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Interstitial Gingivitis 
 
 AND 
 
 PYORRHCEA ALVEOLARIS 
 
 BY 
 
 El'gexk S. Talbot, M. S., D. D. S., M. D., LL. D. 
 
 Late Professor of Stomatology, Woman's Medical School, Northwestern University 
 Late Lecturer on Stomatology, Rush Medical College, University of Chicago; Fellow 
 of The Chicago Academy of Medicine; Fellowship Member op the New York St^^te 
 Dental Society, 1908; Secretary of Section on Stomatology of the American 
 Medical Association; Vice-President American ^Medical Association 1905- 
 Member VII International Medical Congress, 1881, London; Honorary Presi- ' 
 DENT X International Medical Congress, 1890, Berlin; Honorary President 
 Xll International Medical Congress, 1897, Moscow; Corresponding 
 Member, Budapest Royal Society of Physicians; Honorary President 
 International Association of Stomatology, 1907, Paris; Member First 
 French Congress of Stomatology, 1907, Paris; Honorary Secretary 
 Pan-American Medical Congress, 1901, Havana; Honorary Member 
 Odontologischen Gesellschaft, Berlin; Honorary Member 
 Association Generals des Dentistes de France. Paris; Honor- 
 ary Member Sociedad Odontological Espanola, INIadrid; 
 Corresponding Member Dansk-Tandlaegeforening, 1901;' 
 Honorary Member Stomatology Society of Hungary; 
 Corresponding Member of the Italian Stomatological 
 Federation, 1910; Member Chicago Academy of 
 Sciences; Member American Association for the 
 Advancement of Science; Charter Member 
 American Institute of Criminal Law and 
 Criminology; IMember of the Author's 
 Club, London. 
 Author of the following books: "The Irregularities of the Teeth and their Treatment-' 
 Chart of Typical Forms of Constitutional Irregularities of the Teeth;" The 
 Etiology of Osseous Deformities of the Head, Face, Jaws and Teeth;" 
 "Degeneracy: Its Signs, Causes and Results;" "Developmental 
 Pathology: A Study in Degenerative Evolution," etc., etc. 
 
 WITH 102 ILLUSTRATIONS 
 
 TOLEDO, O. 
 THE RANSOM & RANDOLPH CO. 
 
 1913 
 
 r y^..,JU^<^ ni«^'S^'^^.S-»«. 
 
1^)3 
 
 ENTERED ACCORDING TO ACT OF CONGRESS 
 IN THE YEAR 1913, BY 
 
 EUGENE S. TALBOT 
 
 IN THE OFFICE OF THE LIBRARIAN OF CONGRESS 
 AT WASHINGTON, D. C. 
 
 All Rights Reserved 
 
 THE PUBLISHERS' PRESS 
 CHICAGO 
 
To 
 MISS ELLA CLAY 
 
 Aiy Late Faithful Assistant 
 
 Whose scientific ability was recognized and appreciated by scientists 
 
 This work is dedicated 
 
PREFACE. 
 
 In this book the etiology, pathology and treatment of peri- 
 dontal disease have been worked out by actual research which 
 covered a period of thirty-five years. Up to the present time 
 teachers and practitioners have taught that disease of the gums 
 and alveolar process was of a pyorrhceic or infectious nature. 
 All etiologic experiments and treatment are made from this 
 basis. The tendency at the present time is to study diseases of 
 the body from a bacteriological view point. It is now known 
 that many different tissues and organs of the body undergo 
 physiologic and chemic changes which are often due to irrita- 
 tions setting up inflammation and may later under certain con- 
 ditions become infected by bacteria. Inflammations of the 
 mucous membranes due to acid states and burns are of this 
 nature. It has been the aim of the author to classify the 
 inflammations due to infections and those due to chemic 
 changes and local and constitutional irritations. The diseases 
 of the alveolar process due to infections are usually of systemic 
 origin and develop symptoms in other parts of the body such as 
 tuberculosis, typhoid fever, anthrax, actinomycosis, etc., and 
 are rarely referred to the specialist for treatment. The pa- 
 tients referred to the specialists are those with inflammations 
 of the gums, mucous membrane and alveolar process due to 
 irritations and which ma}" or may not later become infected by 
 bacteria. 
 
 The author has observed that every vertebrate having two 
 sets of teeth during life may possess an inflammatory condition 
 of the alveolar process to a greater or less extent after the first 
 set of teeth has developed depending upon environment and 
 the condition of the system. 
 
