of some form substituted. These, if well made, will give excellent service. In watching the progress of many cases of erosion a rather large number will be found that become stationary without known cause, and so remain indefinitely. These cases will, of course, vitiate many of the supposed good results of treatment by filling, or any form of treatment intended to limit or to stop the progress of erosion. 60 PATHOLOGY OF THE HABD TISSUES OF THE TEETH. CARIES OF THE TEETH. HlSTOEICAL. MORE or less vague writings of caries of the teeth are found in ancient literature, most of which are too uncertain in their meaning for us to gain any clear conception of the views held of its cause. Other writings of the specialties in medicine, such as the mention of physicians for the teeth, extraction of teeth and of artificial teeth are not of interest in this connection. Close studies of the conditions surrounding the beginning and progress of dental caries have developed very slowly. The oldest writing that I know which attempts a rational presenta- tion of the cause of dental caries is by an anonymous author in the German language in 1530. I present here a photographic reproduction of a single paragraph. (Eorrofa tfl cine tran&fyeit *wb vefjel her $enwennftcl4d)trigfi vitbtyol werbe weld)$ am meiflen txn bourne $c(d)id)t v$rnemi<$lid>cn fe einet ifl vnnt> fie md)t vw fcer anbanffie fptjfe reimcjet/weldjs favA vcitbt/ vnfc mad)tbavnad) b$c (dp ftrffe feudjtig&te bte fie n eget/ xnb immerall melid) vbtxiyint nynmet ba($ (teie$en verier bet / vnnt> Daroad? nid)t am (djmer^m mdffett fftcFtdjt wcgfc faukn. The statement is remarkable for its close agreement in substance to the views now held, if stated without detail. The wording is very quaint and in some unessential points the mean- ing is uncertain. I should translate it thus : Translation. Caries is a disease and evil of the teeth in which they become full of holes and hollow, which most often affects the back teeth ; especially so when they are not cleaned of clinging particles of food which decompose, producing an acid CAEIES OF THE TEETH. 61 moisture (literally, a sharp moisture) which eats them away and destroys them so that finally with much pain they rot away little by little. In the same volume this writer gives also the oldest authentic mention of the use of gold for filling teeth. The paragraph runs thus: Sumbn'ttert bas mm bteatJe^Tfflffg S»egg mmmet/weld)$ ef fe gefcfytcfyt/ gum ttfkn bmtt cj?e ei'sstey bdrjttbmltd) tt?cl<^6gc|c^ictiniit: (Btolfes epffdwtowilber gdgen fiber $mmfy ber rewtgwrtg barmtt wirbt gcfBUee* The following is very nearly its meaning. The writer is discussing plans of treatment of caries. Translation. In the third plan, the hollow place is done away with (taken away — removed) which is done in one of two ways. First, the soft part of the cavity and the decayed part is cut away with small chisels, knives, files or other suitable instruments, and cleaned, as is well known to practitioners. Then for the saving of the remaining parts of the tooth, the cavity is filled with gold leaf. Otherwise one may use a suit- able gum prepared with nutgalls and hyssop to fill the cavity after cleaning it. This writer mentions Mesu as an authority, a man who lived some two hundred years earlier, who is also mentioned by other writers, but so far as is now known, none of his writings have been preserved. The French writings in dentistry are older than the English, but do not contain very clear statements of view of the pathology of caries. Generally the statements are equivalent to saying the teeth rot away or decay away, without attempt at explana- tion of the process. 62 PATHOLOGY OF THE HABD TISSUES OF THE TEETH. Fouchard wrote in French in 1728 and a translation was made into German by Augustine Duddei in 1733. Second and third editions were published in French in 1746 and 1786. In none of these is there any statement regarding the cause of den- tal caries that is as definite in conception as the one quoted above. This seems to be true of all of the writings of that time. Fouchard mentions filling carious cavities with gold, but con- demns the practice apparently because of the expense, and because certain persons of evil disposition deceived the people by using tin so prepared as to appear like gold. As filling materials, he preferred lead or tin leaf (foil). John Hunter, writing in English (1778), expresses very clearly a different view, in which he says: "The most common disease to which the teeth are exposed is such a decay as would appear to deserve the name of mortification," with which he expresses some dissatisfaction as being an incomplete explana- tion of the diseased process. This, with other writings by the same author, shows that in considering the diseases of the teeth he was following closely the lines of thought of his time of what we now know as necrosis of bones. Fox (1806) expresses a similar view, which, with slight mod- ification, was repeated by Bell (1825), who proposed the term ' ' dental gangrene ' ' to take the place of the more common terms "decay" or "caries." This seems to have been the most common view of medical men of that time, and, with slight modifications, was repeated by most writers. All of these men regarded caries of the teeth as being a result of inflammation and as beginning within the dentin instead of upon the surface of the enamel. Koeker of Philadelphia (1830) speaks of decay penetrating the enamel from within outward, saying that it "had thus formed a natural outlet for the bony abscess." Robertson (1835) expresses a different view, which, in its main features, agrees substantially with the earlier views of the anonymous author quoted above. But Robertson is more explicit in the detail. According to this view, caries of the teeth resulted from the action of an acid generated by the decomposition of food particles or fluids, which lodged at particular points about the teeth and dissolved out the calcium salts of which the teeth are composed. These points of lodgment were shown to be the points at which caries made its beginning, as in pits and deep grooves in the occlusal surfaces, between the teeth (proximal surfaces) or about the margins of the gums. CABIES OF THE TEETH. 63 Begnard of Paris (1838) defined caries of the teeth as "destruction of the teeth by decomposition." His contention was that this destruction took place at the very spot where the acid was formed, or where the alimentary particles lodged and decomposed. This was called the chemical theory of caries of the teeth. A large body of dentists, both in Europe and America, gave simi- lar expressions of view at about this time. The idea that inflam- mation of the dentin had any part in its causation was denied. Also the statements of Fox, Bell, and many others, that caries began within the dentin and worked its way outward, were gen- erally denied. Instead, it was asserted that caries always began upon the surface of the tooth, or in pits, fissures, etc., that were open to the surface. The contentions along these differences of thought were sharp and the lines closely drawn. This brought about a much closer observation and study of the nature and form of the physical injuries inflicted by dental caries, and with this, the opinion became general that caries always began on the outside of the tooth and worked its way inward, forming a cavity. During this period also, comparative anatomists and geologists were studying closely the teeth of the living animals and those remaining of extinct animals, in which prominent differences between the structure of the teeth and the bones were ascer- tained. Owen gave us the word "dentin," distinguishing that which had before been called tooth bone from true bone. A knowledge of histology began to be developed. The cell theory of the construction of organic bodies, animal and vege- table, was propounded and rapidly assumed the general form in which it stands at the present time. Makers of microscope lenses rapidly improved them because of the encouragement and patronage induced by these studies. In the midst of this, John Tomes, of London, was studying the microscopic structure — the histology — of the teeth and bones, and by 1860 this was devel- oped almost completely as it stands to-day. It is true that since then much more exactness of method and greater accuracy of detail has been added. But the full foundation of our knowledge of dental histology and the development of the teeth was laid by John Tomes. It seems that Mr. Tomes began this work with the inflam- matory theory of caries strongly fixed in his mind. He found, however, that inflammation could not take place in the teeth. The histological structure of the teeth was such that there was no provision for the circulation of blood in the dentin, neither 64 PATHOLOGY OF THE HAKD TISSUES OF THE TEETH. was there any provision for processes of repair of injuries. Yet the dentin was a vital tissue and it was the opinion of Mr. Tomes that this vitality must be destroyed before the part could be dissolved out by an acid, thus forming a cavity. He admitted, however, that the same agent — an acid — might do both. This gave rise to the chemico-vital theory of dental caries, which was much discussed from 1840 to 1880. Finally Dr. Magitot of Paris (English translation, 1878) published the most extensive work that has been produced on this subject, detailing much experimentation in various ways in the endeavor to determine the exact cause of the disease. His conclusions were that caries of the teeth was produced purely by chemical substances developed in the mouth or introduced with food. This work seemed, for the time being, to establish the purely chemical theory of the production of dental caries. In the meantime, there had been many suggestions that microorganisms might be found to play a prominent part in the production of dental caries. The first important work published on this subject was by Leber and Eottenstein (German 1867 — English translation, 1868) in which these authors claimed to have determined the presence of these fungi in the dentinal tubules (which were much enlarged) of carious areas. Strong corroborative evidence of the correctness of their view existed in the fact that John Tomes had determined previously that the tubules in carious areas were constantly much enlarged and filled with granules, the nature of which he could not determine. This observation by Mr. Tomes had been confirmed by the obser- vation of others and had become fixed as an essential difference between dental caries and a simple solution of the calcium salts of a tooth by an acid. Still, the work yf Leber and Eottenstein made no considerable impression on the opinions held by den- tists. These gentlemen wrote before the development of the staining methods by anilin dyes, which certainly distinguish microorganisms in tissues. Neither were they able, by means of culture methods then known, to separate microorganisms into distinct species and determine the character of each as to its power of producing fermentation or other special forms of decomposition. Miles and Underwood of London (1881) determined defi- nitely that the enlarged tubules in dental caries contained micro- organisms, by use of the anilin dyes discovered by Dr. Koch, the German bacteriologist, but they were unable to go farther for the lack of better facilities for division of species of micro- CAEIES OF THE TEETH. 65 organisms and the determination of their physiological charac- ters in the production of fermentations or putrefactions. Dr. W. D. Miller was at work with Dr. Koch in his bacteri- ological laboratory when the means of cultivating microorgan- isms on semi-solid media was first established and was at once able to separate the microorganisms found in the mouth or in carious dentin into species, and determine the character of each in the production of acid fermentation or other forms of decom- position. The finding in the dentinal tubules of microorganisms which, when growing in artificial culture in the presence of any form of sugar or starch, uniformly produced lactic acid, which in time dissolved the calcium salts of the tooth tissue, completed the full explanation of the local changes taking place in caries of dentin, but the cause and the nature of caries of enamel was not so clearly made out. This history, briefly as it is written here, shows the principal steps of the unfolding of a knowledge of this disease process extending through many years of labor done by many individ- uals, each building upon the discoveries which were made by his predecessors. The outcome of this work has finally given complete and exact knowledge of the steps in caries of dentin. It will also be seen that the work of Dr. Miller was really the finding of the exact method of the formation of the acids which the older anonymous German writer (1530), Eobertson (1835), Eegnard (1838), and others, described as being formed by decomposition. This brief summary mentions the work of but a few of the men who seem to have been most fortunate in the finding and giving expression to facts that have advanced our knowledge of the processes taking place in caries of the teeth. As a matter of fact, many men have taken part in this work. General, Statement. Caries in its simplest expression consists in a chemical dis- solution of the calcium salts of the tooth by lactic acid, followed by the decomposition of the organic matrix, or gelatinous body, which, in the dentin, is left after the solution of the calcium salts. In caries of the enamel, the whole substance of the tissue is removed by dissolving out the calcium salts, there being so little organic matrix in the enamel that it will not hang together; consequently a cavity is formed by the simple solution of the calcium salts of which it is composed. This solution always begins upon the surface, never in the interior. Decay of the teeth is therefore caused by an agent acting from without the 66 PATHOLOGY OF THE HAED TISSUES OF THE TEETH. tooth, never from within the tooth. It is something extraneous to the tooth, acting upon the surface in the beginning and pene- trating little by little into its substance. Caries of the dentin is different from caries of the enamel, in that the organic matrix is sufficient in amount and consistence to retain its histological and physical forms after the solution and removal of the calcium salts. With the removal of these by an acid, the enamel will have disappeared entirely, but the dentin will not suffer any change of form. Therefore, the simple solution of the calcium salts leaves a softened matrix in the dentin and does not form a cavity. After the solution of the calcium salts, there is a decomposition of this organic matrix progressing from without inward, breaking it up and finally forming a cavity. Between the solution of the calcium salts and the decomposition of the organic matrix, some little time passes. The two seem never to occur at the same time in any given por- tion of the tooth, but the calcium salts are dissolved out first and the decomposition of the organic matrix follows later. Therefore, while, after the full development of the carious proc- ess, both may be progressing at the same time, the solution of the calcium salts is always considerably in advance of the decom- position of the organic matrix, leaving a zone of softened mate- rial between. In the progress of the solution of the calcium salts of the dentin, the tendency is to spread in every direction from the point of penetration of the enamel, and especially along the dento-enamel junction. Then, particularly when the original opening in the enamel has been small, the enlargement of the opening is brought about mostly by what is termed "backward decay of the enamel." This is decay of the inner surface of the enamel that is in contact with the decaying dentin under it, due to the spreading just mentioned. In this case the enamel decays from the inside outward until it is so weakened that it breaks away, enlarging the opening. The rapidity of this back- ward decay of the enamel is exceedingly variable. Cavities may be wide open early in their progress, or they may remain for a considerable time with a small opening. The calcium salts are not dissolved complete from without inward in the first instance, but the acid which dissolves them seems to spread, or percolate, into the tissue and the solution goes on as a gradual softening process. The innermost part affected is less softened than the more superficial parts. In the outer portion of the softening area all, or about all, of the cal- CAKIES OF THE TEETH. 67 cium salts have been dissolved, while in the inner portion but very little is yet dissolved. In this way the action of the acid progresses slowly from without inward. The decomposition of the organic matrix of the dentin pro- gresses in a similar way, the tissue being broken up little by little progressively, from without inward, so that the formation of a cavity, especially when the opening through the enamel is small, follows slowly the solution of the calcium salts. There- fore, it often happens that the solution of the calcium salts has progressed much more rapidly than the decomposition of the organic matrix. In that case, we find a very large amount of material that is soft and spongy, which may be easily cut with a sharp excavator; or, after removing any overlapping enamel that may interfere, a spoon excavator may be passed along the margin of the decayed area, and the whole of it may be turned out in a body, soft enough to be cut with a razor or sharp knife. Occasionally we will see almost the entire interior of the enamel cap, i. e., almost the entire dentin of the crown of the tooth, softened in this way and yet the organic matrix is not yet broken up. This, however, is the exception to the rule. The general rule is that the decomposition of the organic matrix follows fairly closely the removal of the calcium salts. 68 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. CARIES OP DENTIN. ILLUSTRATIONS: FIGURES 63-74. Although in the natural order of the phenomena, caries of enamel always precedes caries of dentin, it is preferred to first describe caries of dentin for the reason that the order and char- acter of the processes in its progress are regarded as having been completely made out, and it is believed that afterward caries of enamel will be easier understood. It is sufficient here to say that caries of dentin can not occur until the enamel has been penetrated. The enamel with its rods cemented together by its cementing substance is a solid. It has no natural open- ings into which microorganisms can grow; and these have no power of penetrating into it, except as it is dissolved and removed by the acids which they form during their growth. Therefore, in decay of the enamel, the microorganisms producing the acid are on its surface. On the other hand, the dentin is everywhere permeated by the dentinal canals into which micro- organisms may grow when the dentin is exposed by the destruc- tion of the enamel. Both caries of enamel and caries of dentin are caused by the same agency; namely, the growth of microorganisms in contact with the surface of the enamel in the first instance, and the formation of lactic acid during that growth, which dissolves the calcium salts of which it — the enamel — is composed. In caries of dentin, the microorganisms grow into the dentinal tubules and form their acid product within the tissue itself. This dissolves the calcium salts of the dentin, converting it into the soluble salt, calcium lactate, which gradually escapes into the surrounding saliva by osmosis. Osmosis. The word osmosis, as used here, is used in phys- ical chemistry to represent the passage of soluble salts through animal membranes. This occurs whenever a fluid containing the specified salt is in contact with the membrane upon the one side and water is in contact with the same membrane upon the other side. In this case, the salt will pass through the membrane into the water until the water on either side of the membrane becomes equally salt. Or again, if two salts, which will commingle in solution without chemical reaction, are placed in solution in water separately, and the one placed in contact with one side of a membrane and the other in contact with the other side of the Figs. 63, 64. Photographs, very nearly full size, of a small dialyzer used for separating the salts from the saliva, or other body fluids, for the microscopic study of the crystals. With this, it is the inten- tion to deal with very small volumes. In Figure 63 the parts of the piece of apparatus are in position. In Figure 64 the lid with the tube passing through it is removed and laid to one side. The tube passing through the lid has a small rubber band around it above the lid, which may be moved to hold the tube at any height above the bottom of the vessel. The lower end of the tube is closed with a piece of gold- beaters' skin stretched over it and tied with a thread. This may have a coating of collodion to close any possible opening. A piece of fresh bladder could be used as well. In use, the saliva or other body fluid is placed in the dish and about two cubic centimeters of distilled water are placed in the tube and the height of the tube adjusted so that the surface of the water in it will be about level with the top of the fluid in the dish. Devised and first used for this purpose by Dr. Edward C. Kirk. This dialyzer was presented to the author by Dr. Kirk. Flo. 65. A photomicrograph of salts dialyzed from the saliva and crystallized on a cover gla Only a minute drop of fluid was used. Fig. 66. Crystals of sugar. A photomicrograph with polarized light. Fig. 67. A bicuspid split mesio-distally through an area of decay and photographed before sepa- rating the halves. When these are opened like a book, the penetration of the decay will be disclosed. These cuts have been made for the illustrations in an especially arranged lathe, in which the tooth is mounted on a slide rest. The cutting is done with a rapidly revolving aluminum disk, twenty-six gauge (thirty-two gauge may be used) charged with carborundum powder mixed with soapy water. With this, slices 1-100 of an inch thick may be cut. Fig. 68. The occlusal surface of an upper first molar was split mesio-distally and is shown in Figure 71. Figs. 69, 70. Other upper first molars showing, apparently, similar decays. decay in the central pit. This tooth Fio. 71. The upper first molar, Figure 68, split mesio-distally, the surfaces polished, laid open and photographed to show the penetration of decay. The specimen shows particularly well the typical conical form of the penetration of dentin as it occurs when the opening in the enamel remains small. It also shows well the spreading of decay along the dento-enamel junction of the occlusal surface form- ing the broad base of the cone of the area of decay. FIG. 72. A lower second molar with a large area of decay which has begun in , the buccal pit The decay has spread along the dento-enamel junction, undermining the greater part of the enamel M the buccal half of the tooth and has destroyed nearly one-half of the dentin. This injury has occurred while the opening into the cavity has remained small. Fig. 74. Fig. 73. An illustration showing the filling of the dentinal tubules with mi dento-enamel junction is at the top of the illustration. The organisms have and by continued growth and multiplication have filled and enlarged them i grown single file into all of the smaller side branches. Only a few slight local are seen. The left of the illustration is near the margin of the invasion, where yet but partially filled. Great differences are found in different specimens smaller side branches. Some have very few after passing a little way fror junction. Fig. 74. Another illustration of the filling of the dentinal tubules with which, as compared with Figure 73, the opposite extreme as to side branches ; iroorganisms. The entered the tubules ery evenly, having swellings of tubules new tubules are as in the number of i the dento-enamel ings of the tubules ings of tubules and with n deeper margin of the invi selected as representing the extremes of sm< and maximum of filled side branches, as seen something near the maximum of irregular s tions between these two illustrations are fou lcroorganisms, in d irregular swell- >f irregular swell- deeper in the tooth close on the i different teeth, and have been of the filling and enlargement of the tubules n Figure 73 ; and absence of filled side branches and ellings of tubules, as seen in Figure 74. All grada- figure represents something like hes. Th two specimens CAEIES OF DENTIN. 