 The pyorrhceic stage which may develop later is observed 
 in only a very small per cent of patients. Happily, to a certain 
 
11 PREFACE 
 
 extent, the profession has come to realize the importance of the 
 two periods and the teaching of the pathology and bacteriology 
 of the disease is much simplified and better understood. 
 
 The great law of medical science, that to know the cause is 
 half the treatment, is as applicable to diseases of the mouth as 
 to any other specialty of medicine, and is as applicable to dental 
 problems as to those of biology generally. Treatment of any 
 disease without knowledge of its pathology is practically a 
 failure. 
 
 While much has been written upon the pyorrhoeic stage of 
 interstitial gingivitis and its treatment, during the past two 
 decades, no new principle has been advanced w^hereby the parts 
 can be restored to a healthy condition, or whereby the disease 
 can be prevented. The disease is admittedly on the increase. 
 This seems at first sight to indicate that dental prophylaxis and 
 treatment, so far as this disease is concerned, are failures. 
 
 Nearly three decades ago I felt and expressed the necessity 
 for more extended study (Dental Cosmos, 1886, page 689) of 
 the clinical aspects and etiology of this disease. Even daring 
 apparently diverse and separated studies, such as those related 
 to dental and maxillary irregularities and degeneracy, the ne- 
 cessity for this has forced itself still further upon me. In the 
 present study, the disease has, of necessity, been considered 
 from the broad standpoint of general pathology. In all in- 
 stances where possible personal elements of error are present, 
 these have been eliminated by having researches made by more 
 than one observer. 
 
 The attempt has been made to summarize all researches on 
 the subject. So much have opinions been intermingled that it is 
 possible that proper credit for priority has unintentionally not 
 been given. 
 
 The author is under obligation to the following scientists for 
 their kind assistance : Dr. Ludwig Hektoen, Pathologist, Rush 
 Medical College; Dr. Jerome H. Salisbury, Chemist, Rush 
 Medical College ; Dr. W. A. Evans, Pathologist, Columbus Med- 
 ical Laboratory, Professor of Pathology, Chicago College of 
 Physicians and Surgeons and Milwaukee Medical College; Dr. 
 J. A. Wesener, Chemist, Columbus Medical Laboratory, Profes- 
 
PREFACE 111 
 
 sor of Chemistry, Chicago College of Physicians and Surgeons ; 
 Dr. Vida A. Latham, Pathologist, Northwestern Uinversity, 
 Woman's Medical School; Dr. Maximilian Herzog, Pathologist, 
 Chicago Polyclinic Hospital; Professor Theo. A. Ed^\an Klebs 
 and Dr. Robert F. Zeit, Pathologists, and Dr. W. L. Baum, 
 Professor of Diseases of the Skin, Post-Gradnate Medical 
 School, Chicago; Dr. G. V. I. Brown, Professor of Oral Sur- 
 gery, Dental Department, Milwaukee Medical College; Dr. 
 Frederick Noyes, Histologist, Dental Department, Northwest- 
 ern University; Dr. J. G. Kiernan, and to Blomgren Bros. & 
 Co. for electrotypes, etc. 
 
 THE AUTHOR. 
 31 North State Street, Chicago. 
 
CONTENTS 
 
 Chapter 
 
 I. 
 
 II. 
 
 III. 
 
 IV. 
 
 V. 
 
 VI. 
 
 VII. 
 
 VIII. 
 
 IX. 
 
 X. 
 
 XI. 
 
 XII. 
 
 XIII. 
 
 XIV. 
 
 XV. 
 
 XVI. 
 
 XVII. 
 
 XVIII. 
 
 XIX. 
 
 XX. 
 
 XXI. 
 
 XXII. 
 
 XXIII. 
 
 XXIV. 
 
 XXV. 
 
 . XXVI. 
 
 XXVII. 
 
 XXVIIL 
 
 PAGE. 
 
 History 1 
 
 Introduction 13 
 
 Transitory Structures : The Jaws 19 
 
 Transitory Structures: The Alveolar Process. . . 24 
 The Alveolar Process Under the Microscope. ... 35 
 The Gums, Periosteum, Mucous and Peridental 
 
 Membranes Under the Microscope 38 
 
 Inorganic Salts and Interstitial Gingivitis 73 
 
 Theories of Interstitial Gingivitis 84 
 
 Uric Acid and Interstitial Gingivitis 87 
 
 Heredity and Environment in Interstitial Gingi- 
 vitis 95 
 
 Degenerate Tissues in Interstitial Gingivitis. . . . 100 
 Bacteriologic Researches in Interstitial Gingi- 
 vitis 104 
 
 Interstitial Gingivitis . 112 
 
 Researches on Animals in Interstitial Gingivitis . 125 
 Researches on Human in Interstitial Gingivitis. 156 
 
 Researches on Human in Pericementitis 175 
 
 Local Causes of Interstitial Gingivitis 182 
 
 Constitutional Causes of Interstitial Gingivitis. 194 
 Climatic Influences in Interstitial Gingivitis .... 211 
 
 Scurvy in Interstitial Gingivitis 218 
 
 Toxins Producing Trophic Changes 223 
 
 Autointoxication in Interstitial Gingivitis 235 
 
 Urinary Signs of Autointoxication 247 
 
 Arteriosclerosis, Endarteritis Obliterans and 
 
 Nerve End Degeneration 261 
 
 Absorption of the Alveolar Process and Calcic 
 
 Deposits Upon the Roots of the Teeth 275 
 
 Pyorrhoea Alveolaris 285 
 
 Constitutional Effects of Pyorrhoea Alveolaris. . 295 
 
 Treatment 310 
 
 Bibliography 330 
 
 Index 335 
 
INTERSTITIAL GINGIVITIS 
 
 CHAPTER I. 
 
 HISTOEY. 
 
 Inflammation of the peridental membrane and alveolar pro- 
 cess is probably coeval with man. Some of the skulls found 
 earliest in the cave-dwelling period exhibit evidences of its 
 presence. In some of these, careful observation has shown de- 
 posits encroaching upon the roots of the teeth and resultant ab- 
 sorption of the alveolar process. 
 
 In the Swiss lake-dwellings and in the earlier Irish cran- 
 noges of like construction and situation, skulls are found, which 
 exhibit deposits of tartar, inflammation of the peridental mem- 
 brane and absorption of the alveolar process. These skulls were 
 those of primitive races in whom disease of the jaws and teeth is 
 supposed to be absent or infrequent. In the skulls of the peo- 
 ples exhibiting the highest civilization at the earliest period — 
 those of the Accadians and Egyptians — similar inflammatory 
 conditions are to be found. This, however, was to have been 
 expected, to judge from the dental directions left among the 
 medical records of these peoples. The Greeks, Syrians, Arab- 
 ians, Dra^ddians and Aryans of India and the early Burmese 
 all suffered from this disorder. In the museum at Constan- 
 tinople are the skulls of soldiers who fought at a battle 328 
 B. C. One of these skulls has the anterior alveolar process 
 entirely absorbed away. The roots of the right central, the 
 right lateral and the left central incisors are exposed. 
 
 Inflannnation of the peridental membranes and alveolar proc- 
 ess, it A\ill be evident, is, therefore, not a modern disease ; not a 
 disease confined either to civilized or primitive races, but one 
 which attacked man early in his evolution. Like most diseases 
 it has been chiefly discussed and analyzed during the past two 
 centuries. 
 
Z INTERSTITIAL GINGIVITIS. 
 
 In 1740 H. A. Fauchard ^ (while recognizing the disease in 
 all its essential features and describing its principal symptoms) 
 advanced no theory as to its origin. 
 
 In 1778 M. Jourdain ^ advanced the opinion that the disease 
 was of scorbutic origin. 
 
 In 1821 L. Kaecker ^ discussed the disorder in an essay on 
 the devastations of the gums and alveolar processes. 
 
 In 1822 M. Joirac* (in a discussion of the disease), while 
 advancing no theory as to its origin, called it '' pyorrhoea inter- 
 alveolo-dentaire. ' ' 
 
 In 1860 Marshall de Calve ^ advanced the opinion that the 
 disorder was of hereditary origin. 
 
 In 1867 Magitot, discussing the disorder, advanced the 
 opinion that the gum, being in all cases only attacked subse- 
 quently, is not the original seat of the lesion. In his opinion 
 systemic disorders like gout, rheumatism, albuminuria, diabetes 
 and angemia had an influence. 
 
 BonwilP during the same year expressed the opinion that 
 the disorder was due to thinness of the alveolar process between 
 the teeth, thus depriving the peridental membrane and gum 
 tissue of proper support. The want of proper articulation of 
 the teeth also exerted an influence. 
 