69 same membrane, the two salts will pass through the membrane in opposite directions until they have become equalized in the two solutions. This process, when used to separate crystallizable salts from colloid substances with which they may be com- mingled, is known as dialysis, for it is found that such substances as gums, resins, albumens, etc., which are not crystallizable, do not readily pass through membranes in this way. Therefore, if there is a solution of sugar in the saliva and a solution of calcium lactate in the depths of a carious cavity, that part of the matrix of the dentin which is already softened by the solu- tion of its calcium salts, acts as a dialyzing membrane, passing the sugar in and calcium lactate out. In this way, the growing microorganisms receive sugar from the saliva, and lactic acid (their waste product) which has become calcium lactate by com- bination with the calcium salts of the tooth, is eliminated. This process naturally goes on very slowly, so that weeks and months are required for any considerable cavity to form, and often several years. Figures 63 and 64 represent a dialyzer used to obtain salts from the secretions free from the gummy substances with which they are associated, for microscopic examination of their crystals. Figure 65 is a photomicrograph of the salts dialyzed from saliva and crystallized. Figure 66 is a photo- micrograph, made by polarized light, of sugar dialyzed from a solution and crystallized. In penetrating into dentin microorganisms follow the den- tinal tubules, simply growing into them as a grapevine would grow through a lattice. The anastomosing loops from tubule to tubule, which are plentiful near the dento-enamel junction, and any other openings such as interglobular spaces which they may encounter, are filled full as they go. There is much dif- ference found in different teeth in the number and size of the anastomosing loops from tubule to tubule. In some these are plentiful, in others very much limited. In all, however, there is a sufficient number of these near the dento-enamel junction to afford a moderately free passage of microorganisms from one tubule to another. In a considerable proportion of teeth there are many small interglobular spaces along next to the dento-enamel junction, known as the "granular layer of Tomes," through which microorganisms may readily grow. Therefore among different teeth there are differences in the facility with which microorganisms will spread along the dento-enamel junc- tion. The organisms having gained access to the dentin by the solution of the enamel, they grow into the dentinal tubules 70 PATHOLOGY OF THE HAKD TISSUES OF THE TEETH. directly toward the pulp. They are continually gaining access to other tubules by spreading laterally along the dento-enarael junction in every direction from the first point of entrance. Therefore, the tendency is to the formation of a conical area of decay with the point of the cone toward the pulp of the tooth and its base against the dento-enamel junction. The breadth of the cavity thus formed, in relation to its depth, will naturally depend upon the comparative rapidity with which the organisms may spread laterally along the dento-enamel junction. For this reason some cavities are broad and some are very narrow as compared to their depth. In the illustrations of this subject many "split teeth" will be used. In these the teeth are cut through the decayed area as shown in Figure 67. The cut surfaces are polished and the parts laid open like a book and photographed as opaque objects. The half-tone engravings are made from the photographs with- out any retouching whatever. In many cases only one of the halves has been used. The form taken by decay in dentin when it has begun in an occlusal surface is well shown in Figure 71, a photograph from a first molar split in half mesio-distally through the central pit, in which the decay began. The occlusal surface of the tooth before cutting is shown in Figure 68. Other photographs of molars showing decays which, to superficial observation, seem to be similar, are shown in Figures 69 and 70. In Figure 71 the wide spreading of caries along the dento-enamel junction forming the base of the cone, and the point of the cone reaching to the pulp chamber are well shown. This is the most common form. In this case, as in most cases of split teeth displaying caries, the cut surface is photographed as an opaque object. In examining such illustrations, it must be remembered that a section through a cone gives a triangular figure. Figure 72, a lower second molar that has been cut bucco- lingually, shows a decay that has begun in the buccal pit. This decay has proceeded very slowly. There is the same wide burrow- ing along the dento-enamel junction related above, and the effect of the continued irritation during the slow progress of the decay is seen in the reduction of the size of the pulp chamber by the deposit of secondary dentin. This condition, resulting from long continued irritation of the dentinal fibrils, is a common effect. It occurs also in abrasion and erosion. Careful observation has shown that microorganisms do not begin to grow into the dentinal tubules until the calcium salts CABIES OP DENTIN. 71 have been dissolved out for some little distance in advance of them. In the natural order of the advance of decay this is accomplished in the beginning by the percolation of acid through the enamel before the enamel rods have fallen away, so as to admit microorganisms to the dentin. This will be more clearly shown in considering caries of the enamel. Therefore, when they are admitted to the dentin, some portion of it has been softened and the organisms begin growing into the tubules at once. As they do so the acid which they are forming percolates into the dentin in advance, dissolving more and more of the calcium salts. ■ In this way it happens that the dentin is contin- ually softened in advance of the growing organisms so that there is a little space softened around them that contains none of the fungi. By removing all overlapping enamel carefully to give good opportunity, a thin, sharp spoon excavator may be passed closely along the hard dentin at the margin of the softened area and the decayed portion turned out, removing with it practically every microorganism in the dentin. As the microorganisms fill the dentinal tubules, the tendency is to become more and more crowded together and the tubules begin to be enlarged. In some cases this enlargement is a very regular increase in size along the length of the tubules, the outer ends of which are enlarged most, as shown in Figure 73. In other cases there is much tendency to irregular swellings of the tubules, as shown in Figure 74. Indeed, these two illustrations have been chosen as showing the extremes of regularity and of irregularity in this respect. Every variation between the two may be found. Also the number of side branches into which organisms may grow varies indefinitely; after passing a little way from the dento-enamel junction some cases show very few or even none at all, while in others they are very plentiful. This enlargement of the dentinal tubules continues until the division walls disappear, uniting two in one, three into one, and so on until there is nothing left but a mass of microorgan- isms mingled with some undissolved shreds of organic matrix, which, if the cavity is exposed to the saliva, wastes out and is washed away. This enlargement of the tubules and destruc- tion of the organic matrix is accomplished by the enzyme of the organisms. It is digested. Dr. Miller, in his examination of this point, decalcified teeth, cut them into slices, completely removed the acid by which the decalcification was done, and planted the fungus upon these as culture media. He found that they make a good growth without other nutrient material. 72 PATHOLOGY OP THE HABD TISSUES OF THE TEETH. "Within my personal observation, caries of dentin has seemed to progress most rapidly when closely shut in by overlapping enamel, and less rapidly when the opening to the fluids of the mouth was broad and ample. Finally, when the carious area is so flat as to be kept clean by mastication and is fully exposed to washings by the saliva, the decay ceases. The fungus is facultative anaerobic, growing ordinarily in the presence of oxygen, but having the faculty of growing quite as well in the absence of oxygen. It grows well in culture media when all oxygen is removed, and therefore grows as well when shut up in a deep cavity. In case the opening of the cavity becomes very broad while the cavity is yet shallow, the progress of decay is apt to be much slower. The explanation for this difference is that when the opening to the cavity is very broad, much of the acid formed by the microorganisms is washed away by the saliva. This must be considered a local factor. The intensity of the condition of susceptibility, which will be discussed later, must also be reckoned with as a general factor when considering the rapidity of caries. The progress of caries is limited, or even stopped, in a number of different ways. The crowding of meats into a cavity and the establishment of putrefactive decomposition, an occa- sional occurrence, is apt to end the progress of decay for the time, and leave the cavity with smooth, hard, blackened walls by the decomposition of all of the organic matrix from which the calcium salts have been removed. Decay may rebegin in this if conditions are so changed as to favor it. When most of the crown of a tooth breaks away, the prog- ress of caries will necessarily be across the length of the dentinal tubules, because these become horizontal on a level with the pulp of the tooth. If the organisms are prevented from entering the tubules from the pulp canals, the progress of decay will be very slow, or there will be no progress at all. WTien the pulp of the tooth has died and alveolar abscess in the chronic form is established with a free discharge through the root canals, the progress of decay is generally stopped as long as this condition continues. If, however, the apical portion of the root canal is choked by debris or otherwise closed, decay may proceed from the root canal, penetrate the tubules and rapidly hollow out the root to a conical shell and destroy it. The breaking away of the lingual or buccal wall of proximal cavities is often a factor in saving a tooth from destruction, especially among those people who live much on coarse food. CARIES OF DENTIN. 73 This has been found in the examination of some of the older Indian remains, especially of those tribes that were supposed to eat much parched corn. The food forced through the cavity in mastication and out through the broken side kept the surface worn smooth. The opportunity to know and to watch this among our own people occurs frequently. The question as to whether caries is produced by a single species of microorganism or whether a number of kinds are acting together is often asked. As to this, there are several organisms found in the saliva of practically every person that have physiological characters which seem to fit them for the production of caries, and no reason is known why they may not be acting together in the same carious cavity. Dr. Miller seems to have found them so. In the deepest portion of the carious area I have usually found but a single variety, the streptococcus. In the decaying mass, however, pretty much all of the varieties found growing in the mouth may be found and some of them penetrate deeply into the softened portion. Especially a white staphylococcus is often found deep in the dentinal tubules, if judged of by the difficulty of keeping clear of it in the effort to get a pure culture of the streptococcus from carious dentin. Note. — I have often spoken of this staphylococcus as the zigzag coccus, because of its habit of forming zigzags in its growth in broth. One coccus of a pair divides on the opposite pole from that upon which the pair has divided, making a square turn instead of a straight or curved line, as is the more usual habit of the strepto- cocci. This organism dissolves gelatin freely in artificial culture. It is frequently found in suppurating pulps and in alveolar abscess, yet it will generally fail to pro- duce pus when animals are infected with it. It is probably the white staphylococcus pyogenes modified by continuous residence in the saliva. The streptococcus spoken of above I have often called "caries fungus," or "streptococcus media," the latter because of finding larger and smaller varieties occasionally in the saliva. These are hardly found so continuously as to make the latter term a good one. 74 PATHOLOGY OP THE HARD TISSUES OF THE TEETH. CARIES OF ENAMEL. ILLUSTRATIONS: FIGURES 75-98. Caries of enamel, differs from caries of dentin in several important particulars. (1.) In caries of enamel, the microorgan- isms are attached to or lie upon the outside of the enamel. They grow and form the acid which causes caries of enamel in that position. They never enter the tissue until the enamel rods are loosened and fall out. The enamel is a solid into which micro- organisms can not penetrate. (2.) The enamel rods are cemented together hy a cementing substance which dissolves more readily in an acid than the rods themselves, and the first effect upon the . enamel is to dissolve out this cementing substance. The general rule is that in decays occurring on the smooth surfaces of the teeth, this cementing substance is dissolved through the entire thickness of the enamel before any enamel rods fall away. In some of the decays occurring in pits, the enamel rods themselves will be dissolved, enlarging the pit. (3.) The decaying spot upon the enamel is always whitened, as the first observable change. This change in color is sometimes not considerable and is very easily overlooked while the teeth are wet, but, when the teeth are dried and examined carefully, the color will be found to be a grayish white, or even very white in some cases, and the out- lines are often very clearly marked. (4.) In such spots an explorer is likely to catch if passed lightly over the surface, instead of gliding smoothly as it will on sound enamel. (5.) For these decays to occur, it seems to be necessary that microorgan- isms become attached to the surface of the tooth, grow there in the form of a colony, or in a zooglea formation, attached together in a gelatinoid matrix, or equivalent covering, and produce fer- mentative decomposition with acid formation at the spot, apply- ing the acid directly to the solution of the tooth. (6.) For this reason, the beginning of caries of the teeth occurs at such points as will favor such lodgment or attachment in which the micro- organisms will not be subject to such frequent dislodgment as would prevent a fairly continuous growth. This is the cause of the localization of the beginnings of caries on particular parts of the surface of the tooth. It had previously been supposed that caries of the enamel might be caused by acids dissolved in the saliva, or introduced with foods from the outside. This CAEIES OF ENAMEL. 75 idea, however, is no longer tenable. If caries of the enamel was caused by acids dissolved in the general saliva, we would not have that strict localization of decay that is found in the mouth. This localization is very important and should be very carefully considered. The points of localization are: (1.) Pits or fissures in the occlusal surfaces of the bicuspids and molars, in the buccal surfaces of the molars, and sometimes in the lingual surfaces also, and occasionally in the lingual surfaces of the upper incis- ors; (2) In the proximal surfaces of all of the teeth; (3) In the gingival third of the buccal or labial surfaces of all of the teeth, and rarely in the lingual surfaces also. Ninety-eight per cent of all of the decays that occur in the human teeth are located at the points included in this mention. Those beginnings of decay located elsewhere in the teeth are usually the result of accidental conditions, proving the accuracy of the rule; (4) The most prominent tendency to wide spreading of decay on the sur- face of the enamel is a direction that, when complete, encircles the tooth following close to the free margin of the gum. Hence proximal decays and gingival third decays spread most in these directions. The tendency in cases of unusual severity is for proxi- mal and buccal, and even lingual decays, to unite across the angles of the teeth, making a complete circle around the tooth near the free border of the gum. It may be laid down as a principle that for caries to begin in the enamel of the teeth anywhere, the caries fungus, which forms an acid, must be attached to the surface of the enamel in some such ivay as to prevent the acid which it forms from being readily washed aivay and dissipated in the general fluids of the mouth. Under all the observations of the surroundings of the occurrence of decay of the enamel, I fail to be able to form a conception of its beginning without the existence of some such conditions. But it is not insisted here that this must always be by the formation of zooglea or gelatinoid plaques. This may be produced in an artificial way by cementing a band on a tooth, as is done in orthodontia operations, and omitting the cement in a part of the area covered. If such a band remains long on the tooth, caries of the enamel will occur, even when the patient is otherwise immune to caries. This has been a matter of care- ful experiment by the author. It has also been observed in many orthodontia cases. Indeed, the amount of injury being done in this way during the treatment of irregularities, is giving rise to much complaint. 76 pathology of the hard tissues of the teeth. Penetration of Enamel in Pits. ILLUSTRATIONS: FIGURES 75, 76, 77. The beginning of caries in pits in the occlusal surfaces of three molar teeth is shown in Figures 75, 76, 77. It is not diffi- cult to conceive of a colony of the microorganisms present in the mouth, establishing itself within one of these pits and grow- ing there, producing acid sufficient to begin the solution of the cementing substance between the enamel rods. These would be covered with debris from foods that is forced in upon them, very completely shielding the acid formed from being washed away by the saliva. It seems to be true that there is a greater intensity of the action of the acid in caries of enamel in this position than in any other, for elsewhere it is very rare to see the carious process extending across the length of enamel rods, or a complete solution of any of the rods before they are loosened from the dentin. Caries usually follows accurately the length of the enamel rods in the penetration of the enamel in all axial surface positions. But in beginning decays in pits, we occasion- ally see progress across the length of the enamel rods, and in Figure 77 particularly, less distinctly in Figure 76, we may note that the pit has been enlarged at its deeper part by the solution of the enamel rods about its walls. This kind of showing occur- ring frequently, indicates that the locality is more completely isolated, or less disturbed by solution of the acid in the oral secretions than elsewhere, and therefore reaches the highest percentage of acidulation. It seems to be for this reason that in this position the rods themselves are often dissolved even before the carious process has extended into the dentin. The spreading across the enamel rods is, however, often more appar- ent than real, for about pits the enamel rods are all inclined toward the pits. It will be noted also, in the examination of these illustrations, that there is no sign of the carious process on the surface of the enamel outside the pit. It is confined exclusively to the walls of the pits and usually to the deeper part. Occasionally pits that are gradually narrowed from sur- faces much inclined, or in a funnel shape, will show caries extend- ing a little out of the pit proper, but this is unusual. This absence of superficial extension is because the surfaces immediately about the pits are kept clean, or reasonably clean, in the process of mastication; and further, because, if microorganisms were growing in such a position, they would be subjected to continual pit decays of occlusal surfaces. See Figs. 75, 76, 77. Photographs from split teeth showing progressively the beginning and progress of decay of the enamel in pits in the occlusal surfaces of molar teeth. Each illustration is from a different tooth. Figure 75 represents almost the earliest beginning of caries in the pit, shown by the whitening of the enamel of the walls of the pit, that can be distinctly recognized in a photograph. Figure 76 is a more distinctive showing of decay made by the deeper whitening of the enamel about the pit and the appearance of slight solution of its walls. In Figure 7 7 more decided advance has been made in the whitening of the enamel and loss of substance in the walls of the pit. The acid has, in this case, passed the dento-enamel junction and an effect in the dentin is seen. In this tooth there is also a smooth surface decay of the enamel beginning in the mesial surface, which has also been cut through centrally. This shows as a faintly whitened area, broad on th? surface and penetrating deepest in its central part. Its form is characteristic of smooth surface beginnings of decay of the enamel, and is placed here in sharp contrast with the forms of beginning decay of enamel in pits. Fig. 78. Caries of enamel. A wnite carious spot on the distal surface of a central has very sharp and definite outlines, though not very regular. Fig. 79. An incisor removed for a girl nine years of age, split through areas of decay and show- ing the broad pulp chamber of that age. A decay in the mesial surface had destroyed the pulp. In the distal surface there is an area of decay in the enamel, which, superficially, was similar to the one shown in Figure 78, but not so white. This is very typical of the form of these smooth surface decays of enamel in its conical shape, with the broad base of the cone on the surface of the enamel and the apex of the cone toward the dento-enamel junction. In this case the apex of the cone has just pene- trated the enamel. A little solution of the lime salts of the dentin has begun by the percolation of acid from the surface through the thickness of the enamel. No enamel rods have fallen away and no microorganisms have been admitted. Notice that a delicate hyaline zone fringed with shade streaks away toward the pulp, following the direction of the dentinal tubules. Fig. SO. A split lateral incisor, with a very white decay of enamel in its distal surface, showing a modification of the conical form of penetration. This has just penetrated the enamel, and the hya- line area, which may already be traced to the pulp chamber, is unusually dark for such a case. These areas of effect in the dentin beyond the area of actual decay vary greatly in light and shade. Pho- tographs of these tooth that has become differently. Fig. SI. greatly, because of differences in the translucency of different teeth. dry, becomes opaque and often fails to show these shadows, or shows them very narrow area of decay penetrating the enamel in the distal surface of a cuspid. In this the action of acid has been confined to a very narrow area of the surface of the enamel. The decay has reached the dentin, following accurately the length of the enamel rods. The enamel rods have fallen out of its central portion, microorganisms have been admitted and decay of the dentin has begun. Other parts of the photograph are indistinct because it was made when the tooth was dry and the surface opaque. For the same reason the hyaline area streaking inward toward the pulp does not show. Some translucence is necessary to snow these by photography. Fig. S2. A photomicrograph showing an area of decay in the enamel in the distal surface of an incisor. The incisal edge of the tooth is upward. All the illustrations from perpendicular sections have been so placed. The letter d is placed on the dentin, e. is on the enamel. The dento-enamel junction is between these two letters. x. The beginning point of the decay of the enamel. z. An extension of the superficial decay toward the incisal. The irregularity of the line of deepest penetra- tion is common, as seen in photomicrographs. In this figure the enamel rods in the decayed area have been disturbed in mounting, distorting the edge representing the surface of the tooth. Areas of decay which show white by reflected light are opaque and show dark by transmitted light. Fig. 83. A photomicrograph of a small area of the beginning of caries in enamel that shows an unusually smooth rounding of the deep line of penetration. d. Dentin. e. Enamel. The dento- enamel junction is between these two letters. x. A distinct swelling of the decayed area. This swelling is common in areas of decay in enamel. Fig. 84. Caries of enamel. d. Dentin. e. Enamel. x. Area of decay. In this figure the outer ends of the enamel rods have been broken away in grinding. Notice particularly the flamelike tongues of penetration sweeping toward the dento-enamel junction, following the lines of the length of the enamel rods. Also the penetration on the margins of the principal area are seen to follow the lines of the length of the enamel rods. This rigid following of the enamel rods is a characteristic of caries of enamel beginning in smooth surfaces. Fig. 85. A broader and flatter area of carious enamel. d. Dentin. e. Enamel. I. Area of decay. Here also we find the same inclination to the formation of flamelike tongues sweeping toward the demo-enamel junction, following the length of the enamel rods. There is no spreading of decay across the length of the enamel rods. All spreading is in new beginning's to the side on the surface of the enamel. CABIES OF ENAMEL. 77 washings by the saliva, which would dissipate the acid formed. Therefore, decays of the enamel, beginning in pits, are in the form of a cone, having the base on or toward the dento-enamel junction, and the apex toward the surface. Peneteation of Enamel is Peoximal Subfaces of Incisoes. ILLUSTRATIONS : FIGURES 78-85. The conditions are entirely different on the smooth surfaces of the teeth, as the proximal surfaces. Here there is no pit or fissure, depression or fault in the enamel. It is a smooth, rounded surface. The teeth round together normally in such a way that the interproximal gum tissue fills the space to the contact point, and the contact point proper is fairly well rounded in most cases. "While this condition continues perfect, there is no place for the lodgment of microorganisms upon the proximal surfaces, but, whenever the gum tissue fails to fill this space completely and a little opening is left to the gingival of the contact point, it forms a harbor or nidus at which microorganisms may lodge and begin their growth. It is probable that by this growth alone they may have something to do with forcing the gum tissue a little bit further away, and, if they are sufficiently protected from wash- ings by the saliva, they may form sufficient acid to produce an action upon the calcium salts of which the enamel is formed. Figures 78-81 are a group showing the manner of the pene- tration of enamel by caries in the proximal surfaces, as may be well seen in split teeth with an ordinary hand magnifier. Fig- ures 82-84 illustrate the same thing in photomicrographs* pro- duced by low powers of the microscope. The first beginning of decays upon these surfaces is often small, as is shown by Figure 78, a photograph of the distal surface of a central incisor with the spot of beginning decay very exactly in the position men- tioned, just to the gingival of the contact point. This was a very white spot on a tooth that was rather dark in its general color, so that the engraver has been able to show it very distinctly. "We might ask here, by what power, circumstance or condition has the action of the acid been confined to this one small spot, while all the rest of the surface of the tooth is free from any action of the acid? * The difference between the photograph and the photomicrograph, constantly- observed in their use in this work, is that the photograph is taken from an opaque object by reflected light, while the photomicrograph is taken from a thin section by transmitted light. Usually the object is much less enlarged in the photograph. 