 In 1870 Brown ascribed the disorder to serumal calculus. 
 
 In 1875 John T. Riggs, after whom the disorder is frequently 
 called, entitled it (in a paper read before the American 
 Academy of Dental Surgery) suppurative inflammation of the 
 gums and absorption of the gums and alveolar process. 
 
 During the same year Scheif "^ of Vienna entitled the disorder 
 periostitis dentalis. He was of the opinion that it originated 
 from external irritation through mechanical, thermic and chemic 
 changes. The real origin of the disorder was, in his opinion, 
 very often obscure. He doubted, however, the influence of 
 rheumatism. 
 
 ^Independent Dental Journal, 1875. 
 
 * Philadelphia Journal of Medical and Physical Science, 1821. 
 ' International Dental Journal, Vol. XIII. 
 
 * Journal of the American Medical Association. 
 
 * Journal of the American Medical Association. 
 « Dental Cosmos, Vol. XXIV. 
 
 ■ Wiener Med. Presse, Vol. XVI. 
 
HISTORY. 6 
 
 In 1876 Sirletti ' (in a discussion of the pathology of the 
 disorder, which he called alveolo-dental periostitis) regarded it 
 as due to constitutional conditions, like rheumatism, scrofula, 
 syphilis, etc., with local causes as exciting factors. 
 
 In 1877 Rehwinkle,^ in a paper on pyorrhoea alveolaris, after 
 citing from Albright (of Berlin) the claim that the disorder 
 was due to uncleanliness, mercury and the suppression of habit- 
 ual secretions, expressed the opinion that acquired and inherited 
 constitutional defect often played an important part as etiologic 
 factors. He was also of opinion that mercury exerted an influ- 
 ence in its causation. Salivary deposits were, in his opinion, 
 without influence. 
 
 Clowes ^^ was of opinion in 1879 that the general cause was 
 lack of nutrition in the parts. The use of wedges often excited 
 the disorder. 
 
 C. J. Essig," in 1880, expressed the opinion that its predis- 
 posing causes were unknown, that it occurred as a rule in healthy 
 persons, and that irregular and crowded teeth acted as an excit- 
 ing cause. 
 
 In another paper during the same year G. A. Mills " ex- 
 pressed the opinion that the disorder was of systemic origin. 
 Various mental and physical influences aided its progress, such 
 as nervous exhaustion and bodily and mental overwork. In his 
 opinion it frequently occurred in children and adolescents from 
 eruptive fevers. The deposit was only a local manifestation of 
 the disorder. 
 
 In 1881 N. S. Niles " expressed the opinion that constitu- 
 tional conditions were, as a rule, without influence, and that local 
 irritating deposits were the cause in twenty-five per cent of the 
 cases coming under his observation. He was of opinion also 
 that the amount of lime salts taken into the system in drinking 
 water exerted an influence. A calcic and phosphatic diathesis 
 had an influence in the production of the disorder. 
 
 * Gazzetta Medica di Roma, 1876. 
 
 » Dental Cosmos, Vol. XIX. 
 
 '"Ibid., Vol. XXT. 
 
 " Dental Cosmos. Vol. XXI. 
 
 " Ibid., Vol. XXTTI. 
 
 "Ibid., Vol. XXIV, 
 
4 INTERSTITIAL GINGIVITIS. 
 
 In 1881 (when there seemed to have been many contributions 
 to the literature of the subject) Atkinson " expressed the opinion 
 that nervous debihty or original defect in innervation exerted an 
 influence in the production of the disorder. The deposits of 
 tartar were a secondary consequence. In the course of his paper 
 he cited the opinion of Hamilton CartAvright that Riggs's disease 
 commenced in an unhealthy condition of the gums with a sec- 
 ondary deposit of tartar. 
 
 In a paper read before the Dental Section of the Inter- 
 national Medical Congress, Walker ^^ claimed that the starting 
 point of the disease was subacute inflammation passing into the 
 depths of the alveolar process adjacent to the inflamed gum. In 
 the discussion of this paper, Archovy and Joseph Izklai, of 
 Buda Pesth, ascribed the disorder to minute organisms. Oakley 
 Coles thought that systemic states were the predisposing factors, 
 while minute organisms exerted an exciting influence. 
 
 In 1882, L. C. IngersolP*^ regarded sanguinary calculus as a 
 manifestation of the disorder, and distinguished it from salivary 
 deposits. 
 