78 PATHOLOGY OF THE HAED TISSUES OF THE TEETH. Figure 79 is a photograph from a central incisor that has been split mesio-distally through a white spot upon its distal surface but little larger that the one shown in Figure 78. In this we see the penetration into the enamel in the form of a some- what flattened cone, or a cone with a broad base on the surface of the enamel, and the point just reaching through to the dento- enamel junction. As we will see quite distinctly later, in caries of the enamel more highly magnified, the solution of the cement- ing substance between the enamel rods follows directly the length of the enamel rods and continues spreading upon the surface from a spot of much smaller beginning than that now seen. At the central beginning point, or nidus, the effect of the acid has reached through the enamel to the dentin and is beginning to dissolve it, while the depth of penetration is less and less about that central point in every direction, until it runs out to quite a thin edge at the surface of the enamel. This is characteristic of beginning decays in enamel upon all of the smooth surfaces of the teeth. They begin at a central nidus, or beginning point, and spread sometimes in every direction, but generally spread most in some particular direction from that beginning point, as will be described later. Not infrequently decay begins at several points close together in a more or less even row, which takes some particular direction. In Figure 80 we have another illustration similar to that in Figure 79, also a photograph from a lateral incisor, cut mesio- distally, with a cavity in the distal surface. This was a very white decay and shows to advantage. It will be seen that there has been considerable spreading both ways from the central nidus, and that the central portion has just penetrated to the dento-enamel junction and is quite a little in advance of the general conical form of the invasion of the enamel. Decays occur, however, that show very little or none of this spreading upon the surface, even upon the proximal surfaces of the teeth, as will be seen from an examination of Figure 81. The tooth is a little more enlarged in order to show this spot to better advan- tage. Here it will be seen that a cavity has formed in the enamel. Some of the enamel rods have fallen out and the effect of the acid has passed entirely through the enamel and begun to dis- solve the calcium salts from the dentin, and yet the opening, or the area, of the enamel affected, as seen in this dimension (the tooth having been cut mesio-distally from occlusal to gingi- val), is no larger than the shaft of a large pin. The enamel rods have been exactly followed lengthwise, and the enamel about CARIES OF ENAMEL. 79 it seems free from the action of acid. Again it might be asked : By what power, circumstance or condition has the action of the acid been confined to this narrow area? This following of the enamel rods is better seen in photo- micrographs, in which the enlargement is only just sufficient for the direction of the enamel rods to be made out. If a very high power is used, a sufficient area of the tissue of the tooth can not be included in the picture to give a correct idea of the general form and relation of the different parts. It must be understood that a decayed area that is white to reflected light, shows an opacity to transmitted light and is dark in the photo- micrograph unless it is ground excessively thin. This group of sections, Figures 82, 83, 84, 85, are all cut from occlusal to gingival. Beginning decays of the enamel cut in this direction show but little superficial spreading as compared with that seen in cross section, which will be given later. The characters as to penetration, however, are the same, only less extended laterally. Figure 82 is a photomicrograph from a lateral incisor with a beginning decay of the enamel that was very similar to that shown in the photograph, Figure 80. The form of the penetration and of the spreading on the surface are quite remarkably alike in the two cases. There has been a little disturbance of the injured tissue by crushing it together just above x forming the notch midway between x and z. There has also been some loss of the outer ends of the enamel rods from this notch to the letter z, but the main feature of the illustration, the line of penetra- tion, is in perfect form. The starting point of the decay was about the position of the letter x, and it has spread superficially in both directions. In this case, the spreading has been most toward the incisal angle, as was the ease in the photograph, Fig- ure 80. The tendency of the line of invasion to be broken up into flamelike tongues shooting forward of the general line may also be noted. Figure 83, a photomicrograph from a proximal decay, is almost unique in the smooth roundness of its deeper portion. It shows almost none of the flamelike tongues shooting toward the dento-enamel junction that are common characteristics of the deep border of advancing caries of enamel. The accretion lines of Betzius are brought out much more clearly in the decayed area. This is quite general when the direction of the section is squarely across them. In many instances, however, this seems not to occur. The swelling of the decayed area is well seen at x. 80 PATHOLOGY OP THE HARD TISSUES OF THE TEETH. This is constantly seen in decays at this stage when no enamel rods have been lost during the preparatory work. Figure 84 is a photomicrograph from a proximal decay of the enamel at x, which is very narrow on the surface and pene- trates almost to the dento-enamel junction at the point of the cone. This cone is of somewhat irregular outline. In this case the outer ends of the enamel rods were lost in grinding. Notice particularly that at different points the tendency is for decay to advance in little namelike tongues or projections, each fol- lowing the length of the enamel rods. This is a characteristic of caries of enamel, and often, when examined in the very early beginning, the starting points are divided from each other with these little namelike tongues projecting inward toward the dento-enamel junction. This is seen also in Figure 85 in a decay at x, which is much broader and natter, showing less of the coni- cal form. In this, a nidus, or beginning point, upon the sur- face of the enamel has been just above the letter x, and it has spread quickly over the surface to the gingival and the occlusal of this point by the increase in size of the growing colony of microorganisms on the surface. Each new beginning, with indi- vidual enamel rods, or groups of rods, follows exactly along its length toward the dento-enamel junction. Other illustra- tions will show this tendency more prominently than these two. In examining many photomicrographs of caries of the enamel, we find this tendency constant and the following of the length of the enamel rods very rigid. We never find caries of the enamel spreading laterally in the interior of this tissue. It always goes straight from its starting point to the dento-enamel junction and then spreads out in the dentin. In order for decay to spread out, involving a larger area of enamel laterally in any direction, the spreading must be in the form of new beginnings on the surface. In other words, all spreading of decay of enamel from the beginning point is brought about by conditions which allow of growth and spreading of colonies of microorganisms on the surface of the tooth. No matter how broad the carious area, it projects inward in these little flamelike tongues along its deeper border. Therefore, decays of the enamel, beginning in smooth surfaces, are generally in the form of a cone, having the base at the surface of the enamel, and the apex toward the dentin. caeies op enamel. 81 Superficial, Spreading op Caries in Proximal Surfaces op Bicuspids and Molars. illustrations: figures 86-95. We pass now to the superficial conditions as seen in the proximal surfaces of the bicuspids and molars. If we examine the whitened outlines seen upon the surfaces of the teeth before any enamel rods have fallen away, we will find these decays taking certain definite forms by reason of spreading, and often starting at several points instead of at one central nidus. A knowledge of these forms and the reasons for them, is of great importance in the treatment of caries. The group of illustrations, Figures 86-89, inclusive, shows the principal varieties of form produced by the spreading bucco- lingually of beginning decays in the proximal surfaces of tha bucuspids as seen in whole teeth. This tendency is practically the same in the molars, as seen in Figure 91. These may be confined to a round spot, as is often the case in the incisors, as shown in Figure 78, but the more general tendency is to spread buccally and lingually from the beginning point. This is shown progressively in the different pictures of this group and illus- trates the common tendency of caries of the enamel to spread in these particular directions. Occasionally the tendency to spread gingivally is seen, as is illustrated in Figure 90. The cause of this will be more explicitly discussed later. It should be noticed particularly here that the tendency is to spread bucco- lingually rather than gingivally, though, as will be shown later, wide spreading gingivally occurs under certain conditions. Spreading occlusally does not ordinarily occur, because that part of the surface from the contact occlusally is cleaned by mastication. As we shall see later, decays that begin much to the gingival of the contact point may spread occlusally. These beginning decays are characteristic of the surface areas of beginning decays in the proximal surfaces in the bicuspids and molars. It will be readily seen that if the cut is made horizon- tally instead of lengthwise of the tooth, as in split teeth herein before shown, the area of decay presented would be very dif- ferent. In the group of illustrations, Figures 92-95, inclusive, cross sections are shown illustrating the conditions from that view. Here, instead of the narrow area of decay seen in the whole teeth, as in the group 86-91, the teeth are cut crosswise through similar areas of decay. These have the additional value of show- 82 PATHOLOGY OF THE HAED TISSUES OF THE TEETH. ing both the spreading buccally and lingually and at the same time the penetration of the enamel along this line in its rela- tions to the individual teeth as a whole. In three of the four figures, the decay has spread across the proximal surfaces to the rounding of the angle which opens the embrasures, both to the buccal and to the lingual, practically before decay of the dentin has begun. Figure 92 is from a mouth with thick necked, squarely built teeth, in which the lingual surfaces of the second bicuspids are equally broad with the buccal, and with very fiat proximal surfaces. On the distal, the decay reaches fully from angle to angle. It is easily seen in this that there were two nearly equal beginning points which have run together on the surface, but are still divided in the deeper part. On the mesial surface, it is noted that the original beginning was much to the lingual at the point where whitening completely penetrates the enamel for a little space. The spreading is toward the buccal and toward the lingual from that point. It spreads a little around the mesio-lingual angle but does not reach the mesio- buccal angle. It is easy to determine by this that the position of the first bicuspid was abnormally to the lingual of the line of the arch. This gave the opportunity for decay in this unusual position. It was prevented from reaching the mesio-buccal angle by the cleaning of this part by excursions of food crushed along this portion of the surface in mastication. In Figure 93 there has been an unusual number of very small beginning points forming a line which had just fused together by the superficial spreading. It is particularly inter- esting from that fact. The tooth seems out of form for the reason that the decayed side was cut farther from the occlusal surface than the sound side. Figure 94 shows an area of decay on the distal surface of a molar that is of the more regular type, showing a solid advance of decay of the enamel, except as it thins out at the angles of the tooth. This photograph gives in relief, to speak figuratively, the reason for many cases of recurrence of decay after filling. The cutting had been carried to hard enamel, but not far enough to remove the thin portion of the decay spreading farther around toward the angles. If the filling were finished without sufficient separation of the teeth having been made, so that a little of the mesio-distal breadth of the tooth was lost, the area of near contact was increased by that much, giving better opportunity for decay to rebegin. Therefore, the filling is quickly undermined. Many of the beginning decays observed in the proximal sur- Figs. 86, 87, 88, 89. Photographs from four bicuspid teeth with superficial proximal decays. To show distinctly the gingival line, the first two have been stained slightly with eosin, which does not stain the enamel. The four teeth have been arranged to show progressively the disposition of caries to spread bucco-lingually on the proximal surfaces of these and the molar teeth. While decay is apt to begin first just to the gingival of the contact point and is confined between that and the free border of the gum oecluso-gingivally, it is free to spread bucco-lingually as far as the sweep of food through the embrasures, formed by the rounding of the angles of the teeth away from each other, will allow. In Figure 86 the area bucco-lingually is very narrow. In Figure 87 a little broader, and in Figure 88 it reaches fully to the embrasures. In Figure 89 something of the disposition of decay to begin at numbers of small points along this bucco-lingual line, is seen. Flu. 90. A bicuspid in which there is seen a disposition to broader spreading occluso gingivally. Sometimes this is very extensive, as will be illustrated later. Fig. 91. An upper molar in which is seen the same disposition to spread bucco-lingually as occurs in the bicuspids. This form of spreading is common to the bicuspids and molars. In this case the enamel rods have fallen out of a small area at the point of first beginning. CABIES OF ENAMEL. 83 faces are of much less extent than in these three figures. Indeed, the general rule is that the enamel rods have fallen away in the central area quite a little before the spreading has reached its bucco-lingual limit. In this case, the spread of decay in the dentin, along the dento-enamel junction, backward decay of the enamel and breaking away of enamel, so change the conditions as to stop the superficial beginnings in the enamel. Figure 95 sufficiently illustrates this. In this case, the spreading bucco- lingually is not yet great, but the decay has penetrated the enamel at two minute points, and solution of the calcium salts of the dentin has begun. In a little more time the enamel rods would have fallen away from all of the central part of the area and so changed the conditions that the superficial spreading of caries would have ceased. A Closer Examination of the Injury to the Enamel. ILLUSTRATIONS: FIGURES 96-98. Before studying further the cause of the localization and tendency to the spreading of caries in particular directions on the surface of enamel, it may be well to examine more closely the injury produced. For the illustration of this, the photo- micrographs have been taken from thin sections of decays begin- ning in the enamel that were in every way similar to those shown in other illustrations, but with an amplification that is sufficient to display the condition of the tissue without being excessively magnified. This enables a larger area of tissue injured, in com- parison with the uninjured tissue, to be shown on the ordinary book page than seems practicable with a higher amplification. In Figures 96, 97, special preparation of the tissue has been made to show the removal of the cementing substance from between the enamel rods by filling the spaces left with common yellow shellac, which takes dark in the photomicrograph. Figure 98 is without this. In Figures 96, 97, which are both from cross sections, but from different teeth, the darker portion marked with the letter x is the injured enamel, while that portion marked by the letter e is uninjured. In each case the border line between the injured and uninjured tissue is dark. The sections from which they were made were prepared as follows : (1.) The cross section of the tooth was ground flat and polished. (2.) It was then placed in absolute alcohol for twenty-four hours to remove all traces of water. (3.) It was placed on a cover-glass which was covered with a solution of ordinary yellow shellac in abso- 84 PATHOLOGY OF THE HAKD TISSUES OF THE TEETH. lute alcohol, which had been filtered to free it from all insoluble particles. (4.) It was allowed to lie in an abundance of the shellac solution for several hours. (5.) It was then placed on a steel disk and the specimen was clamped down onto the cover- glass with a heavy weight, the excess of shellac removed and then left until the shellac had become hard. (6.) The cover-glass to which the specimen was attached was then cemented to a grinding-disk, which was placed in the grinding machine and tbe specimen ground thin enough for examination with a twelfth- inch immersion lens. (7.) The glass, with the specimen, was then removed from the grinding-disk and at once mounted upon an ordinary slide, using for the purpose xylol balsam, which does not dissolve the shellac by which the section is attached to the cover-glass. In this way, every part of the frail tissue is retained in its normal position. From the photomicrograph of this the engraving is made without the slightest retouching. It is seen by examination of the illustrations that the spaces, formed between the enamel rods by the solution of the cementing substance by the acid causing the injury to the tissue, have been filled by the shellac, which photographs dark. This divides the carious area, marked by the letter x, sharply from the sound tissue, marked by the letter e, and displays the enamel rods, or the undissolved central portions of them, lying in a dark field, each in its normal position. The adjacent undecayed enamel does not absorb the shellac and remains white. In Fig- ure 96 the sound enamel shows scarcely a trace of structure, while in Figure 97 the enamel rods in the sound tissue are very well brought out. This difference in unetched sound enamel is often met with. In both specimens the area decayed is also sharply divided from the normal enamel by a broad, dark band, which occurs in many specimens in which no shellac has been used, as will be seen in most of the photomicrographs of decayed enamel in this volume. If we examine carefully these illustrations as to the com- parative sizes of the enamel rods in the undecayed and the decayed areas, it is found that they are much reduced and more slender in the decayed areas. This may be made out also in Fig- ure 98, which has not been filled by shellac, but not so clearly. In the grinding of this latter specimen, the machine was adjusted to stop when the specimen was one one-thousandth (1-1,000) of an inch thick. Such specimens are extremely frail. When the solution of the enamel rods has gone a little further than shown in these illustrations, the whole structure falls to Fig. 92. A cross cut of a bicuspid crown showing decay on both the mesial and distal surfaces. This has the advantage of showing the spreading of the decay bucco-lingually in its relations to the angles of the teeth. On the right side of the picture the spreading of decay is from angle to angle ; indeed, somewhat around the curve on the lingual. Also the decay is seen to have begun at several points along the line from buccal to lingual. Some solution of the calcium salts of the dentin is in progress, though no enamel rods have fallen away and microorganisms have not been admitted. A broad area of decay is shown in such an illustration, because the cut is along the length of greatest spreading on the surface. A section lengthwise of the tooth would show a narrow area of decay. On the left margin of the illustration, the area of decay is not central because the first bicuspid was in lingual occlusion. Hence the anomalous position of the beginning of decay. Fig. 93. A cross cut of the crown of a bicuspid with a decay that has begun at a number of points, which have penetrated the enamel separately, leaving some areas of sound enamel between them at the time of extraction, but on the surface all had united. Fiq. 94. An upper first molar cut across the crown, showing a solid area of caries of the enamel stretching buccolingually from angle to angle of the distal surface, which has just reached the dento- enamel junction at one point. One should note especially the thinning out to the surface of the decay of enamel rounding slightly toward both the buccal and lingual angles, and the amount of sound enamel that would have to be removed in order to remove the hist of the carious enamel in the prepa- ration of such a case for filling. Fig. 95. An upper first molar with a less extensive decay of the enamel, which has reached the dentin at two points. In this case the beginning of the decay was much further toward the gingival line than usual, and the enamel is very thin. Fig. 96. A photomicrograph showing a portion of a section of enamel in which caries has pro- gressed part way through its thickness. e. Enamel that is perfect. x. Decayed enamel. The decayed portion of the enamel has been filled with yellow shellac, which has taken the place of the cementing substance dissolved out from between the rods, and takes dark. The sound enamel, being solid, does not absorb the shellac. The plan of doing this is given in the text. In this particular section not much of the structure of the enamel can be seen in the undecayed portion. Fig. 97. A photomicrograph of enamel in which caries has made considerable progress. d. Dentin. e. Enamel. r. Carious enamel. The dento-enamel junction is seen between d and e. In this case, the enamel rods appear fairly well in the sound enamel and a considerable irregularity in their course may be observed. The decayed area is filled with yellow shellac. The enamel rods appear smaller in the decaved area. CARIES OF ENAMEL. 85 pieces at a touch, and most generally through the whole thick- ness of the enamel at once. This seems to be due to the complete loosening of the ends of the rods from the dentin. In unpro- tected places, however, such as decays of buccal or labial sur- faces, and decays of proximal surfaces in which there has been interference by the crowding of food through the contact, a considerable number of cases are found in which the outer ends of the enamel rods are broken before the enamel has been pene- trated. In the greater number of cases, however, in any of these positions, a considerable solution of the dentin has occurred by the acid which has penetrated through the enamel before any enamel rods have fallen away. This is well attested in many of the illustrations presented. The Relation op the Occlusion to the Localization of Caries. ILLUSTRATIONS: FIGURES 99-103. When we come to study carefully the forms of the teeth in their relations to each other as they stand in the arch, and their uses in the mastication of food, we find that there are certain points or areas of their surfaces that are comparatively free from rubbing, or abrasion, while much the larger part of the tooth surface is exposed to friction and washings by the fluids in the mouth. The occlusal surfaces particularly are exposed to severe abrasion in the mastication of food. The lingual surfaces, both above and below, are exposed to the fric- tion of the tongue and of the food that is washed over them during mastication, so that these surfaces are fairly well cleaned. The buccal surfaces are less exposed to friction during mastication and to washings by the saliva during the motions of the tongue, cheeks and lips, particularly in their gingival thirds. The proximal surfaces are shielded from abrasion and from washings by the saliva by the contact and areas of near approach of these surfaces with adjoining teeth. Decays begin- ning in the depths of the pits of the occlusal surfaces have no opportunity to spread upon the surface of the enamel, for the reason that these surfaces are so continually cleaned by abra- sion in mastication and by washings by the saliva. It seems to be for these reasons, principally, that decay does not spread superficially upon these surfaces. It is prevented by the forms and the uses of the teeth. It seems to be purely these local con- ditions that are the basis of the strict localization of the begin- 86 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. nings of dental caries in certain positions in the enamel to the exclusion of all others. These are physical conditions controlling lodgments of debris. They are also physical conditions prevent- ing the removal of anything which may become attached to the enamel in these positions. If we study the relations of the proximal surfaces of the different teeth to each other, we find that various forms of con- tact and near approach of these surfaces serve to .shield certain areas from all friction from mastication and in which the deposit of a very little gummy material will shield colonies of micro- organisms from all washings by saliva. This may be studied in the illustrations. Figures 99, 100, show the buccal and the occlusal surfaces of the upper bicuspids and molars as they stand in the arch. The teeth are in the same relation to each other in each figure. The soft tissue filling the interproximal spaces has been removed in order that the forms of these may be better seen. In studying the buccal view, it will be seen that the points of near approach of surfaces are very narrow and rounded in form from occlusal to gingival, so that the actual touch point of unworn teeth is very small, like that of two mar- bles coming in contact, while, in the view of the occlusal surfaces, the points of near approach of the teeth to each other are shown to be very much broader in the bucco-lingual direction. The decays in the proximal surfaces of the bicuspids and molars, in Figures 86-91, inclusive, correspond in form with the areas of near approach of the surfaces of the teeth so closely and so constantly that we must connect these relations as cause and effect, controlling both the localization and superficial form of the beginning and spreading of caries in the enamel. To gain correct expressions of this, the study must be confined to those beginnings of decay that have not yet penetrated the enamel, or in which the enamel rods have not yet fallen out, for, with the breaking away of the enamel after decay of dentin has begun, the particular form of the beginning upon the surface of the enamel is often quickly lost. A study of the forms of the surfaces making the contact of different teeth as seen in the occlusal view, will show great variations in the bucco-lingual length of near approach of these surfaces. The area of near approach of surfaces is much longer bucco-lingually between the second bicuspid and the first molar than that between the two bicuspids. Therefore, a beginning decay between the second bicuspid and first molar will spread and become longer bucco-lingually in these than a beginning Fia. 98. A photomicrograph from a very thin section of carious enamel ground on the cover glass in hard balsam. b. Perfect enamel. X. Carious enamel. The line between the sound and carious enamel is fairly sharp, and follows closely the leng-th of the enamel rods. ** * xk -** r*S, %* Fias. 99, 100. Photographs of the upper molars and bicuspids of the right side in their norma) relations to each other, with the soft parts removed to show the interproximal spaces, interproximal contacts and areas of near approach of the surfaces of the teeth. The two pictures taken together, the first showing the buccal surfaces and the second the occlusal surfaces, give a good view of the inter- proximal spaces, breadth of contact orehiso gingiva lly, and breadth of near approach of surfaces bucco-lingually, with their variations. They also show the openings of the embrasures buccally and lingually, with their variations in depth. CARIES OF ENAMEL. 