 Malasses and Gallippe, " in 1884, expressed the opinion that 
 the disorder w^as of microbic origin. 
 
 In 1885, A. 0. Rawls ^^ expressed the opinion that the causes 
 were environment with morbid factors, such as malaria, exces- 
 sive sodium, etc., chloride and mercury. 
 
 In 1886, Reese ^^ expressed the opinion that the disorder had 
 its source in the uric acid diathesis resultant on abuse of alcohol. 
 
 During the same year, J. D. Patterson -° expressed the opin- 
 ion that the disorder was of catarrhal origin. Later, in 1886, J. 
 N. Farrar "^ regarded the disorder as a combined result of sys- 
 temic tendencies and local irritants. There was a peculiar con- 
 dition of the system associated with hypersecretion laden with 
 increased earthly deposits. 
 
 " Dental Cosmos, Vol. XXIV. 
 
 ^^Transactions of the International Medical Congress, 1881. 
 
 1" Dental Cosmos, Vol. XXV. 
 
 " Ibid., A^ol. XXVI. 
 
 " Ibid., Vol. XXVII. . 
 
 " Independent Practitioner, Vol. VI. 
 
 =" Dental Cosmos, Vol. XXI. 
 
 °^ Independent Practitioner, Vol. VII. 
 
HISTORY. 
 
 A. R. Starr later also expressed the same opinion. He, how- 
 ever, was unable to determine the local irritation factor, but 
 regarded it as the same as that which causes exostosis of the 
 cementum. He had found most cases in the upper jaws. 
 
 Black " designated the disorder phagadenic pericementitis. 
 It was a specific infection of an inflammatory character, having 
 its origin in the gingiva, and was accompanied with destruction 
 of the peridental membrane and alveolar walls. 
 
 E. S. Talbot -^ during the same year regarded the disorder as 
 a local one, due to both local and constitutional causes. The 
 disorder began with simple inflammation of the gums, which 
 afterward became chronic. 
 
 He laid particular stress upon the anatomy, physiology and 
 pathology of the parts involved, there being no other struc- 
 tures in the human body like them, hence their eas}^ suscepti- 
 bility to disease. 
 
 We may consider, then, as predisposing and exciting causes 
 a perverted condition of the secretions, low vitality of patient or 
 tissues or both, calcic deposits and all diseases which affect the 
 circulation such as drugs and auto intoxication, and as among 
 the local causes catarrh, fistulae, salivary calculus, irritation 
 from foreign substances, which are included as modern dentis- 
 try, such as detached bristles from the tooth brush, too great 
 friction in brushing, injudicious use of the toothpick, the use of 
 ligatures and regulating apparatus, application of the rubber 
 dam and clamps, artificial dentures and regulating plates, ac- 
 cumulation and decomposition of food under artificial dentures, 
 and at the necks of the teeth, drugs which over-stimulate the 
 parts, the use of tobacco, fillings extending beyond the cervical 
 margins, digestive derangements, contagion from unclean in- 
 struments," and improper mouth washes and tooth powders, 
 especially charcoal. In a word, whatever irritates the gums, 
 alveolar process and peridental membrane is likely to produce 
 the lesion under consideration. The devitalization of pulps and 
 tlie filling of roots, which throw increased work upon the mem- 
 
 " American System of Dentistry. 
 =» Dental Cosmos, Vol. XXVIII. 
 
b INTERSTITIAL GINGIVITIS. 
 
 brane, are also to be accounted as among the factors responsible 
 for this pathological condition. 
 
 Talbot pointed out that the disease is contagious so far 
 as- one tooth becomes infected from another in the same mouth. 
 
 Of the status of this disease at the close of the year 1887, 
 the following analytic picture was drawn by W. X. Sudduth '* : 
 ''Pyorrhoea alveolaris is a term applied to the secondary stages 
 of a disease that has its inception in a catarrhal stomatitis. Be- 
 ing confined, as a rule, to the margin of the gums surrounding 
 the teeth, it might be called a 'gingivitis,' were it not for the 
 general catarrhal tendency shown by the entire mucous mem- 
 brane of the mouth and nasal passages. The intimate relation 
 between a general catarrhal idiosyncrasy and pyorrhoea alveo- 
 laris is more than mere coincidence." Its common occurrence in 
 persons who have irregular teeth has also been often noted by 
 Dr. Sudduth, who considers that this fact has, besides the matter 
 of uncleanliness, a direct bearing upon its pathogeny. It is well 
 known that the irregularities of the teeth present an indication 
 of a degenerative taint, and that persons in whom irregularities 
 occur are very prone to catarrhal affections of the respiratory 
 organs, including the nasal passage. Their skin is usually very 
 susceptible to inflammatory affections. Another feature is the 
 offensive ordor of the saliva of individuals who show this partic- 
 ular tendency to catarrhal affections even in persons who take 
 most scrupulous care of the teeth. In the majority of cases, 
 pyorrhoea is a stomatitis in which the local and constitutional 
 factors in the production of the disease are largely dependent 
 upon hereditary catarrhal dyscrasia for their ability to engraft 
 themselves upon the tissues. This position is borne out by the 
 clinical experience of Patterson, of Kansas City, Missouri, who 
 reports thirty-eight cases of well marked pyorrhoea observed 
 by him, thirty- three of which presented undoubted evidence of 
 nasal catarrhal conditions ; two were the result of direct irri- 
 tation of misfitting partial plates, and the remaining three were 
 apparently caused l)y calcific deposits. Patterson remarks that 
 a close examination of the history of the above quoted cases 
 
 Sajoiis' Anuiial, 1888, Vol. Ill, page 365. 
 
HISTORY. 7 
 
 confirms the opinion that the disease is, as a rule, an "oral 
 catarrh. ' ' 
 
 From the foregoing W. X. Sudduth feels justified in class- 
 ing the disease as a localized catarrhal stomatitis which may be 
 either acute or chronic. Acute catarrhal inflammation of the 
 gums begins in circumscribed points which present a bright or 
 rose-red color, and which are generally located on the margin 
 or the rugae of the palate. There is but little swelling because 
 of the dense nature of the sub-epithelial connective tissues. 
 The gums present the same stages as are found in inflamma- 
 tion of other mucous surfaces — first dryness, followed by an 
 increased secretion of mucus. The parts are very sensitive to 
 pressure; the patient complains of an annoying, burning sen- 
 sation. The appearance of the gums is noticeably smooth and 
 glistening. They bleed easily when the brush is used or even 
 during a meal. This stage does not last very long, but soon 
 heals by resolution or passes into a chronic catarrhal stomatitis 
 in which condition the gums become markedly swollen and tur- 
 gid. They present a condition of tumefaction that sometimes 
 rapidly passes into hypertrophy; at other times there is an 
 indurated appearance that may last for some time. Granula- 
 tion tissue may be produced as the result of overstimulation. 
 The gums become detached from the necks of the teeth; and 
 pockets are formed from which a fetid discharge may be 
 pressed, giving a peculiarly disagreeable odor. Bullae are apt 
 to form, which, by rupturing in the process of mastication, 
 give rise to intense smarting. The tongue constantly seeks the 
 surface if the bull» are on the inner side. 
 
 The pathologic changes which take place are, according to 
 Newland Pedley, of England, "hypertrophy of the muco-peri- 
 osteal fold around the teeth, accompanied by dilatation of capil- 
 lary loops, enlargement of the papillae and rapid proliferation of 
 epithelial cells. Later the gums become firm and contracted and 
 display increase of fibrous tissue. The changes which go on in 
 the socket have not been as yet satisfactorily worked out. The 
 examination of the jaws of carnivora, apparently affected mth 
 pyorrhoea alveolaris, leads to the supposition that osteitis of the 
 alveolar process -spreading toward the apex of the socket is pres- 
 
8 INTERSTITIAL GINGIVITIS. 
 
 ent. Later tlie alveolar walls become absorbed and are at times 
 more or less denuded, while the fangs of the teeth become coated 
 with a layer of thin, hard, green-brown tartar. Ultimatel}^ the 
 disease progressing, the teeth, one after another, drop out." 
 
 From what has been said it will be seen that the pathology 
 of pyorrhoea alveolaris may be explained in several ways. The 
 general causes are local or symptomatic, or both combined. The 
 most common cause of catarrhal gingivitis is found in local 
 irritation, combined with some hereditary disposition to catar- 
 rhal affections. The next greatest etiologic factor is sympto- 
 matic — the local manifestation of a constitutional vice. The 
 most common manifestation is that of syphilis and of its anti- 
 dotes, mercury and potassium iodide, both of which sometimes 
 find expression in a localized inflammation which may be the 
 starting point for pj^orrhoea alveolaris. As a complication of 
 the disease in its secondary stages there can be no doubt of the 
 action of micro-organisms, but Sudduth does not feel justified 
 in conceding to them a position of specificity. 
 