87 decay would do between the two bicuspids. Tbe differences in this respect among the teeth of the same mouth, and especially among the teeth of different mouths, are very great. As this study of forms of contact and near approach accounts for the differences seen in forms of decay in this respect, as shown in illustrations given of the bicuspids and molars, Figures 86-91, inclusive, it also accounts for the differ- ences shown of the breadth of decay in illustrations made from cross sections of the teeth, Figures 92-95, as compared with sections made lengthwise of the tooth. A section made length- wise of a tooth may show a very narrow injury to the enamel, while, if the section were made crosswise of the tooth, cutting through the length of the injury, it would show a very broad beginning of decay. This will be seen more clearly by a com- parative examination of sections cut in these different directions which show the great difference in the form and extent of the injury to the enamel. This will be appreciated hy comparing the cross sections, Figures 92-95, with the photographs of split teeth, Figures 107, 108, 112, 113, 117. The embrasures, or the openings formed on the buccal and on the lingual by the rounding of the surfaces of the teeth away from each other, vary greatly in depth among the different embrasures of the same mouth, and particularly they vary in depth among the teeth of different persons, owing to the forms of the teeth and the form and prominence of the proximal con- tact points. It must be remembered that in normal conditions in young people, the interproximal space is filled with gum tissue to, or very nearly to, the contact point, and that the gum tissue arches up to this from the buccal and the lingual. In studying this, it will be found that the beginning of decay is close to the line of the margin of this arch of gum tissue, and it does not spread to the gingival unless the gum tissue has been pushed away by lodgments of food between the teeth. There- fore, unless lodgments of food have occurred, the forms of beginning decay will retain that narrowness from occlusal to gingival that has been shown, and the spreading bucco-lingually will generally coincide with the length of the close approach of the surfaces to each other. If we study the teeth in their occlusion under normal con- ditions, we will find a provision of very considerable importance in the relation of the cusps of the upper teeth to the embrasures between the lower teeth, and, vice versa, the arrangement of the cusps of the lower teeth with respect to the embrasures in 05 PATHOLOGY OF THE HABD TISSUES OF THE TEETH. the upper teeth. This will be seen in Figure 101. Beginning with the third molars, we find that the cusp of the lower third molar occludes directly under the embrasure between the second and third molars of the upper jaw and will force food through that embrasure especially, while the second molar of the upper jaw has its distal cusp over the embrasure between the second and third molars of the lower jaw and will force food through it. This arrangement is repeated among all the molars and bicuspids. The result is that, in mastication, the food is caused to run through the embrasures by the crushing action of the teeth. The effect of this arrangement will perhaps be better understood by comparison with the occlusal surfaces of the same teeth as seen in Figures 102, 103, noting carefully the forms of the individual embrasures and their variations. This abrasive action by the food is increased by the cheeks and tongue also pressing upon the food laterally, causing it to be crushed down over the buccal and lingual surfaces of the teeth, and more par- ticularly through these embrasures. In fact, this lateral pres- sure on the food is an endeavor to hold it between the occlusal surfaces of the teeth. The result is that the food is forced through the embrasures especially, causing it to rub the angles of the teeth from their occlusal surfaces to the gum margin. This abrasive action of the food serves to limit sharply the distance that attached colonies of microorganisms may spread toward the buccal or lingual angles of the teeth because of their removal from the surfaces by the passing of food through these embrasures during mastication. It also explains another fact of great importance in the treatment of caries of the teeth by filling, for it was found by actual count of ten thousand persons examined that only in about one case per thousand, decay was found to have spread superficially, or upon the surfaces of the teeth, across the angles. Therefore, near to, or along these angles, is the safest place to lay cavity margins. Caries never regins on the angles of the teeth nor spreads superficially past these angles in any case in which the teeth are in normal relations and the person is making active use of them in mastication ; this may be stated without fear of successful denial. All of the cases of such spreading that have come under my observation in twenty-five years of close study of this point, have been in persons who have practically ceased to use their teeth in the mastication of food because of some interference. This has generally been sensitiveness of exposed pulps in decayed teeth, and at the same time the persons had CABIES OF ENAMEL. 89 become entirely careless as to artificial cleaning. The study of this phase of the spreading of caries and its limitations is of the utmost importance. The student and the practitioner should be continually studying it in the mouths of his patients, making out carefully areas of spreading decay and their normal limitations under the conditions which he finds. This, if carefully carried out, will serve as a guide of great importance in the extensions necessary in the preparation of cavities to prevent recurrence of decay about cavity margins. In the consideration of the beginning of caries of the enamel with reference to treatment, it may be stated, as a fundamental proposition, that the nidus of each beginning of caries will be found at that particular point on the surface of the tooth attaclced, or that may be attached in the future, that offers the best position for the lodgment and undisturbed growth of colo- nies of microorganisms. These colonies and the caries will spread superficially on the surface to those lines where their further spread is limited, (1) by the position of normal gum tissue; (2) by abrasion of mastication by excursions of food through the embrasures; or (3), by artificial cleaning. "When this nidus is destroyed by the falling away of the enamel rods because of caries of the dentin, before such spreading has reached its limit, as often happens, the conditions are usually so changed that the growth of colonies on the surface of the enamel is prevented. This at once limits further superficial spreading buccally and lingually on the lines thus far illustrated. Further superficial spreading gingivally, may or may not occur, as will be illustrated later. The lateral superficial spreading seems to be stopped by the frequent catching of stringy foods on the roughened area and the worry of the parts in its removal, or by the frequent forcing of these lodgments further to the gingival at each meal time. In many of the cases the loss of the central and best attachment of the organisms may of itself be sufficient to produce this effect. However this may be, much careful observation shows that after the opening of the cavity this stoppage occurs in many cases. But if a good and perfect filling is made, restoring the original form and conditions with- out reference to the possible further spreading of the growth of colonies of microorganisms, such filling will reestablish the nidus for growth and this will jrecur on the filling and extend to the full limit that it might have done if the original nidus had not been destroyed, thus reestablishing caries beyond the margins of the filling. In this way, a well-made filling in the mechanical 90 PATHOLOGY OF THE HARD TISSUES OP THE TEETH. sense, restoring the original contour perfectly but without ref- erence to the superficial spreading of caries, may become the cause of wider spreading of decay on the surface than would have occurred without it. Further, in practice, it will be found that when proximal fillings are made without separating the teeth to gain room for the finishing of the fillings to the full original contour, with the original fullness of the contact points, but necessarily losing a little of the original mesio-distal breadth, the area of near approach of the proximal surfaces is increased, the embrasures are made shallower and the opportunity for recurrence of caries at the bucco-gingival and linguo-gingival angles of fillings is increased. Penetration of the Enamel in Buccal and Labial Surfaces. Caries beginning in the buccal and labial surfaces presents the same characters as to penetration of the enamel and spread- ing in definite directions as decays beginning in the proximal surfaces. In this case the line of beginning is along the free margin of the gum in the middle third of the surface mesio- distally. The lines of extension in spreading are toward the mesial and the distal angles of the tooth. The beginning of these decays often forms a narrow whitened line, the length of which is from mesial to distal. These, taken with the decays of the proximal surfaces, tend to form lines encircling the teeth along the free margins of the gum. This is very generally defeated by the failure to spread across the angles of the teeth. But when the angles are passed and when connected by decay on the lingual surfaces, which sometimes occurs, the complete girdling of the teeth is accomplished. Frequently we may find, in the first beginning of the decay on buccal surfaces, several starting points which later run together, forming a continuous line of whitened enamel. This gives, in cross sections of the tooth, appearances almost exactly similar to those shown in Figures 92-95, inclusive. As the very general rule, the extension of decay on the surface of the enamel is stopped at the mesial and distal angles of the surface. While these decays occur in a much less number of persons than proximal decays, they often attack tooth after tooth in quick succession, and progi'ess very rapidly in the enamel, destroying considerable areas of enamel tissue. They become wide-open cavities, and, in the mouths that have very little care, are apt to run a rapid course. This subject will be presented in greater detail under the heading, "Caries as a Whole," Fig. 104. Photograph of a split upper first molar with an occlusal decay of ordinary form. Note a small beginning of decay of enamel in the distal surface, and a decay beginning in the cemen- turn. This latter is characteristic of decays which occur because of crowding of food into the inter- proximal space, with resulting absorption of the interproximal gum tissue. Figs. 105, 106. Photographs showing decays in occlusal pits, in which the opening through the enamel has become larger and the decayed areas are of less depth in proportion to their breadth. Some proximal decays are also shown. CABIES AS A WHOLE. ITS CLINICAL FEATUREa 91 CARIES AS A WHOLE. ITS CLINICAL FEATURES. In the further consideration of the injuries inflicted by caries of the teeth, we may include caries of both the enamel and dentin. In this we may consider the processes as a whole, noticing the various characters presented in the beginning and progress, controlled purely by local or clinical conditions. These conditions have no special signification as to immediate or remote cause of caries further than location or condition of tissue which may influence the action of these causes. Yet these causes which are brought into action, seemingly because favorable conditions for their active development have been presented, can not be lost sight of in any consideration whatever. It may truly be said that, without the presence of the principal causes no decay could occur, and also that, without reasonably favorable conditions for their action, these causes would not produce decay. This may be said to constitute the clinical features of dental caries, and in its consideration frequent reference will be made to the clinical management of cases. One of the surprising features of the study of dental caries that comes sharply in view when the history of the development of our knowledge of it is closely scanned, has been its complete divorcement from all clinical consideration. It seems to be correct to say that a large number of even the most earnest workers in dentistry are doing their work of treatment by rote, without any proper thought of the relations which their plan of treatment may bear to the conditions that have localized the decay being treated at that particular spot, and making inadequate provision, or too often no provision at all, for the prevention of a recurrence of the trouble. It is only recently that there has been any special study given to the conditions of the beginning of caries of the enamel, which really is the all-important question in the study of dental caries considered from the clinical standpoint. One of the noblest pieces of scientific work in pathology was Dr. W. D. Miller's investigation of dental caries. It not only developed the questions at issue, but completed the investigation so that the rest of us, in repeating his experimental work, could only say, well and correctly done. But this investigation was con- fined exclusively to the immediate active cause of caries as it occurs in dentin. Decay of enamel, or the conditions localizing 92 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. beginnings of this, which constitutes the initial lesion, without which caries of dentin never occurs, was left untouched. These constitute the principal clinical features of the disease we are treating. Our knowledge of them is, as yet, but partially devel- oped, particularly in that the systemic conditions of suscepti- bility and immunity are but indefinitely known; and observers do not yet agree as to the especial relations of acid saliva and of microorganisms to the particular processes in the earlier parts of the beginning of caries of enamel. Occlusal, Surface Decays in Molars. ILLUSTRATIONS: FIGURES 68-71, 104-106. Principal clinical features: (1.) Beginning in pits, absence of superficial spreading. (2.) Rapid burrowing along the dento-enamel junction. (3.) Spreading in the dentin in true conical form. (4.) Great softening of dentin in advance of the decomposition of the organic matrix. (5.) Very large decays often occurring while the opening to the surface remains small. These characters are common to decays beginning in pits and fissures wherever found. The conical form of decays of dentin beginning in pits, in the occlusal surface or elsewhere, the spreading along the dento- enamel junction, and the absence of spreading superficially on the surface of the enamel, have been considered in previous articles and some principal illustrations, Figures 68-71, given. For the further illustration of the clinical features, the Figures 104-106, inclusive, are here provided. It will be seen that Figure 104 and other figures of this group show the same form of decayed area more or less perfectly, the detail being different in some degree on account of size of the decayed area or the particular form of the surface of the tooth about it. In each case illustrated, the direction of force in the use of the chisel in opening the cavity so as to fully uncover the area of decay, may be studied. The case illustrated in Figure 104, considering the tooth as a whole, is complicated by two other decays, both of them in the distal surface ; one a very shallow decay, begin- ning in the enamel at the usual point of beginning decays, and the other a decay beginning in the cementum and penetrating into the dentin at the gingival line. This latter is a serious complication in the clinical sense, which has arisen from neglect of the leakage of food into the interproximal space. In Figures 105, 106, the openings through the pits, in which the decay has CABLES AS A WHOLE. ITS CLINICAL FEATURES. 93 begun, are unusually large. This has occurred by the breaking away of the enamel about the pit much earlier in the progress of the decay than usual. In response to this early widening of the pit, giving a greater opportunity for washing out acids formed in the dentin, the penetration of the dentin presents a much less pointed cone, the penetration is less in proportion to the breadth than in cases in which there is less breaking of enamel about the pit. This is seen most distinctly in Figure 106. In studying these illustrations, one must divide the area of actual decay from the cloud (hyaline area) stretching away toward the pulp. In Figure 105 there is really very little decay of dentin. The triangular (in section) cloud stretching toward the pulp chamber is not softened dentin. In Figure 106 the area of decay is more definitely outlined by the distinctly darkened area which is flattened or rounded rather than in the typical conical form. This is characteristic of a wide opening through the enamel. The rate of progress of decay is quite apt to be greater where it is hidden away under the overlapping enamel than in the central parts. The tendency, therefore, is to form broad, flat cavities. Both of these cases, considering each tooth as a whole, are com- plicated by proximal decays. On account of ease of access and the absence of the tendency to superficial spreading of decay, these cavities and pit cavities, wherever they occur, are the simplest of cavities in the clinical sense. The only thing requir- ing special attention outside of the area of decay and its full exposure by trimming away the undermined enamel, is to see to it that all grooves are cut out to such a point as will give opportunity for a smooth finish of the filling. Proximal Surface Decays in Molars. ILLUSTRATIONS: FIGURES 107-111. Principal clinical features: (1.) The beginning decays of this class are hidden from view in the proximal surfaces of the teeth, making their early discovery difficult. (2.) A tendency to wide spreading on the surface of the enamel, bucco-lingually, making extension for prevention necessary in filling operations. (3.) Tendency to the early undermining of the marginal ridge by the extension of decay along the dento-enamel junction and the exposure of the cavity by its breakage. (4.) Wide secondary spreading gingivally in a considerable number of cases which is liable to be overlooked in the preparation of cavities. (5.) Recurrence of decay at the bucco-gingival and linguo-gingival 94 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. angles of fillings when judicious extension for its prevention is neglected. (6.) Recurrence at the gingival margins of fillings where contacts are of bad form, allowing food to leak into the interproximal space. (7.) Hence the requirement that correct forms be given contact points in the finishing of fillings. The conical form of cavities in the dentin is a little different in proximal cavities, where seen in sections cut mesio-distally, from those in occlusal surfaces, because of the difference in the trend of the dentinal tubules from the line of the dento-enamel junction toward the pulp of the tooth. It is still a cone, how- ever, with its base placed diagonal to its length, or in section it is a triangle, having one of its basal angles obtuse. The tendency to this form is best displayed in the decays in Figure 110. In general, there is a greater tendency to rounding of the general line of invasion of dentin than is seen in the decays beginning in occlusal surfaces. There is the same tendency to wide soften- ing of the dentin more rapidly than the decomposition of the organic matrix when the opening in the enamel is small, as is seen elsewhere; but this disappears when the enamel breaks away, exposing the cavity to the occlusal surface. As the time in relation to the progress of the decay at which this breakage of the enamel occurs is very variable, extensive burrowing with large amounts of softened dentin is liable to be found unex- pectedly in that which seemed, upon superficial examination, to be a small cavity. The large proximal decays in Figures 110 and 111 show something of the extent to which these cavities may burrow before the marginal ridge breaks away, exposing them to the occlusal surface. A lower molar is shown, in Figure 107, with a mesial surface decay and a distal surface decay, both of which are excellent types of the early beginnings of caries in these surfaces. In that in the mesial surface, the decay has just passed through the enamel, no enamel rods having yet fallen away. In the distal surface the enamel rods have fallen out and the extension of caries along the dento-enamel junction is making progress. This is seen best in the picture to the right. From this the hyaline zone stretches away to the pulp chamber. This picture is a most excellent study. It is well to note the small amount of dentin between the occlusal surface and the pulp in this case, and also the great extension of the mesial marginal ridge of the pulp. The frequent extension of the mesio-buccal horn of the pulp in both upper and lower first molars is a menace in cavity prepara- tion that should be carefully guarded against when possible, by Fig. 107. A photograph giving an excellent showing of a mesial and a distal decay in a lower molar that have made but little advancement. The two halves of the tooth are shown, giving two views of each decay. In the decay in the mesial surface the enamel rods have not yet fallen out from any part. The enamel has been penetrated, however, and in the half on the left side some solution of the dentin is apparent. In this, another feature not so frequently met with, is the compression of the decayed area by contact with the next tooth, which is apparent in both halves but is most prominent in the half on the left side. It is not uncommon to find a decay that has progressed about as this has done (but situated just to the gingival of the contact), swollen so as to have become flattened against the proximating tooth or even to take its form for a space. But for the area of decay to occupy the contact point as in this case is infrequent. In the decay in the distal surface, the enamel rods have fallen out of the central area, and in the half on the right side, there is an excellent show- ing of the projection of decay along the dento-enamel junction. The illustration is also an interesting one because of the showing of the unusual nearness of the pulp to the occlusal surface and the danger of exposing the mesial marginal ridge of the pulp, or horn of the pulp. Fig. 108. An upper first molar with a distal decay which has made considerable progress, ana has undermined the distal marginal ridge. Fig. 109. This photograph discloses three decays; one in the mesial surface, one in the distal surface, and one in the occlusal surface. The decay in the distal surface is not well shown because of the loss of a part of the enamel. The decay in the mesial surface is cut tn one side of its central area and shows the undermining of the enamel buccally beyond the area of penetration of the enamel, and shows well the area of whitened backward decay of the enamel. The extraordinary prolongation of the mesio-buccal horn of the pulp is also an interesting feature of the specimen. Fig. 110. The decay on the right side of the illustration shows a very prominent clouding extending to the pulp. This also shows particularly well the form of the clouded area, with the base of the cone placed diagonal to its length, caused by the relation of the direction of the dentinal tubules to the proximal surfaces. The actual decay of the dentin in this case is marked by the very dark area about the small opening in the enamel. The spreading along the dento-enamel junction is very wide. The decay in the mesial surface has exposed the pulp before the mesial marginal ridge has broken so as to expose the cavity. Fig. 111. This tooth has an unusually heavy enamel cap. This seems not to have been any bar to the penetration of caries, but has prevented the breaking of the marginal ridge disclosing the cavity to the occlusal surface, though it is extensively undermined. CAKIES AS A WHOLE. ITS CLINICAL EEATITBES. 95 avoiding cutting through its recessional line. This recessional line is usually nearly a direct line from the point of the cusp to the present location of the point of the horn of the pulp. Where the point of the horn may be located along that line in any indi- vidual case can not be told in advance, but that it will not be much out of that line is a certainty. When it is possible, cutting that line should be avoided. In this group of pictures, and in the next following, the clouded areas stretching away from the areas of decay toward the pulp are particularly prominent. The best examples are in Figures 110, 113 and 117. It is an almost constant appearance in some form, even in the freshest decays, after the acid has begun to dissolve the calcium salts of the dentin, but it never appears before the enamel has been penetrated. It was first described by John Tomes and by him was called the hyaline area in advance of actual caries. It finally became known as the hyaline area of Tomes. At first Mr. Tomes supposed this was caused by an increased deposit of calcium salts, filling the den- tinal tubules. While the chemico-vital theory of caries was held, this was looked upon as an effort to bar the further progress of caries by building against it. With further studies, this expla- nation became untenable. It now seems more probable that it is caused by the death of many of the dentinal fibrils. The appearance differs much in different cases. It may be either a cloud fringed with white, or a white area fringed with cloud, an irregular distribution of these, or it may be wholly of the one or the other. It appears to the best advantage in photo- graphs of split teeth by reflected light, and its prominence in the photograph depends much upon the condition of the dentin as to translucence at the moment of photographing. A freshly cut tooth is apt to show it best, and, if it is photographed at once on being removed from water, the surface being simply wiped dry, the appearance will be much stronger than it will be if the tooth has been allowed to dry. Therefore, it has happened occasionally in the pictures presented that the photograph of one of the halves of a tooth has shown this strongly, while the other half of the same tooth has scarcely shown it at all. How much actual injury to the tooth is done by that influence which causes this hyaline zone can not well be told. That there is a distinct injury is certainly true. It seems now that the most rational explanation is that in this zone many of the dentinal fibrils are dead from the irritation caused by the progress of caries. If this is true, the extension of this to the pulp may be 96 PATHOLOGY OP THE HAKD TISSUES OF THE TEETH. the cause of the hyperemia of the pulp that so often occurs in carious teeth before the pulp has become involved or exposed to the actual carious process. In studying the decays of this tooth, Figure 107, or others of this group, it will be seen that any effort to prepare these smaller cavities as simple proximal cavities, would inevitably produce conditions which would cause failure of the fillings, for the reason that they are situated so close to the marginal ridges that the enamel rods slope very much toward the ridge. Further cutting in that direction to obtain a clean enamel wall, or to remove the decay projecting along the dento-enamel junc- tion, would bring the margin of the filling to an impossible point, because of the direction of the enamel rods. Therefore, the marginal ridge should be cut through and anchorage made in the form of a step in the occlusal surface. This is more sharply illustrated in the undermining of the distal marginal ridge in Figure 108, in which decay has made a little further progress. In such positions, this undermining is generally done very early in the progress of the decay and the marginal ridge breaks away, exposing the cavity corre- spondingly early. This generally gives the patient the first sug- gestion of the presence of a cavity. Often, also, the dentist overlooks these decays until this breakage reveals them. This is often fatal to the pulp of the tooth, especially in cases in which the decay has begun farther to the gingival, as in the decay on the left, in Figure 110, or in those cases in which the enamel cap is unusually strong, as in Figure 111. In the decay seen in the right of Figure 110, the undermining of the enamel seems extreme. This is often the case in those decays that have pene- trated the enamel as a small opening without much superficial spreading, as is apparent in this case. In Figure 109 there is an excellent showing of backward decay of enamel in the decay seen on the left of the figure. In this case the cut is to one side — the buccal side — of the central area of the decay, and shows the projection of the decay buccally, along the dento-enamel junction, its progress in the dentin and the whitened area show- ing the backward decay of the enamel. Incidentally this cut has been in the line of the projection of the mesio-buccal horn of the pulp, which is unusually long, demonstrating again the clinical necessity of avoiding the recessional line of this horn of the pulp in the preparation of cavities, both proximal and occlusal. For here it may also be noticed how very close the small occlusal cavity is to this horn of the pulp. Finally, it is suffix Th6 P " d ^ " >»-<> to b eco me J* »32X1^ettSF£ ^ Fig. 113. A beginning decay i tion of the dentin is just beginning, fringed with deep cloud. surface. lesial surface of a small three-cusped molar, in which solu y characteristic light-colored hyaline area in the dentin is The deeav of the enamel has extended considerable toward the occlusaJ CAEIES AS A WHOLE. ITS CLINICAL FEATURES. 97 well to notice that the very heavy enamel cap shown in Figure 111 has been no bar to the invasion of caries, but that, on the other hand, has been rather a menace in that the failure to break away early has kept the cavity hidden and maintained condi- tions favorable to the rapid advance of caries of the dentin. Occlusal and Proximal Surface Decays in Bicuspids. ILLUSTRATIONS: FIGURES 112-118. Principal clinical features : (1.) In pit and fissure decays, the danger of undermining the mesial and distal marginal ridges by extension of caries along the dento-enamel junction, involving also the enamel of the proximal surfaces. (2.) In proximal sur- face cavities the clinical characters are the same as in proximal surfaces of the molars. The positions in which pit decays occur in the bicuspids are well shown in Figure 112. The occurrence of these, inde- pendent of caries of the proximal surfaces, is not nearly as frequent as in the molars, yet a considerable number are met with. If these are treated before considerable progress has been made, they are very simple cases ; but, as decay progresses, it quickly undermines the marginal ridge and is liable to weaken the enamel of the proximal surface to such an extent that this must be cut away to make a safe treatment by filling. In the illustration, Figure 112, which presents decays of the enamel in each pit and in its distal surface, it will be noted that, as these progress in the dentin, they will quickly undermine the enamel of both the marginal ridge and the proximal surface, and the enamel of these parts will be weakened by backward decay. This undermining often makes a proximo-occlusal filling neces- sary even though there may have been no proximal decay. Many of the proximal decays in bicuspids begin near the marginal ridges, as in the molars. This is illustrated in the beginning of decay of the enamel in the distal surface in Figure 112. These undermine the marginal ridges and disclose the cavi- ties early in their progress. In Figure 113 the beginning of the decay has been farther toward the gingival, and spreading on the surface of the enamel toward the occlusal has occurred. This is seen also in Figure 114 in the decay on the right side of the figure and is much more plainly seen in the photomicrograph of the same decayed area in Figure 116. The excellent photo- graph of the split bicuspid in Figure 117, shows the most usual points of beginning and direction of progress of these decays to 98 PATHOLOGY OF THE HABD TISSUES OF THE TEETH. great advantage. It will be noticed that in the cavity on the left side of Figure 117, decay has already begun to undermine the enamel forming the marginal ridge, and the distance to the pulp is so great that the breakage of the marginal ridge would prob- ably occur, disclosing the presence of the cavity before the pulp would become involved. But this tooth shows that the pulp has receded and is smaller than usual. In many cases the pulp is involved before the breakage of the marginal ridge. This brings us to the necessity of discovering these decays at an early date in their progress in order to limit the injury to the dentin by caries and prevent the exposure of the pulp. In the split bicuspid, Figure 118, there is a mesial cavity which has extended in the dentin to the exposure of the pulp before the mesial mar- ginal ridge is broken. This shows well the extension along the dento-enamel junction under the occlusal surface of the tooth. This great extension along the dento-enamel junction and the general form of the cavity is typical of this class of cases in which the opening of the cavity remains closely covered by the proximating tooth. Taken all together, the principal clinical differences between the proximal decays of the bicuspids and the molars are to be found in the smaller comparative size of tbe bicuspid in relation to the exposure of surface to the beginnings of decay. For this reason, the amount of sound tissue in proportion to carious tissue quickly becomes much less than in the molar teeth, and their suc- cessful treatment is for this reason rendered more difficult. These facts intensify the demand that closer examinations be made and filling resorted to earlier in tbe progress of caries in the bicuspids. If this will not allow the cutting to be made much narrower on the surface, it can be made much shallower, giving proportionally a much greater mass of healthy tissue to support fillings and to limit the danger of breakage. The photograph from a split bicusjDid, Figure 114, shows a cavity in the mesial, and also one in the distal surface and is of especial interest. The forms are fairly well outlined, showing particularly in the one on the left of the picture, that the enamel rods have not fallen out. Yet the clouding of the dentin reaches to the pulp chamber. The acid, which has percolated through tbe decaying enamel, has begun dissolving away the calcium salts of the dentin. This extends along the dento-enamel junction, both to the occlusal and to the gingival. In this picture the backward decay of the enamel, in the extension toward the occlusal, is particularly well shown. It is this backward decay the Fig. 114 The photograph in this case was taken with the surface dry, with the expectation that of decay would show whiter. This succeeded well with the decay on the left side, but not right. The hyaline area of the left decay is well shown. The extension occlusally very white backward decay of the enamel are inter- cover glass with the one of decay along the dento-enamel junction and tin. ,. esting features. After this photograph was made, the polished surface was cemented and ground thin for photomicrographing, and Figures 115, 116 were made. F.c, U5. Photomicrograph « U-^VdJS? ^ v h6 L^ - ET&ffifTg ass.^ ,v"S".. vjg- HirT^r^s ^n« light, but is dark by transmitted l.ght In 1 Id r.v m . ^^ ni( , s h . )s rred fallen out. however, and microorganisms have not been admitted CABIES AS A WHOLE. ITS CLINICAL FEATURES. 99 of the enamel which, so weakens it that it often breaks away early in the progress of the decay. The decay in the mesial sur- face, or right-hand side of the picture, has not been well shown by the engraver, but in this, in the central area of the decay in the enamel, the enamel rods are broken down and lie in a tangled mass near the dento-enamel junction. After the photograph of this tooth was made, the cut sur- face was cemented to a cover-glass, and this in turn to a grinding-disk, which was placed in the grinding machine, and a section ground thin enough for microscopic examination by transmitted light. From this, photomicrographs were made which show the carious areas in greater detail. The sides to which each belong have been preserved as they appear in the small photograph. If the decay on the left in the photomicrograph, Figure 115, is studied, the amount of the solution of lime salts from the dentin, as it is shown at y, is easily followed. The injury to the dentin, however, extends from the point of the dentin cusp near the occlusal, down past the decay of the enamel toward the gingi- val. At z the outline of the backward decay of the enamel, seen in the small photograph, is quite plainly shown, but by trans- mitted light it is dark. A backward decay toward the gingival is not so well shown, because of some little cracking of the enamel in that region, which mars the picture. The occlusal portion of this picture is upward, as it is in all of the photomicrographs. The decay on the right of the small picture, Figure 114, is represented in Figure 116. Although this decay has not caused enough solution of calcium salts in the dentin to show shrinkage in drying, the injury to the dentin seems to be considerable. The enamel rods are broken down in the central area, which occurred, I am persuaded, in the process of grinding, for my notes say that the surface of the enamel showed no loss of enamel rods. The grinding of the surface from which the small photograph was made, was without any protection by cementing the enamel rods together by solutions of balsam or shellac to prevent move- ment, and some distortion of the enamel rods on the superficial portion of the cut surface would easily be overlooked. It will be seen in the photomicrograph that many of the partially dissolved enamel rods lie in a tangled mass in the deeper parts of the cavity. The very unusual extension of the carious process in the enamel toward the occlusal at z will also be noticed here, sepa- rated partially from the principal area of decay, a flamelike tongue shoots inward from the surface and is making progress, 100 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. following directly the length of the enamel rods. This represents a new decay of enamel in the form of an extension, but begin- ning upon the surface. It is not a lateral extension within the tissue, but marks the spreading of microorganisms on its surface. It is well to note particularly the direction of the enamel rods along the occlusal side of the flamelike tongue of decay shooting down from z, with reference to the inclination of the enamel wall that would be required if this were prepared as a simple proximal cavity. It will be seen that this inclination of the enamel rods is too great to fill against safely, for it is in such a position that the thinness of the margin of the filling material would be insufficient to give it the necessary strength. MISPLACEMENT OF BEGINNING PROXIMAL DECAYS. ILLUSTRATION'S: FIGURES 119, 120. It has been noted, in considering Figure 92, that the proxi- mal decay upon the mesial of the bicuspid is out of the ordinary position to the lingual, passing partially around the lingual angle of the tooth. Such displacements from the normal position occur frequently on account of irregularity of the teeth bringing their surfaces together in unusual relations to each other, or some such accidental condition. In Figure 119 a peculiar shaped cavity is presented in the mesial surface of the central incisor, having a prolongation running labio-incisally. When the tooth is seen standing alone, such form of beginning decay might seem difficult to explain, but examination of Figure 120 explains the reason for this unus- ual form. The relative position of the two teeth is such as to bring very near contact directly along the line which this decay has taken in the enamel, and is the local influence which has caused this peculiarity. In any case, if a tooth, a bicuspid for instance, is turned one quarter around upon its axis, so that the buccal surface, proper, becomes the mesial surface, and the lingual surface, proper, becomes the distal surface, decay, if it occurs, will start in the portion of the enamel that is in near contact with the neighboring tooth. Therefore, we see again in this that the nature or perfection of the enamel is in no wise an element in the localization of decay on the smooth surfaces of the teeth. These unusual forms, and apparently unusual positions, of beginning caries are always traceable to some condition that serves to invite lodgment and Fig 116 FlG ' 116 ' Fig. 117. This excellent photograph of a split bicuspid with mesial and distal decays is remark- ably similar to the last, but in many ways a more perfect picture than Figure 114. In the decay on the left, the enamel rods are broken down and are lying in the cavity in the enamel in a tangled In the been adn dentin ii flamelike features. the right, the enamel rods are still in perfect position and no microorganisms have itted to the dentin. The dark portion of the dentin accurately exhibits actual decay of the both decays. The hyaline areas are both very well shown. The forked projection of the tongue on the left, formed by the border of cloud, is one of the singularly interesting Fig. 118. The halves of a split bicuspid in which decay, through an opening through the enamel that has remained small, has involved the pulp before the marginal ridge has broken, though it is extensively undermined. Figs. 119, 120. Drawings showing an unusual form of decay in a cential incisor in Figure 119. and the overlapping of the two central incisors in Figure 120, in such a way as to bring the sur faces of the teeth in very near approach in such a direction as to produce this form of beginning decay. CARIES AS A WHOLE. ITS CLINICAL FEATURES. 101 to protect colonies of microorganisms. In the examination of many teeth, such unusual positions of beginning decay are not very rare. SECONDARY EXTENSIONS GINGIVALLY OF PROXIMAL DECAYS. ILLUSTRATIONS: FIGURES 121, 122, 123. In proximal surfaces another condition arises frequently that deserves especial attention on account of its great clinical importance. Figure 121 shows a large carious area of enamel at x that has just passed through the enamel and begun the solu- tion of the calcium salts of the dentin. In this case, a secondary beginning of caries of the enamel has occurred toward the gingi- val at y, running farther gingivally than the illustration shows. This occurs in somewhat less breadth in a considerable number of cases on account of lodgment and retention of food between the teeth. Because of roughening of the surfaces, by the swelling of the decayed area, or because of the falling away of enamel rods in one or both of the proximating teeth, the food, instead of gliding out laterally in the normal way, will be held, and will be forced more and more onto the gum tissue as other food is forced in upon it. In this way the interproximal gum tissue will be absorbed and a pocket will be formed between the teeth that will be well enclosed by the festoons of the gum to the buccal and lingual, and by coverings of debris from washings by the saliva. Acid fermentation will become established in this pocket. The acid formed by this fermentation will be in contact with the surface of the enamel and its calcium salts will be dissolved. Another case of similar character is illustrated in Figure 122. The progress toward the gingival line is less extensive, but in depth its progress is more pronounced and it has a more evident separation from the original beginning point of decay in this surface. As in most of the decays of enamel at this stage, the swelling of the carious enamel is very apparent in the principal decayed area. There seems to be some effect upon the partially dissolved enamel rods that causes them to lengthen slightly, causing this swollen appearance. Further, when these rods are disturbed, they often collapse into a tangled mass in which they seem bent and twisted together in such a way as to suggest that they have become softened and in a degree pliable. See Figure 116. This swelling appears in a number of the photomicro- graphs. I do not remember that any other writer has mentioned it. In the hand grinding that I had done before this had not been 102 PATHOLOGY OF THE HAKD TISSUES OF THE TEETH. noticed, but in many of my recent grindings with the machine, in which the final thinning down of the specimen is done, with all such frail parts held together in hard balsam or shellac, it has become too prominent to be overlooked. Indeed, in the grinding by the machine, the preparation is more delicately done than heretofore and much carious tissue is saved in form that formerly was lost. This is giving a closer insight into the actual conditions existing in the beginnings of caries of enamel. The roughening of the surface of the decayed area is evidently a factor in the holding of food and the establishment of a pocket between the teeth. This is aided later by the falling out of the enamel rods and the more general roughening of the surface on that account. Those conditions, which cause the food to lodge, become a cause of the wide secondary extension of the carious area toward the gingival line, which creates a very ugly clinical con- dition, and one that is too often overlooked at a time when it might be easily remedied. During the preparation of the cavity, such an extension of decay as is shown in Figures 121, 122, will show a white line of more or less thickness on the cavo-surface angle of the gingival wall, while the remainder of the enamel wall will be hard and firm. This is further illustrated in Figure 123, another photomicrograph from the same specimen as that in Figure 122, but made with less amplification in order that more of the relation of the carious areas to the tooth and its pulp chamber may be shown on the ordinary book page. In this case, if the occlusal portion of this proximal decay had extended into the dentin and the cavity had been discovered by the breaking away of the enamel at a time when the secondary extension of decay gingivally, as shown, was at its present stage, which often occurs, it would have been easy to overlook this extension and prepare the cavity with its gingival wall cut at the line d, instead of cutting the cavity to the line c. Such an error as cutting the gingival wall at d would inevitably have resulted in disaster within a short time. In practice, the only way in which to make a filling that will not soon be undermined at the gingival wall is to -continue the extension until all appearance of this secondary caries of the enamel has been removed. The perfect enamel will then show the usual solid vitreous appearance at the cavo-surface angle of the gingival wall. Then the contact point must be so formed and the filling so finished as to later on prevent the leakage of food into the interproximal space. Afterward, the regrowth of the interproximal gum tissue should be encouraged m oIar F ' G - 'o'-Dentif 0t0m E iC ESd ° f "I aSTS $"** °! the "J"™ 1 on the P™ 1 ™ 1 sur ' a « of a proximal ^m tis^e '"dements of food between the teeth and absorption of the inte* Fig. 122. A photomicrograph of caries of the enamel on the proximal surface of a molar, with an extension gingivally. The decay from the original point of beginning has penetrated the enamel almost to the dento-enamel junction. The extension gingivally is partially separated from the prin- cipal decay. See Figure 123. CARIES AS A WHOLE. ITS CLINICAL FEATURES. 103 by local stimulants and the case kept under observation in the effort to have it refill the interproximal space. Any condition which allows food to leak into the interproxi- mal space, be held and forced onto the gum tissue, will cause the absorption of the gum tissue and result in the formation of a pocket. In time, one of two things is certain to happen : (1) acid fermentation will become established in the pocket and decay will occur farther toward the gingival line, or (2) putrefactive decomposition will become established, and finally disease of the peridental membrane will result. Careful clinical study has shown conclusively that much the greater number of the decays met with in practice that extend far toward the gingival line, or past it into the cementum, have occurred in this way. It is true, however, that a considerable proportion of these have occurred in what may be called the more normal way by the spread of decay along the dento-enamel junction and backward decay of the enamel. This later can occur only in the badly neglected cases. The crowding of food between the teeth after the placing of so-called contour fillings in the earlier days of cohesive gold work was the cause of widespread loss of fillings by under- mining by decay at the gingival margin. The former employ- ment of the separating file as it had been developed in the use of non-cohesive gold was continued for the finishing of cohesive gold fillings. Flat contacts were made and the forms of proxi- mal surfaces were left otherwise in imperfect form. There had not been that close study of tooth forms which enabled men to copy them with accuracy, or to appreciate the correctness of forms of interproximal contacts ; neither did they have suitable instruments. It is only by the complete relegation of the sepa- rating file to past history, the study of the best natural forms of interproximal contacts and their function in the protection of the interproximal spaces, the copying of these in the shaping of proximal surfaces of fillings, which are made to restore the full mesio-distal breadth of the teeth, that this difficulty in the treatment of caries of proximal surfaces is being overcome. Decays recurring from these causes are especially difficult of treatment, often requiring the removal of a filling previously made, in order to reach them from the occlusal snrface. They are also complicated with great difficulties in getting the rubber dam far enough to the gingival to protect them from moisture. Therefore, in practice, a complaint of pain being produced by food lodgments, or of food being held between the teeth in 104 PATHOLOGY OF THE HABD TISSUES OF THE TEETH. the chewing of meats or other stringy foods, should receive immediate attention, the canse found and the condition remedied. It may occur from a number of causes besides the beginning of caries, and will occasionally be found in one, two or more teeth, in mouths in which no caries has previously occurred. The proximal contacts may be bad from faulty forms of the teeth themselves, they may have become bad from movements of the teeth after extractions, the contacts may have become flattened by interproximal wear, but oftenest of all, they have become bad because of beginning of proximal decay. I may say that, personally. I have done no other thing for my patients that has elicited keener expressions of appreciation than the correction of this class of evils. If the dentists of this country would unite in looking closely after these conditions and be careful in their correction, it would add greatly to the comfort and welfare of their communities, save thousands of teeth for useful service and enhance the usefulness of dentistry. INJURIES BY INTERPROXIMAL WEAR. ILLUSTRATIONS: FICCRES 124-128. The clinical consideration of caries of the proximal sur- faces of the bicuspids and molars should not be passed without more special mention of the injuries that result from interproxi- mal wear and the flattening of the contact points from this cause ; though it will be again presented from the technical view in the second volume. The general principles governing the lodgment of food debris between the teeth have been given under the last heading, to which the reader is referred, in which interproximal wear of the contact points was mentioned as one of the causes. A certain indefinite amount of wear of the mutual points of proximal contact between the teeth as they stand in the arch, must be regarded as normal. Almost any tooth extracted after the age of twenty-five or thirty years will show a facet of wear on its point of contact with its fellow. A number of measure- ments of these give an average of a loss of about one centimeter in the length of the arch from this cause when measured on the labial and buccal surfaces of the teeth around the arch from the mesio-buccal cusp of one third molar to the other at the age of forty years. This wear increases as the person grows older. "When this wear is fairly even in its distribution among the several teeth, it can not be regarded as abnormal, nor is it a cause of material injury. Such wear does not loosen the normal Ftg. 123. Another photomicrograph from the decay shown in Figure 122, made with less ampli- fication in order to show the relation of the decay to the pulp chamber and other parts of the tooth. It includes a little less than one-half of the mesio-distal section of the crown. In the preparation of a cavity for rilling in such a case, it would be an error to cut the gingival wall at d. The true cavity lines would place the gingival wall at the line c ; the axial wall on the line b ; the occlusal wall of the step on the line A. Figs. 124-128. This group of five teeth, all of which were extracted by the author because ot neglected disease of the peridental membranes, caused by the crowding of food between the proximal surfaces, flattened bv interproximal wear. These should have been protected at the proper time by building prominent contacts for the cure of the difficulty. Figures 127, 128, illustrate the position in which decay most usually occurs in these cases. CAEIES AS A WHOLE. ITS CLINICAL FEATURES. 105 pressure of the contact of tooth with tooth as they stand in the arch in any degree. In the balance of forces which confine the teeth in normal form and occlusion in the arch, there is a mod- erate but continuous pressure exerted to hold them firmly one against the other, which, when conditions remain normal, con- tinues through life. This is much more than sufficient to take up any loss of length of the arch around its curve that may be occasioned by the wear of the contact points. This is often shown by the quickness with which the teeth anywhere in the arch will close together when a contact point has been lost by reason of caries or the reduction of an intervening space where a tooth has been removed. This wear is produced by the slight movement of the teeth in their alveoli allowed by the peridental membrane. It is not equal in all parts of the mouth, but is greatest among those teeth which do the heavier work in chewing food, especially the second bicuspid and the first and second molars. In these teeth it is frequently excessive. The five first molars, photographs of which illustrate this subject, were each removed by the author because of injury done to their peridental membranes by the food which was held by the flattened sur- faces and crowded against the interproximal gum tissue. The flat facets shown in the photographs exhibit the amount of interproximal wear that may be expected to occur frequently in persons fifty to sixty years old, who have made good use of their teeth. Many cases may be observed that have become worn as much as these, or nearly so, in which no special harm has resulted, and they require no attention. But in a certain number of these, food that is unusually tough and stringy will some time be forced between the teeth and not be removed. At sub- sequent meals more will be forced in, until finally the pressure of the contact will be loosened and remain so. Then trouble has begun in earnest, which, if not relieved promptly, will cer- tainly result in disaster. Within my personal observation, certain persons have manifested a remarkable unconcern as to this condition, claiming that they had never experienced any uneasiness whatever, even when large amounts of gum tissue had been destroyed by the pressure of food debris. Such cases are often hopeless when first seen. But when the dentist dis- covers such cases in time to act successfully, he should express the necessity for treatment by proceeding at once to do that which is necessary. Such a course will save his patient from the loss of the teeth concerned. Others, and much the greater number, are in constant trouble from the beginning of the lodgments 106 PATHOLOGY OP THE HARD TISSUES OF THE TEETH. and gladly accept anything that promises relief. The number of persons who have complained that they have been unable to obtain relief when applying to their dentist indicates that the body of the profession have been slow to realize the necessity for treatment, or to see the way to make it successful. As said in the previous article, one of two things is sure to result if this continues: (1) acid fermentation will become established in the pocket formed between the teeth as a result of the absorp- tion of the interproximal gum tissue, by the pressure of the accumulations, and caries beginning near the gingival line, as shown in Figures 127, 128, will result; or (2), putrefactive decomposition will occur, resulting in disease of the peridental membrane. In Figure 124 a considerable absorption is shown on the side of the mesial root of the lower molar, which seems to have been caused by the continued irritation of the peridental membrane, a thing that has been observed in a considerable number of such cases. The common habit of dentists of throw- ing extracted teeth into the waste-basket or elsewhere without examination of the condition of their roots, is accountable for the slowness of the development of our knowledge of the effect of pathological conditions upon the peridental membranes and the hard tissues which they invest. In this illustration, Figure 124, the surface flattened by wear is very broad. In Figure 125 the enamel has been worn entirely through, exposing the dentin. In Figure 126 a decay of the enamel had begun near the contact point but had ceased to progress because of some favorable change of conditions. This has become blackened and the facet of wear has later spread over it. The location of the decays that have begun in Figures 127, 128, is typical of the beginnings of decay in these conditions and speak for themselves as to the difficulty of treatment. From every point of view cases of this class call for immediate, careful consideration and treatment in the very early stages of their progress, or just so soon as it is noticed that there is trouble that seems to persist. Only one thing promises relief, and, fortunately, has proven very effective when carefully done. This is to cut a cavity in one of the worn teeth that shall fully include the worn area, make a good and sufficient separation of the teeth and build out a prominent contact that will hold the surfaces sufficiently apart and prevent further leakage of food into the interproximal space. This treat- ment is given in detail in the volume on technical procedures in filling teeth. Flo. 129. A blackened spot on the mesial surface of a central incisor caused by a beginning decay of the enamel, which was stopped by a change of conditions, and afterward became very dark It shows the most common position of beginning of decay in these surfaces. Flo. 130. An open cavity in the mesial surface of a central incisor with a superficial extension of decay running away from it, toward the linguo-gingival angle of the surface. A similar superficial whitening leads away to the labio-gingival angle, which was lost in the high light in photographing Fio. 131. A beginning decay in the distal surface of a lateral incisor from which the enamel rods are falling away and progress of decay has begur away toward the pulp chamber. Fig. 132. A decay in a worn cuspid that has give a false impression for the reason that the cut is the enamel penetrated with the enamel rods still i through the enamel. the dentin. A delicate hyaline area stretches iade greater progress. This picture is liable to little to the side of the central area and shows position, when, in fact, the cavity was open Fig. 133. A more considerable undermining o£ the enamel is less tha may be found undermined. the distal surface of a central incisor in which the In such a case the labial or lingual plate of the enamel Fig. 134. A photograph of a cuspid with a decay across its labial Burface. There is a decayed area running across the surface mesio-distally that has penetrated the enamel and is making progress in the dentin. Undermined enamel has been breaking away, leaving more or less jagged margins. The beginning of this decay occurred when the free margin of the gum was about at the gingival margin of this carious area, and covered the portion of the tooth to the gingival of it. As the tooth protruded farther through the gums, more of the enamel became exposed and the conditions producing decay continuing, or recurring, another band of whitened enamel — beginning decay — has occurred to the gingival of the first. Fro. 135. Another cuspid, similar tc that in Figure 134, in which a decay, beginning in the enamel when the tooth was still half covered with gum tissue, has become fixed in the dentin and later produced a round opening by the breaking away of undermined enamel. When the tooth had protruded farther through the gum and the conditions causing the beginning of decay in the enamel having passed away, this appeared much removed from the free border of the gum. caries as a whole. its clinical featuees. 107 Proximal Surface Decays in Incisors and Cuspids. ILLUSTRATIONS: FIGURES 78-81, 129-133. Principal clinical features: (1.) The V-shaped form of the proximal surfaces. (2.) The necessity that cavities be approached through the labial or lingual embrasures, differing from the approach through the occlusal surface in the molars and bicuspids. (3.) The curvature of the surface at the usual point of initial attack carries extensions of decay along the dento- enamel junction quickly to the undermining of the lingual or labial enamel plates, or often both. (4.) The frequent danger of the spread of decay incisally along the dento-enamel junc- tion, destroying the support of the incisal angle. (5.) The ten- dency to spreading of caries to the linguo-gingival and labio- gingival angles of tbe surface, especially after fillings have been made. (6.) The triangular forms of prepared cavities, with extensions at the labio-gingival and linguo-gingival angles only, instead of the square-cut cavities in proximal surfaces of the bicuspids and molars. (7.) The necessity for forming incisal anchorages of a form not used elsewhere. (8.) The greater necessity for esthetic considerations in all parts of the treatment, and especially in the preservation of the stronger parts of under- mined labial enamel. (9.) The great danger of injury to the attachment of the soft tissues to the tooth at the crest of the arch of the gingival line on the mesial and distal surfaces in the use of ligatures. The two groups of Figures, 78-81, 129-133, taken together, present a progression from the very early beginnings of caries in the enamel in proximal surfaces of incisors and cuspids to a very considerable invasion of the dentin. They give a fair view of the usual conditions found, including the place of beginning and the manner and direction of the invasion. Particular atten- tion should be given to the arch of the gingival line as it passes from labial to lingual across the proximal surfaces. This is well shown in Figures 129, 130, which exhibit plainly the danger of serious damage to the attachment of the soft tissue to the tooth at the crest of the arch of the gingival line by tying liga- tures tightly and forcing them to the gingival line on the labial and lingual surfaces. This danger is found particularly with the incisors and cuspids, and great damage is frequently done by inattention to this point. 108 PATHOLOGY OF THE HAED TISSUES OF THE TEETH. Figure 129 shows particularly well the most common posi- tion of the beginning caries on the mesial surfaces of the incis- ors. It is sometimes a little closer to the incisal angle and sometimes a little farther away, though it does not often vary very much from the point shown. The spot shown is a begin- ning decay which had penetrated the enamel but little appar- ently, and, having been stopped by a change of conditions, became very dark. Figure 130 was intended to show the broad spreading of caries which sometimes occurs on the proximal surfaces of these teeth. This is plainly shown on the lingual in the rounded tongue of superficial decay extending away from the dark, open cavity toward the linguo-gingival angle of the sur- face. A somewhat similar extension toward the labio-gingival angle was apparent, but the high light in the photograph has hidden that point. Such extensions as that seen upon the lingual in this photograph are particularly liable to occur in very sus- ceptible persons after fillings have been made, unless extensions of the angles of cavities have been made to include the area of danger. Otherwise, this case presents a wide-open cavity in which the undermined enamel has broken away most toward the lingual surface. The penetration of dentin and its direction of progress is progressively shown in Figures 131, 132, 133. In the first of these, the enamel rods have fallen out, and the spread- ing of decay along the dento-enamel junction is in progress. The faint hyaline zone is seen reaching almost to the pulp cham- ber. This decay is rather nearer the gingival line than usual, because the strong rounding of the distal surface inciso-gingivally placed the contact point unusually far from the incisal. We see in this that the form of the particular tooth plays its role in the particular locality of the point of attack in the enamel by caries. The next photograph, showing decay in the mesial surface of a cuspid, Figure 132, gives a false impression in that it shows the enamel rods in position, while, in fact, the cut is slightly to one side of a small area from which they had fallen out, admitting microorganisms to the dentin. The same spreading along the dento-enamel junction is present, though in less degree than the average of cases. An examination of this case will show the liability of extension along the dento-enamel junction under- mining the incisal angle before an exposure of the pulp would occur, a thing that frequently happens to the incisors when there is a lack of watchfulness of the progress of decay. This was not a young tooth, as shown by the wear of the cusp, which has exposed an area of dentin. A trace of a hyaline zone is CAEIES AS A WHOLE. ITS CLINICAL FEATURES. 109 seen streaking away to the pulp chamber from that as well. These shadows occur in abrasions the same as in caries, but usually are not so prominent. Whatever else these zones of shadow may be, they express a decisive injury to the dentinal fibrils. A still more extended invasion of dentin is photo- graphed in Figure 133. This is not an inordinately large cavity, but one that is easily managed in filling operations. However, even in this, one is liable to find the labial or lingual enamel plates considerably undermined by extensions of decay along the dento-enamel junction. It should be noted particularly that many of the incisors are thin labio-lingually at the point first invaded by decay, and a comparatively moderate extension along the dento-enamel junction may cause such injury to the labial enamel plate as to make a decisive esthetic blemish. This can be avoided only by careful watchfulness over these teeth to see that caries in them receives early attention. Material for the illustration of this class of decays is exceed- ingly difficult to obtain and much dependent upon accident. This is exhibited in Figure 79. In this, decay had practically de- stroyed the central incisor by exposure of the pulp before the apex of the root had closed sufficiently to permit of a root filling. The case exhibits in a striking manner the breadth mesio-distally of the pulp chamber at this tender age of the child, the proximity to the pulp of the usual points of the beginning of caries, the small amount of dentin through which decay must penetrate to expose the pulp, and strongly suggests the watchfulness that should be had over such teeth in families highly susceptible to caries. This is an ugly thing to happen, but it gave an excellent picture of beginning caries and the form of the penetration of enamel in the distal surface of the tooth. Gingival Thied Decays in Labial and Buccal Surfaces. ILLUSTRATIONS: FIGURES 134-141. Principal clinical features: (1.) The earliest beginning of decay is a line of whitening of the enamel running mesio- distally near the free margin of the gum in the middle third of the surface mesio-distally. (2.) The spreading of the decay on the surface of the enamel is usually confined closely to exten- sions mesially and distally toward the angles of the tooth, following the curve of the free border of the gum. (3.) In cases of neglect of cleanliness, and especially in neglect of the use of the teeth in chewing food, there may be extensions occlusally and also across the angles of the teeth to connect with proximal 110 PATHOLOGY OF THE HAED TISSUES OF THE TEETH. decays on the mesial and distal surfaces. (4.) In many cases of this class of caries the disposition is seen to spread quickly from tooth to tooth, or to attack a number of teeth at the same time. (5.) Yields to prophylactic treatment by the patient, when prop- erly instructed, more readily than any other class of decay. (6.) Protection from recurrence of decay after making fillings is had only by extension of cavities nearly to the angles of the teeth in the ordinary cases. (7.) Attacks fewer persons than other classes of caries, but is often very destructive when a beginning is once made. (8.) The most general rule is that gingi- val third decays occur later in the life of the person than the other classes, but attacks in early youth are not very infrequent. Gingival third decays in the labial or buccal surfaces, or in both together, have been much dreaded by dentists because of persistent recurrence to the mesial and the distal of the margins of fillings, or to the gingival when these have been made for young people. This difficulty has arisen from a failure to study the clinical characters and conditions of occurrence closely enough to properly direct the treatment for its eradication and cure. If the conditions which have given rise to the beginning of the decay are not materially modified by prophylactic meas- ures, or spontaneous cessation, the disposition to spread mesially and distally is one of its most persistent characters. Nothing less than the extension of cavities very nearly to the angles of the teeth attacked, will be effective. Figure 134 is a photograph of a cuspid with a gingival third decay which began before the tooth fully reached its position in the arch, or when the crown had yet more than one third of its length covered by the free margin of the gum. Decay spread rapidly across the surface mesially and distally from the begin- ning point and became established in tbe dentin. In the process of growth, more of the crown of the tooth was uncovered to the gingival of this decay, the conditions which caused the first beginning remaining or recurring. The result is another whit- ened band of enamel, a new beginning of decay, to the gingival of the first. This is what may be expected to occur when such decays are treated by filling, when they occur in young persons, unless the free margin of the gum is pushed well away and the cavity margin extended so far to the gingival as to include the new area of liability that must become exposed. In early youth the sufficient persistence of attention to prophylactic measures for the prevention of such extensions is not likely to be so well kept up as to be a very safe protection. Fia. 136. A photograph of the lingual surface of a cuspid with a broad open cavity. From what remains of the surface of the tooth, it is seen that there is an unusually prominent lingual groove on the left side of the picture, in the line of which a small dark pit appears. This indicates that there were other and deeper pits in this surface in which decay in this unusual position started. The case illustrates the fact that often decays in unusual positions have occurred because of some imperfection which has furnished a place of lodgment, and the imperfection has been wholly destroyed by the decay, leaving no sign explaining the cause. Fia. 137. running n A molar showing two beginning points of decay on the buccal surface, ■sio-distally was apparent on this tooth, but the engraver failed to show it Figs. 138, 139. Two photographs of a lower molar tooth, in which caries proceeding- from a buccal surface decay and a mesial surface decay have met across the angle. Figure 138 shows the wide range of the decay of the buccal surface. Figure 139 shows the mesial surface decay as a broad, whitened area, from which no enamel rods have fallen away. This meets the buccal surface decay across the angle of the tooth. This picture also shows the breaking away of the undermined enamel of the buccal surface to advantage. The cementum of this tooth was stained selectively with an anilin dye to bring the gingival line into prominence, showing the influence of the free border of the gum in protecting the enamel from beginnings of caries. showing the more CARIES AS A WHOLE. ITS CLINICAL FEATURES. Ill The most essential condition for the occurrence of decay of this class is a saliva favoring certain kinds of deposits upon the teeth which will cover in attached colonies of microorganisms in such a way as to protect the acids formed from free dissipa- tion in the general oral secretions. This may be such a condition as will enable microorganisms to protect themselves by the for- mation of gelatinous plaques (zooglea aggregations), or possi- bly by other kinds of deposits from the saliva that will form a membrane-like covering that will afford a sufficient protection. It is a notable fact that where any kind of deposits are found upon the teeth, they are first to be seen on the buccal surfaces at the points where gingival third decays begin. It is not any and every kind of aggregation of filth on the surfaces of the teeth that gives rise to decay. Indeed, some forms of filth seem to prohibit decay instead of causing it. Some of the filthiest of mouths have no caries, and in some cases where caries has been in progress it seems to have been actually stopped by extreme filthiness in the same way as decay not very infrequently is stopped in certain cavities by the establishment of putrefactive decomposition in their interior, as has been mentioned. Neither will loose aggregations of saprophytic microorganisms, or of leptothrix buccalis, or the leptothrix of Vignon, or other harm- less varieties which may form thick masses over the teeth, through which water will run as freely as through a sieve, have any influence favoring the production of caries. The covering must be of a kind that will protect from free washings by the fluids of the mouth, and in and under which the caries fungi will grow and produce acid fermentation. This may be so thin and so transparent that the teeth may appear clean and yet afford an effective protection against the too free dissipation of the acid products of fermentation. It has become evident enough from clinical observation that the conditions which favor the formation of these plaques is one that is liable to be inter- mittent. It comes and goes. Decays of the gingival third of buccal and labial surfaces are especially liable to start, to stop, and to start again. Their exposed situation renders them more sensitive to fluctuations of conditions than decays situated in protected localities. This is said of decays of the enamel in which enamel rods have not fallen away exposing the dentin to invasion by microorganisms. Once caries is implanted within the dentin, it will most generally persist, even when there is complete immunity to the beginnings of caries on the enamel. Figure 135 shows a decay, situated centrally in the labial 112 PATHOLOGY OP THE HARD TISSUES OP THE TEETH. surface of a cuspid, which has progressed in the dentin, under- mining the enamel, which, by breakage, has now formed a round opening. At a time when this tooth was taking its place in the arch and was uncovered by the gum tissue, only to about that point, a decay penetrated the enamel and became seated in the dentin. The particular form of the beginning in the enamel is now lost by breakage from backward decay, but we know from many observations of such cases that it was in a line across the central portion of the present dark area. As the tooth pro- truded farther through the gum, the conditions causing the beginning of decay in the enamel passed away and did not return, but the decay established in the dentin continued. Had the orig- inal beginning failed, ever so little, to penetrate the enamel and admit microorganisms to the dentin, the progress would have ceased entirely. Later, a blackened blemish of the enamel would have remained to show where decay had begun. Many of these may be found in any box of extracted teeth. A rare position of decay on the lingual surface of a cuspid is shown in Figure 136, which, from what is left of the lingual surface, seems to have begun as a pit decay, beginning, probably, in pits at the junction of the lingual developmental grooves with the linguo-gingival groove or pits along the lines of these. (See "Descriptive Anatomy of the Human Teeth" — Black, Figures 5 and 20.) These grooves are unusually prominent, and one undecayed pit remains in view. The case shows how decays may sometimes begin in the most unusual positions and how difficult it may become to define the local conditions causing them after the immediate surroundings have been destroyed. The gingival third decays in the buccal surfaces of the bicuspids and molars are not materially different from labial surface decays. They exhibit similar characters in both their beginning and in their disposition to spread along the gum margin mesially and distally. In the photograph of the upper molar, Figure 137, two considerable areas of loss of enamel rods appear in an area of rather faint whitening stretching across the buccal surface. Figures 138, 139, photographs of a third molar, show the wild race of destruction that sometimes befalls these teeth when caries is allowed to go on unchecked by any sort of cleaning. For these illustrations, the cementum has been tinged with a selective anilin stain to show the gingival line distinctly in order to bring prominently into view that por- tion of the enamel covered by the free border of the gum, illus- trating its protection from the beginnings of caries. This part^e^e/ «SS4 Wff^fi^Sffi Wl*^ "'" Figs. 142-145 inclusive. Photographs of a lower first molar with beginning decay completely encircling the crown, following closely the free margin of the gum in every part. Figure 142, the mesial surface; Figure 143, the buccal surface; Figure 144, the distal surface; Figure 145, the lingual surface. CARIES AS A WHOLE. ITS CLINICAL FEATURES. 113 appears to Dest advantage in Figure 138. In Figure 139 it is seen that the decays beginning in the mesial and the buccal sur- faces have become connected across the mesio-buccal angle of the tooth by a comparatively narrow neck. The pictures illus- trate the riotous progress sometimes seen in buccal decays under exceptionally unfavorable conditions. Figure 140 exhibits another neglected buccal decay, which is a more ordinary exam- ple of the form and extent of these when they are left to take their own course. It will be noticed that this has not passed the angles of the tooth. These decays will, of course, burrow along the dento-enamel junction, the same as others, and in that way destroy the enamel by backward decay to the gingival line, allow- ing the free margin of the gum to fall into the cavity. Figure 141, a photograph of an upper third molar, presents an anomalous condition. In coming into position it deviated backward and to the buccal from the normal, and seemed to have stood for some time with but a part of its crown through the gum. When removed, the whole of its exposed surface was whitened by beginning decay. Spreading of Decay Around the Teeth. ILLUSTRATIONS: FIGURES 142-145. In what has been written thus far of dental caries, the idea has been developed that, when decay occurs on proximal sur- faces, the tendency to superficial spreading is from the starting point both buccally and lingually toward the angles of the teeth. Also, that, when caries begins on the buccal surfaces, the ten- dency is to spread mesially and distally from the place of begin- ning toward the angles of the teeth. This is true of caries in these positions in all of the teeth, but more especially of the bicuspids and molars. A fewer number occur in the front teeth as well. It has also been stated that in a few instances under specially unfavorable conditions this decay crosses the angles of the teeth and the proximal and buccal decays join each other. This crossing of the angles of the teeth is the rarest of all of the spreading. It then requires only that decay shall also occur similarly on the lingual surfaces in order to complete the circle of the tooth. This, though much more rare, occurs also. This appears in the case of the lower second molar tooth, four photo- graphs of which are shown in Figures 142-145, inclusive. Fig- ure 142 shows the mesial surface with a broad, whitened area of carious enamel stretching from angle to angle, in which the 114 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. enamel rods have begun to fall away at one point only. Figure 143 is a photograph of the buccal surface with the whitened area also stretching from angle to angle, the shadow obscuring a small part at the mesial angle. The distal surface, Figure 144, shows dark, but the decay is apparent, and on the buccal surface, as seen in this photograph, the whitened line of carious enamel is seen to advantage as it rounds to the occlusal follow- ing the free margin of the gum to join the distal surface decay. Finally, the whitened decay on the lingual surface, Figure 145, is seen streaking away from the decay in the mesial surface in a curved line, which is lost in shadow as it approaches the distal angle, completing the circle of the tooth. The pictures of this series are the final illustrations for the explanation of the tendencies to spreading superficially on the surface of the enamel and the direction of that spreading as one of the principal clinical features of caries of the teeth, which every dentist should fully understand and appreciate as his guide in the preparation of cavities for the prevention of recur- rence of decay about the margins of fillings. Every one should understand distinctly that the spreading on the surface of the enamel is a thing entirely different and apart from spreading along the dento-enamel junction and destruction of the enamel by backward decay, together with the general invasion of and destruction of dentin by caries. This latter spreads in every direction from the point of penetration of the enamel, having no respect whatever for any particular surface or any of the angles of the teeth. The spreading along the dento-enamel junction this way or that has no clinical significance in connection with the recurrence of caries about fillings. This invasion may pro- duce broad cavities, cavities of awkward shapes, may weaken the tooth by the destruction of dentin, and, in these and other ways, has its special points of clinical importance. But this is all secondary, occurring only after the enamel is broken. The clini- cal importance of a full appreciation of the superficial spreading of caries on the enamel has to do especially with the prognosis, with the probable future of every case individually, and the rational management of the teeth of each person under our care. On the details of this management, the success or failure will depend more than all else, supposing always that the details of manipulation, as this may be planned, be skillfully executed. Together with all of this, judgment must be stimulated and quickened by a careful study of the conditions of immunity and susceptibility to dental caries. SYSTEMIC CONDITIONS. 115 SYSTEMIC CONDITIONS. ILLUSTRATIONS: FIGURES 146-158. In what has been presented thus far, the immediate active cause of dental caries only has been mentioned, namely, the acid produced at the spot by growths of microorganisms. This presentation would be incomplete without the mention of other factors. While caries of the teeth is the most prevalent disease known to man, those in dental practice who have not made a careful study of the teeth of persons who have no need for dental operations perhaps do not realize how many are immune to caries of the teeth. Many grow up from childhood and pass on to old age, without ever having a carious tooth. These persons are aways to be found, if we look for them. In the mouths of these persons the same microorganisms are found growing, and growing as abundantly, as in the mouths of persons who are very susceptible to caries. In an examination of the fluids of the mouth in these persons, it is also found that the saliva is as acid, as shown by tests with litmus paper, as in persons who have caries of the teeth. Cultures of micro- organisms from those immune persons have been made over and over again, and it has been found that these microorganisms are of the same character and species and produce the same results in culture media as do microorganisms taken from the mouths of those who are very susceptible to caries. Some of these persons have been followed for years, occasional examina- tions and cultivations being made, so as to leave no possible doubt as to the general facts. Therefore, there is something lying over beyond the active growth of microorganisms and acid formation by them, controlling caries of the teeth. We have, therefore, persons who are predisposed to caries of the teeth and persons who are immune to caries of the teeth. A predisposition to disease is generally considered to be a condition of the body juices and cells which renders the person liable to that particular disease. We do not always know in what that condition consists, but, from the developments thus far, we know it to be dependent upon some material form or combination of matter. We do not know this now of all diseases, but we do know it of some. Bacteriologists and chemists are succeeding in demonstrating the material nature of the causes of disease by finding alexins, antitoxins, etc., and the conditions in which these are produced and in which they are not produced. 116 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. An antitoxin will prevent persons taking a certain disease. For instance, the antitoxin of diphtheria, if properly applied in time during a diphtheria epidemic, will prevent children from taking diphtheria. It acts as a control. Here we are introducing into the blood a material, or combination of matter, which con- trols or prevents the development of disease. So many of these have now been proved as to give the strongest possible evidence that all of them are material. We go through the process of vaccination to produce a material condition in our own bodies that will prevent us from taking smallpox. An antitoxin is produced in the blood, in the juices in the tissues of our bodies, which is antagonistic to the disease known as smallpox. In these ways we are learning to control a number of the most destructive diseases. Disease is also said to be hereditary. Tuberculosis has been reputed to be intensely hereditary. That condition depends upon some material element in the body; just what this is, we may not know now. A person is not born with tuberculosis ; it is not transmissible from parent to child, but the child is born with a material constitution of body which renders it particu- larly liable to contract the disease, but it will not have tubercu- losis unless exposed to the tuberculosis infection; but it contracts it more readily than other people. There is that ele- ment in the body juices and tissues which enables that particular microorganism to grow more freely or produce more injury than in other persons. That is what constitutes a hereditary predisposition to disease. "We find in certain families a hereditary predisposition to caries of the teeth that is strongly marked. If a family of chil- dren is presented for treatment and it is found that the father or mother, or both, have suffered severely in early youth from caries of the teeth, we may be reasonably sure that the children will suffer likewise. "We find this almost universally true of families. Not only this, but we find in very many instances that the first beginning and the order of progress will be in the same teeth, and otherwise similar in character and form. I have followed these peculiarities now through four generations of persons, and find these particular characteristics to be heredi- tary. There are certain conditions, however, that seem to influ- ence these hereditary peculiarities in a very marked degree. It is noted perhaps most in those families that come from Europe and settle in America. In these, where the parents are immune, or very nearly immune, to caries of the teeth, we find them pre- SYSTEMIC CONDITIONS. 117 senting us with children who are very susceptible to caries. There seems to have been some change brought about in the change of climate or conditions under which they live. The reverse of this has been noted in a few instances. Also, it has been noted that parents who have come to the city from the country and who did not suffer much from caries, present us children reared in the city who suffer greatly from caries. Here again a change in the mode of living seems to have influenced the hereditary factor. These changes are quite frequent. The predisposition to caries is much stronger in youth and tends to disappear as persons arrive at mature age. Indeed, caries of the teeth is a disease of youth rather than of adult age, for it is now found, after much careful observation on this point, that if caries of the teeth occurring in youth is well and successfully managed, very little caries will occur in after life in the majority of persons. Cases of persistence, however, of the beginnings of caries at new points are sufficiently plentiful ; and, also, cases are frequently occurring where persons have been immune from caries for many years, and suddenly we find their teeth decaying very badly, showing that there has been a marked change in the predisposition to this disease. Again in pregnant women there is often a renewal of the conditions giving rise to caries of the teeth that are apt to con- tinue also during the period of lactation. It has happened that girls who have grown up under the best of care and arrived at adult age with many fillings, perhaps, but with teeth in good condition and showing unmistakable signs of immunity to decay, have married, and, during their first pregnancy, developed a considerable number of new cavities in which decay progressed rapidly. This recurrence of susceptibility is not at all uncom- mon, and marks a change in bodily conditions with consequent changes in the oral secretions, favoring the development of caries of the teeth. The fact that caries of the teeth is more prevalent in chil- dren than in adults, conforms with what is known of many other diseases. We have a whole list of diseases that are peculiar to children, as measles, chicken-pox, diphtheria, whooping-cough, scarlet fever, etc. As persons arrive at adult age, the predispo- sition to these diseases passes away, or immunity comes; and this is so complete that it is rare to find an adult person suffering from this class of diseases. They are practically confined to children. Generally also they are self-limiting diseases. This term 118 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. "self -limiting" is applied to those diseases which run a specific course and, if the patient has withstood the attack, tend to recov- ery at about a certain period. In all of these, it is found that there has been a change in the blood, which renders the person immune, and this is known as the development of an antitoxin, which remains more or less permanent in the blood. In some of the diseases it seems to become a permanent fixture, as in small- pox. In others, it disappears after a time more or less com- pletely, and the person again becomes susceptible. In this way, children may have scarlet fever and some other of the chil- dren's diseases more than once before they become permanently immune. In other cases, susceptibility to disease seems to go and come. At one time a person exposed to a contagious disease apparently under all conditions that would favor its develop- ment, goes free. The same person at other times, with probably otber conditions of the body juices and cells, will take the disease readily under otherwise similar conditions. Most of the microbic diseases have some one or more of the peculiarities that have been mentioned, but there are some that are not in any wise self- limited. Tuberculosis is one of these. Although purely a microbic disease, there seems to be no self -limiting effect.' Something similar to the changes that happen in suscepti- bility and immunity to other diseases must occur in caries of the teeth, for to-day it is only upon this ground that we can explain the conditions of susceptibility and immunity that are so prominently before us. Formerly, the susceptibility or immunity of the teeth to decay was differently explained. It was supposed that hardness or softness of the teeth, the amount of calcium salts they contained, was in a large degree the con- trolling factor, and under that supposition, when the teeth of children were seen to be decaying badly, the interpretation was that the teeth were soft or poorly calcified. If the child grew up without decay of the teeth, the interpretation was that the teeth were hard and firm and for that reason did not decay. It was on this ground that the effort was made to explain the variations of susceptibility and immunity of which we have spoken. Physical Characters of the Teeth. The idea that some teeth are hard and some teeth are soft, grew up in the minds of the dental profession and of the laity many years ago, and this was generally regarded as a fixed fact. SYSTEMIC CONDITIONS. 119 These differences were supposed to be considerable, and caries was supposed to be severe in teeth that were very soft. The fact is, that heretofore, when it was discovered that the teeth of an individual were decaying very rapidly, the inter- pretation was that the teeth were poorly calcified and were soft. If, after careful treatment, little or no decay occurred, it was supposed that the teeth had become hard and firm. Again, if a person had arrived at maturity with little or no decay of the teeth and later it was discovered that the teeth were decaying very badly, the interpretation was that, while the teeth had been very good in their structure, sometbing had happened to cause them to become soft, and therefore they decayed badly. In this, the observation of clinical facts has been correctly reported. Many persons have grown to maturity without decay of the teeth and afterward their teeth have decayed very badly. It was quite generally held that, during pregnancy and lactation, tbe teeth of the mother were robbed of calcium salts to build up the bones of the fetus. This was because of the general observation that during such periods the teeth of women suffer more from caries than during other periods. These observations were shown to be correct by the testimony of many observers, and lines of treatment were undertaken for tbe correction of the supposed loss of calcium salts in tbe teeth. A large proportion of people who have decay in their youth, will, if that decay is well cared for, cease to have much decay later in life. This gave rise to the general opinion that the teeth were inclined to become hard with advancing age. These observations were carried on and discussed more or less for years, serving to fix the interpretation mentioned in the minds of both the dentists and the people. In fact, there seems to have been no question as to the correctness of the interpretation. In 1895 I published a series of studies (Dental Cosmos, Vol- ume 37, page 353) which were undertaken to determine the facts as to the differences in the physical properties of the teeth with reference to hardness and softness, as represented by the per- centage of calcium salts in tbe dentin, and the relation this held to caries. The results of this investigation are given in great detail, but for our purpose very little of it need be repeated. The results surprised myself as much as they surprised others, for it was found that there were no differences of consequence. I give here a summary of that investigation, which will show the actual facts and also tbat the interpretation of soft teeth and hard teeth, as that interpretation then stood in the minds 120 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. General Summary of Results of Physical Examinations of the Teeth. No of cases. Average Age Xo of Teeth. Specific Gravity Per cent of Per cent of calcium salts Per cent of organic matter. Average for total number of The lowest percentage Ill 32.33 268 2.092 2.133 2.036 .097 11.06 13.56 9.32 4.24 63.54 65.75 61.08 4.67 25.36 27.59 23.26 4.33 Average for persons under 15 Average for persons 15 years 11 8 20 15 26 12 10 10 11. 17. 21.55 25.93 33. 42.66 53. 63.60 13 9 48 43 72 38 19 27 2.066 2.080 2.081 2.086 2.092 2.094 2.105 2.109 11.89 11.46 11.47 11.27 10.84 10.91 10.85 10.66 62.26 63.18 63.43 63.44 63.42 63.73 63.83 64.56 25.92 25.33 Average for persons 20 years 25.23 Average for persons 25 years 25.28 Average for persons 30 years 25.66 Average for persons 40 years 25.34 Average for persons 50 years 25.29 Average for persons 60 years 24.81 Average for males 20 years old 12 26 12 14 6 6 24 67 18 54 19 19 2.082 2.083 2.090 2.094 2.093 2.094 63.30 63.51 63.35 63.48 63.54 63.92 Average for females 20 years old and under 30 Average for males 30 years old and under 40 Average for females 30 years Average for males 40 years old Average for females 40 years .043 1.29 10.88 11.25 11.16 10.95 11.03 11.06 2.30 1.12 Average for persons who lost their teeth from diseases of the peridental membranes . . 15 32 63 16 42 91 50. 28. 33.53 36.19 36.26 31.5 51 121 105 42 103 165 2.101 62.90 25.19 Average for cases in which the teeth are classed as bad Average for cases in which the teeth are classed as good. . Average for cases in which the teeth are classed as fair .... Average for perfect teeth Average for carious teeth . . 2.087 2.090 2.090 2.095 2.091 63.33 63.53 63.56 63.59 62.50 25.49 25.31 25.48 25.36 25.36 Fia. 146. _ A photomicrograph of a section of enamel having straight parallel rods running through its entire thickness. Such enamel splits away from the margins of a break very easily. Fig. 147. A photomicrograph of curled enamel in which the inner two-thirds of the enamel is composed of interlaced bundles of rods. These straighten up and become parallel in the outer one- third of the thickness of the enamel. Such enamel splits away from the margin of a break with great difficulty as compared with enamel having parallel rods. '^■jwi^sttsroje^w ■% M- Fig. 148. A photomicrograph of curled enamel. FlG. 14!*. A photomicrograph of the gingival portion of the enamel on the proximal surface of an incisor having curled enamel, showing the direction of the enamel rods in the extreme gin- gival portion. The cracks in the specimen indicate the direction of cleavage. SYSTEMIC CONDITIONS. 121 of the dental profession and of the laity as well, was wrong. There had never been any substantiation of that interpretation by careful physical examination of the teeth themselves. This summary speaks for itself and shows that the greatest difference in the calcium salts in the dentin, including all exag- geration that might arise from errors, was 4.35 per cent, and the usual range of difference was very much less than this. The dif- ferences due to age are also given, and it is found to be 2.30 per cent. When we consider that ivory, or the tusk of the elephant, has 20 per cent less of calcium salts than the human teeth, and we consider its hardness as compared with the human dentin, we will see that these slight differences in the amount of calcium salts can amount to nothing whatever as rendering the teeth more or less liable to dental caries. It is clearly shown in the comparison of the amount of calcium salts in the teeth of those whose teeth decayed badly with the amount in the teeth of those immune to decay, that there is no difference whatever. Teeth that decay badly have just as much calcium salts, are just as heavy and just as hard, as teeth of persons immune to caries. Therefore, while the fact in regard to caries being severe in this person's mouth, while the teeth of another person escape caries entirely, was a perfectly correct observation, to attribute this to the softness of the teeth in the one and the hardness of the teeth in the other, was a wrong interpretation; but this interpretation has become so fixed in the minds of men that it is very difficult indeed for many of the older men, particularly, to change their minds upon this point. It is perhaps well for the human family that opinions so widely held should have great weight in all matters pertaining to human welfare. They should not be cast aside without the very best reasons for so doing. At the close of the paper communicating these results, the suggestion was strongly made that the causes of immunity and susceptibility to dental caries would necessarily be found in conditions of the general system, influencing the qualities of the mixed fluids of the mouth by which the teeth were surrounded. The composition of these fluids influences the action of the micro- organisms growing in them in such a way that caries occurs in one person and not in another. While the elements entering in to produce these differences in dental caries might be totally different from those in systemic conditions controlling suscepti- bility or immunity to other diseases, the search for them would be conducted on the same general principles. The storm of disapproval that arose when these results 122 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. were published was what might be expected under the circum- stances. They were regarded as revolutionary, and rightly, for the results proved that many of the ideas of dental caries that had existed before were necessarily wrong, and other opinions must take the place of those which had been regarded as correct. Many arguments were advanced from time to time in the effort to sustain the older view, most of which have disappeared. The hardness and softness of the teeth to cutting instru- ments has troubled a considerable number of men. It has been difficult for them to feel that all teeth were of equal hardness, or nearly so, as had been represented. A further careful study of the subject shows that this has generally been due to differ- ences found in cutting the enamel of different teeth, rather than in cutting the dentin. With the exception of its tubules running through it, the dentin seems to be very homogeneous in struc- ture. There is no disposition to split in any one direction more readily than another. Generally no accretion lines are discoverable, though these may often be brought in view by decalcification. We can not find them in the calcified dentin with instruments. In careful experimental work in cutting dentin, I have been unable to distinguish differences that seem to be of con- sequence. In the crushing strength, quite a little difference has been noted, which will be found in the tables of the strength of dentin accompanying the studies to which I have referred. In the enamel there are wider differences in the apparent hardness to cutting instruments. These are due (1) to the direc- tion of approach, (2) and to differences in the relation of the enamel rods to each other. The enamel is not a homogeneous structure like the dentin, but is composed of the enamel rods cemented together by a cementing substance which is less strong than the rods themselves and allows them to part on the line of their length more easily than in other directions. "When the rods lie parallel with each other, the enamel splits in their direc- tion easily when a breach has been made and a sharp chisel is used in the right direction on the margin of the breach. If we undertake to cut it in other directions with steel instruments, it is found to be very hard. This is called straight enamel. Figure 146 is a photomicrograph of straight enamel in which the rods lie parallel and are straight from the dento-enamel junc- tion to the surface of the enamel. This enamel with straight parallel rods is found on very many teeth; perhaps in the majority of cases we will find the enamel rods straight and parallel, except over the cutting edges of the incisors and the SYSTEMIC CONDITIONS. 123 cusps of the molars and bicuspids. "We will find only a variation from the straight line in these positions on many teeth without intertwining of bundles of rods. Enamel with straight, or paral- lel, rods may, when undermined, be split off about the margins of a breach that has been made in it almost as easily as straight grain pine, if it is touched just right with a sharp instrument. If not approached in the right direction, it is very hard to cut. On the other hand, many teeth have enamel over most of their surfaces that is curled; that is, the enamel rods, instead of pursuing a straight course, are much interwoven among each other, usually in the form of small bundles of rods, twisting in among other bundles of rods. This gives to the enamel, when cut in sections and etched, a wavy, twisted appearance. This is called curled enamel. See Figures 147, 148. This form of enamel does not split nearly so readily as enamel with parallel rods. In fact, it is much more difficult to cut it by ordinary means. It should be noted, however, that in nearly all cases of curled enamel, the rods straighten up and become parallel before reaching quite to the outer surface. The checking of this straight portion to the part that is curled in Figure 147 is suggestive. Often the inner half will be curled and the outer half of the thickness straight. There are all sorts of differences to cutting instruments between the perfectly straight enamel, as shown in Figure 146, and the abundant intertwining of bundles of rods seen in Figure 147. The gingival portion of the enamel from the labial surface of an incisor is represented by photomicrograph in Figure 149, which presents much variation in the direction of the rods in its different parts. Some places they are parallel but much bent. Then, for another short space, they are much interwoven. In this respect the specimen is rather remarkable. In the cross section of the tooth at the point where the section was taken, shown in the photomicrograph, Figure 150, the rods are neither quite straight nor quite parallel, but do not depart much from either. But it may be seen how the rods are split up and clinging across the crack near the letter a, reminding one of what occurs in splitting cross-grained wood. One would, however, split off chips from the cut surface at a very easily. But to split off chips from the cut surface at b would be very difficult, not because the rods are more interwoven, but because of the direction of rods toward the cut surface. These differ- ences seem to have no reference to the calcification of the enamel, nor the amount of calcium salts it may contain. In studying the difference of structure in its relation to caries of the teeth, no 124 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. differences whatever are found. Caries seems to pass through the one just as readily as through the other. Therefore, from this phase of the question, these differences are of no conse- quence whatever. Faults en the Structure of the Enamel. Faults in the structure of the enamel, such as pits and fissures, have already been spoken of as of importance in the localization of beginnings of decay. The importance of these has probably been overrated in the past. Very few of the pits are properly termed faults. They are normal to the teeth. They become faults only when they are abnormal in depth. Grooves along the lines of junction of the lobes of the teeth are normal. "When these are of such depth as to merit the term "fissure" they are abnormal and are faults. These, even when faults, are in no proper sense a cause of dental caries, but they furnish favorable conditions for the action of that cause. They must be regarded as giving opportunities for the beginning of decay when conditions otherwise are favorable. But decay does not begin in the pits of the teeth of immune persons, though these pits may be just as deep and just as sharp as the pits in other teeth which do decay rapidly, and even among those who are very susceptible to decay, many pits will be seen without decay, in those teeth that are decayed upon their proximal sur- faces. This is so frequent that they are coming up continually in the laboratory study of caries. In the illustrations accom- panying this article, these will be seen in Figures 107, 108, 110. Here we see that the pits have escaped the beginning of caries when the patient has been sufficiently susceptible for proximal decays to start and run a rapid course. So many of these occur that we must regard the condition of immunity as entirely suf- ficient to prevent decays starting in pits, unless the conditions locally are particularly inviting. This may be said to be true of all teeth which would be regarded as of normal conformation. We occasionally find malformed teeth in which the pits and fissures have failed of closure and in which some area of dentin is actually exposed. This, however, is rare. Ordinarily, all of the deeper pits have a fairly good layer of enamel covering the dentin, but this forms no considerable barrier to the beginning of decay, for. in susceptible persons, the enamel seems to decay readily in such positions, while in those who are not susceptible there is no decay in pits or elsewhere. I once obtained fourteen teeth, mostly bicuspids and molars, from the mouth of a woman II" -til a q. p g>g g-g -Eg "tin's • g— £ £3s Kio. 151. A photomicrograph from a cross secti<: ."'"''". "flSi JH ^i*?** : ■ ^%^>^$^Z Fig. 152. Lengthwise section from the same bone, as illustrated in Figure 151, showing the Haversian systems and their canals cut lengthwise. a. Subperiosteal bone. b. A Haversian canal. "St SYSTEMIC CONDITIONS. 125 over fifty years old, who had reared a family of children, but had never had a decayed tooth. The teeth were lost because of disease of the peridental membranes. I split these with a fine saw and examined carefully the pits found in them. They were unusually deep and sharp, forming what seemed to be unusually favorable places for caries to begin, yet the enamel was perfect in the bottoms of all of these pits. Still, from my experience, I am convinced that a well-fitted band of some considerable width, immovably fixed, but with a buccal surface left without cement, would have produced caries in that mouth. There are certainly differences in the saliva that favor microorganisms becoming fixed upon and clinging to the teeth of some persons, while in other persons there is that which opposes this, and every part is washed so freely as to carry away all acid formed by any growths that may temporarily lie upon the enamel. The band prevents this dissipation. These pits occur in the occlusal surfaces of the teeth of all animals that are omnivorous in their diet, and should not be regarded as abnormal in man. The fact, however, that decay in them occurs so frequently, gives abundant evidence that they furnish the opportunity for its beginning. Therefore, if the teeth are really faulty in their structure so that there are open fissures as well, decay is the more certain to occur. There are some faults in structure within the dentin which give rise to unusual forms of cavities. Sometimes the granular layer of Tomes is very much more considerable under some parts of the enamel than others, inviting the burrowing of decay in special directions, causing irregular forms of cavities. Often, also, we find irregular groups of interglobular spaces in the dentin into which microorganisms grow very readily and in that way pro- duce irregularities in cavity forms. This occurs when there is no appearance of atrophy upon the enamel. In cases of atrophy, particularly where the occlusal surfaces of the first molars have been wrecked, caries is very likely to run through the sheet of interglobular spaces in the dentin, usually only a little below the dento-enamel junction. This often forms a broad, open cavity with the decay still following this sheet of interglobular spaces until finally the whole occlusal surface is cut away, the decay having extended but little in depth. The result is that the whole occlusal surface of the tooth has decayed, leaving a blackened stump, which may come to occlude with its fellow of the opposite jaw and do excellent service in mastication. It too often hap- pens, however, that decay persists in those portions of the sheet 126 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. of interglobular spaces that dip down on the axial surfaces and finally reaches the pulp of the tooth. As the atrophy occurs in all four of the first molars, it is rather rare that some one or more of them is not destroyed. These are the principal faults in the structure of the teeth that seem to influence caries. It will be noted that all of these faults are such as are discoverable by macroscopic or microscopic examination. No faults in the chemical structure of the teeth have been found which seem to influence caries in any marked degree. Even some of those rare cases in which the cementing substance between the enamel rods has failed, leaving the enamel rough and chalky, have been found almost immune to dental caries. It would seem that such teeth would be especially liable to decay early and quickly, and they certainly would do so if they were in the mouths of suscepti- ble persons. Physiological and Pathological Differences Between Bone and Dentin. illustrations: figures 151155. Some persons have seemed to suppose that the teeth and the bones, being calcified tissues, should have similar physiological processes of nutritional change and of repair, and that similar changes might be expected as results of pathological conditions. It is well known that, in certain diseases, as in rickets, the bones become soft and may become hard again; and that nutritional changes are going on continually in the bones up to an advanced age, if not during the whole life, and that the bones are very apt to become hard and brittle as persons grow older. In the study of the bones, we find that, continuously, or at least frequently, portions of the bone are being removed by absorption and replaced by Haversian systems, so that the shaft of a bone that has been formed largely as subperiosteal bone, is finally converted almost or quite into bone composed of Haver- sian systems. This is shown in Figure 151, which is a photo- micrograph from a cross section from the femur of a young per- son. In this figure the line drawn from the letter a passes over laminae of subperiosteal bone, which have not yet been cut away. The lines drawn from b point to Haversian systems, where the subperiosteal bone has been cut away and new bone supplied in the form of circular whorls, with a canal in the center of each, which is called a Haversian system. In Figure 152, a photo- micrograph from a section cut lengthwise of the same bone, SYSTEMIC CONDITIONS. 127 shows the Haversian canals cut lengthwise for the most part. In studying these, it will be seen that nearly the entire substance of the bone as first formed has been cut away and is replaced in the form of Haversian systems, and in many of the bones we find no traces of subperiosteal bone left, except, possibly, on the outer surface. In this cross section, however, we find many patches of subperiosteal bone scattered through it, though most of it is occupied by the Haversian system bone. Each Haversian canal has its blood vessels. In many bones we find the Haversian systems have been cut out again and again and new Haversian systems built in their places. This is not done by removing the old Haversian systems individually, but by absorptions that seem to run through the bone at random, often cutting out parts of these systems and leaving parts by which such additional cutting and rebuilding is readily recognized. This is nature's manner, or the physiological plan of making nutritional changes in the bones; a plan perfectly well known to histologists and physiologists. There is no such plan for nutritional changes in the human teeth. Normally, there is no absorption of the roots of the permanent teeth, nor any absorp- tional changes going on. Normally, as a physiological process, however, the roots of the deciduous teeth are removed by absorp- tion in the shedding process. Figure 153 is a photomicrograph from a line of absorption at a in a cross section of a deciduous tooth, showing the peculiar notching known as the lacuna? of Howshijo, where the dentin and cementum were being removed by the process of absorption. In the bones the process of absorp- tion is practically the same in kind and quality, and though we name the cells which absorb bone, osteoclasts, and those which absorb the roots of teeth, odontoclasts, there is really no differ- ence in the two processes physically or physiologically. Figure 154 is a photomicrograph from an example of this in bone, which may be compared with that in dentin and in cementum. An absorption of bone is always repaired with bone. It may, if it is on the surface, be repaired by subperiosteal bone. If within the bone, it is repaired by Haversian system bone. An absorp- tion of any portion of a tooth, dentin or cementum, if repaired at all, is repaired with cementum ; no matter how deeply it may have cut into the dentin, it is never repaired by dentin. Many of these repairs are found in the study of the histology of the teeth, where, for some cause, an absorption has occurred, cutting deeply perhaps into the root of the tooth. Several pictures show- ing this are published in my book on "Periosteum and Peri- 128 PATHOLOGY OF THE HABD TISSUES OF THE TEETH. dental Membrane." The photomicrograph, Figure 155, shows the repair of an absorption which had occurred in the root of a tooth in which the full contour is rebuilt with cementum. These illustrations are brought prominently forward in this place as the histo-physiological expression of the fact that den- tin possesses no means of physiological repair. Additions may be made to it by the action of other tissues, but dentin never repairs itself. It is never repaired by dentin under any circum- stances, excepting such as may be done by calcifications occur- ring in the pulp chamber. These may sometimes effect a repair of an exposure of the pulp. This latter is a physiological process, however, in which the pulps of teeth are inclosed by further deposit of calcified matter, by cells whose physiological purpose has been the building of the dentin originally. Their sphere of action is always within the pulp chamber, never elsewhere. The suggestion has been made that some additions of calcium salts may be made on the walls of the dentinal tubules, narrowing their caliber. This is plausible, but, as yet, no sufficient series of measurements have been made to determine the facts. An injury of any character occurring to the dentin during its devel- opment remains an injury for life. In the study of atrophy, we find sheets of interglobular spaces passing throughout that por- tion of the dentin being formed at a time of malnutrition. These are never repaired. They form an injury that remains perma- nently. Dentin, or enamel, once formed, is formed for all time ; it never can be re-formed, changed, or improved in its character or qualities. It is fixed material; nature has furnished it with no physiological means of repair or betterment. Studies by Dk. J. Leon Williams. ILLUSTRATIONS: FIGURES 156-158. Dr. J. Leon Williams, of London, published a series of studies (Dental Cosmos, 1897) of faults in the teeth of animals as compared with faults in the teeth of man, and of the beginning of caries under plaques formed on the surfaces of teeth, which he found to be composed mostly of microorganisms agglutinated together. He found the structure of the human teeth much more perfect than that of the teeth of the animals. The faults in structure were less frequent in man and generally of less con- sequence, notwithstanding the fact that animals do not suffer from caries of the teeth, except in a few rare instances of captive animals kept in cages, some domesticated house-dogs, etc. a^ni^ H Uto° miCr0SraPh °' b ° ne iD pr ° CCSS ol »*-»»«<»■ *■ L»e of absorption showing the lacunse of Howship. Flo. 155. A photomicrograph of a porti which an absorption has been repaired by p. Peridental membrane. ] of the root and peridental membrane of a tooth in growth of cementum. D. Dentin. C. Cementum cementum built in, in repair of an injury by absorption. ^«t1fe3 Fig. 156. A photomicrograph of a plaque covering the surface of the enamel in which caries beginning. Williams. Fig. 157. A thick gelatinoid plaque over the surface of decaying enamel. Williams. Pig. 158. A photomicrograph showing a stained film of microorganisms over the surface of decay ing enamel. In pressing down the cover-glass in mounting the specimen, the microbic film has been parted slightly from the surface of the enamel. Williams. SYSTEMIC CONDITIONS. 129 It will be found by a review of the dental literature, that decay of the teeth of man was generally supposed to be because of imperfection in their structure, and many times it has been said that the teeth of man were degenerating and were not so well calcified as the teeth of animals. After a long series of studies, Dr. Williams' opinion was exactly the reverse; and further, that the decay of the teeth of man was not to be attrib- uted to their faulty structure. This opinion seems to have been well supported by the histological structures developed by his microscopic work. His work took a wide range among the lower animals. As I had been studying gelatinous masses formed on the teeth by microorganisms and their influence in shielding the organisms growing in them from washings by the saliva, which would dissipate the acids formed, I was much interested in this phase of his work. But later, in the study of his illustrations and methods, comparing these with my own work along similar lines, it seemed that he had included all manner of material that contained microorganisms (practically any material clinging to the teeth contains them), going wide of the line of those forms of fungi known to produce caries. He seems also to have included deposits through which water would run so easily that they would be no bar to washings by the saliva. Such coatings are found plentifully over the surfaces of the teeth of immune per- sons, and also in others where there is no decay of the enamel. Careful study shows that many kinds of deposits upon the teeth present similar appearances, when seen in microscopic sections, to those produced by gelatinous plaques, and yet seem to have no influence whatever in the localization of caries. A plaque, to have any considerable effect, certainly must have sufficient firm- ness in the moist state to act more or less perfectly as a dialyzing membrane. In the technical sense, Dr. Williams' work was beautifully done, and there is no doubt that caries was shown under the aggregations of organisms in many of his photomicrographs. Three of these, Figures 156, 157, 158, are reproduced from the Dental Cosmos, of 1897, by permission. SlALO-SEMEIOLOGY. Dr. Joseph P. Michaels, of Paris, presented a brochure under the above title to the International Dental Congress, Paris, 1900, which has been translated into English and published in the office of the Dental Cosmos, 1902. 130 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. In this, Dr. Michaels claims to have found the means of determining definitely the existence of the conditions of suscep- tibility to, or immunity from, dental caries, by the examination of a few drops of the individual's saliva. Persons who have spent some time in Dr. Michaels' laboratory and looked over his work, seem convinced that he can do what he asserts. In this writing, the qualities of the saliva are summarized thus: (1) Normal, (2) Hypo-acid, (3) Hyper-acid, and (4) Cacochymic. In the first, the normal, little or no caries occurs. In the hypo-acid condition, the susceptibility is intense or moderate, according to the intensity of the condition. In the hyper-acid condition there is immunity from dental caries. The cacochymic denotes a bad condition of the saliva, due to some functional derangement or organic disease without further specification, and includes very variable conditions. It has no special reference to dental caries. The terms, hypo-acid and hyper-acid diathetic states, do not refer to reactions to litmus. He says: "The abnormal vital processes tend in mankind to pathological conditions, which we may classify under two humoral conditions, viz., hypo-acidity and hyper-acidity. The first state (lymphatism) is the expres- sion of a vital over-activity and has as consequences the con- tagious diathesis (scrofula, tuberculosis, syphilis). The oxida- tions are over-active and the hydrations superior to the normal, hence there is a decrease in organic acidity and an increase in the saline chlorids excreted by the economy. Hypo-acidity, according to Duclaux, favors chemical changes in the tissues. In the hypo-acid diathesis all of the oxidations are exaggerated and above normal. . . . Hyper-acidity is a particular state of the organism characterized in a general way by slowness in the biochemical changes. ... It is not doubtful that the activity of caries in some individuals and the immunity from or the slowness of decay in others are in correlation with diathetic states well determined, resulting from a lack of proper balance of the general factors, and in particular of the blood plasma." Many of the expressions in this brochure seem difficult for many who have read them to understand, but it has seemed evi- dent that, while many other substances in the saliva are found to influence conditions as to caries of the teeth, the absence or pres- ence of the sulphocyanids, or the large or small proportions present, is the most constant mark separating the condition of susceptibility to caries from the condition of immunity. Much of the work is done by the examination of crystals by SYSTEMIC CONDITIONS. 131 the microscope and micropolariscope, and is necessarily qualita- tive rather than quantitative. Recently the committee of the New York State Dental Society on dental science has taken up the question of the influ- ence of the presence of the sulphocyanids in the saliva as a special piece of work, and is making numerous examinations by clinical and laboratory methods. Its last annual report is not yet at hand, but from the information derived from private sources, it seems that this test alone is giving correct indications as to the susceptibility to, or immunity from, caries, in about ninety-sis to ninety-seven per cent of the individuals examined. This is indicated by the absence of, or only very slight reactions, indicating the presence of none or a very small quantity of the sulphocyanids of potassium in susceptibility, as compared with more decisive reactions indicating a large quantity of the sulpho- cyanids in the saliva of immune persons. In the prosecution of this work, another point has developed which may prove of much significance upon further examination. In some cases which were examined a number of times, the teeth, after being well cleaned, were found again coated over with gummy material so quickly as to attract special attention. This gave rise to the suggestion of precipitation from the saliva of some material in it that was not held in solution. Therefore, this saliva was com- pared with the saliva of others, in whom there was an absence of such material, as to its power of dissolving the residue of saliva that had been dried. The result was that the saliva from which such deposits occurred would not dissolve such residue at all, while saliva from persons whose teeth remained free from such deposits dissolved them readily. It will be of much interest to know whether or not such deposits will form films that will act as dialyzing membranes and so inclose colonies of micro- organisms as to protect the acids formed from a too free dissi- pation in the fluids of the mouth, and, in this way, become a factor in the production of the beginnings of caries of the enamel. This may lead to some important discoveries in the near future. Dr. Carl Rose, of Dresden, Germany, is doing an immense amount of work on the saliva, especially with reference to its amount under different conditions of living and the variations in the salts it contains. In this work he is collecting an immense amount of data with reference to the effects of the salts found in the water used for drinking and cooking purposes. In this work he is developing important facts regarding the relation of 132 PATHOLOGY OF THE HARD TISSUES OF THE TEETH. these salts to the percentage of dental caries, the relation of the amount of saliva secreted by the person to the percentage of caries, the relation of salts in drinking water to the development of the salivary glands, etc. The examinations have been mostly made in children. These have been widely distributed in Ger- many, Switzerland, Denmark, Sweden, etc. The work is still in progress. This mention of work being done is given here to show the direction which thought is taking and the activity manifested, rather than for the purpose of giving specific information of its detail. The questions are of very recent origin. The question of immunity and susceptibility to dental caries as a systemic con- dition as known to-day, was first propounded in 1895. Years will probably be required before this problem, involved in such obscurity and difficulty, can be so unfolded and simplified that the general profession may make practical use of it in the treat- ment of dental caries. In the meantime, the general discussion of it belongs to the journal literature rather than to books. The Saliva. When the saliva is mentioned without designation of its special parts, it is most generally understood that the mixed fluid found in the mouth is meant. This is made up of secretions from several sources, any of which may be examined separately. These are the saliva from the parotid gland, saliva from the submaxillary and sublingual glands, and mucus from the mucous follicles situated in the mucous membrane of the mouth. The different salivas are much alike. Though variable, they are generally very limpid, watery secretions. The mucus, on the other hand, is more generally found to be a thick, ropy secretion. If the parotid saliva is collected directly from Stenson's duct it will generally be found to be about neutral in its reaction with litmus, varying from slightly alkaline to slightly acid. If the mucous membrane of the mouth, say the roof of the mouth, is dried and the mouth held open for some time, one will generally find here and there globules of fluid collecting on its surface. Sometimes many of these will be seen ; sometimes very few, and, occasionally, none without a very long wait. The secretion seems to be very variable. Touching litmus to this generally brings a very definite acid reaction. In the lips, I have usually found much larger glands than elsewhere in the mucous membrane. Some of the larger of these seem to emit a much more watery fluid than the usual submucous glands. It is more of the nature THE SALIVA. 133 of that from the salivary glands. This seems to have to do with the moistening of the mucous membrane of the lips especially. The mucus is very variable, both in amount and consistence. Often it is very thick and viscous, so much so that, by touching the finger to a globule, it may be drawn out into a very long thread. The variations in the viscosity of the general saliva have been commented upon by most of those who have examined it in many individuals. Often it is found to be very thin and watery. Not very infrequently it is almost as thick and viscous as the mucus itself. I have met with persons whose saliva was so viscous that I could at any time draw out threads two or three feet long by touching my finger to it and drawing it away. In filtering this, it will leave an unusually large amount of gummy material on the filter. In such cases an excitation of the flow of saliva generally causes the thinning of the mixed fluid for the time, which seems to be due to the larger proportion of the parotid, submaxillary and sublingual salivas. There are great differences in the saliva as to deposits. Many persons are found whose teeth are free from deposits of gummy or slimy material. The saliva seems to hold all of its ingredients in complete solution, and is capable of dissolving quickly all of the ordinarily soluble things with which it comes in contact. Therefore, the mouth is always clean and free from debris. In others the saliva seems habitually incapable of hold- ing its own ingredients in solution. The teeth especially are continually covered with a slimy, viscid coating, and more solid deposits are frequently found. Many writers have noted these differences in persons, and also at different times in the same individuals. The salts of the saliva seem to be very variable. If a person consults many authors, who have reported their findings, he is soon lost in a maze of discrepancies. Dr. Michaels quotes the following from Hammerbacher as representing normal saliva in an analysis of 1,000 parts :