 His position above quoted is sustained by Pedley, who finds 
 that in most instances it is due to some constitutional condition. 
 The fact that it is often symmetrical and frequently hereditary 
 gives support as to this view. It occurs in mouths of patients 
 whose health has been undermined by debilitating influences and 
 injudicious habits of living. It is a common sequel of malarial 
 fever. Young persons recovering from eruptive fevers are some- 
 times subjects of pyorrhoea alveolaris. Frequent pregnancies 
 are a fruitful source of the disorder. Attention has been lately 
 drawn to the shedding of the teeth in tabes dorsalis, but it does 
 not, however, seem to be a constant symptom. Pedley 's view, 
 although tending entirely toward the constitutional character of 
 the disease, does not militate against its catarrhal nature. 
 
 Bland Sutton has found shedding of teeth frequent in rheu- 
 matoid arthritis in animals. He has also met \vith it in mollities 
 ossium and other wasting diseases. Magitot (who views the 
 alveolar dental periosteum as a ligament and not of the same 
 nature as osseous periosteum) calls the disease symptomatic 
 alveolar-arthritis, and mentions especially as causes, chronic 
 
HISTORY. 
 
 Bright 's disease and glycosuria, in which latter condition the 
 phenomenon is absolutely constant. 
 
 Patterson holds that "mouth-breathing has, in his expe- 
 rience, been a very common accompanying condition which he 
 cannot help connecting with the production of the disease. By 
 it the gums are kept dry, their functions destroyed and the way 
 paved for catarrhal inflammation. The majority of the patients 
 he has been called upon to treat have been otherwise healthy, 
 robust persons. From this fact he does not favor the idea of the 
 disease being dependent upon constitutional derangement. It 
 is, however, a Avell-known fact that these are the very class of 
 people who when irritation is once set up in their system, present 
 the most aggravated cases, by reason of their superfluous vital- 
 ity. He says he has occasionally met with cases where the local 
 condition w^as evidently aggravated by constitutional derange- 
 ment and cure w^as thereby retarded. The great majority of 
 cases, however, have shown no indication of constitutional pre- 
 disposition, but have pointed unerringly to local irritation by 
 means of which the function of the mucous membrane had been 
 destroyed." 
 
 Syphilis and other aifections may engraft themselves upon 
 the gums without a predisposition of the parts toward an inflam- 
 matory condition, and having disturbed the normal status of the 
 gingival margins they pave the way for subsequent disease in 
 the alveolus. Certain drugs, such as mercury, phosphorus, lead, 
 etc., have a known deleterious action upon the ligamentous at- 
 tachment of the teeth. 
 
 In 1890 Miller ^" expressed the opinion that the disorder was 
 of a parasitic nature. 
 
 In 1892 C. N. Pierce '' charged the disorder chiefly to sys- 
 temic predisposition and enthusiastically advocated the theory 
 of Reese as to the influence of the uric acid diathesis. 
 
 In 1894 W. X. Sudduth" strongly urged the influence of 
 lactic acid as a local factor in the disorder. 
 
 M. L. Rhein ^^ presented a method of classifying pyorrhoea 
 
 -^ ^Micro-Organisms of the Human Mouth. 
 
 -" Internationa] Dental Association, August, 1894. 
 
 -' Ibid., Vol. Xiy. 
 
 "^ The American'Dental Association, August, 1894. 
 
10 INTERSTITIAL (ilNGIVITIS. 
 
 alveolaris in the following manner: "This classification is 
 made by prefixing to pyorrhoea an adjective stating the name of 
 the disease which is causing the pathological symptoms in the 
 oral cavity as 'gouty pyorrhoea,' 'diabetic pyorrlia'a,' etc." 
 
 The author,-^ after further researches, makes the positive 
 statement that the etiology of the disease is due to both consti- 
 tutional and local causes. He again reiterates and makes the 
 positive statement that modern dentistry is producing more 
 ''pyorrhoea" (interstitial gingivitis) than any other one cause. 
 
 He again lays stress on the anatomy and physiology of the 
 parts involved and that the alveolar process is a transient bony 
 structure, simply for the purpose of holding the teeth in place 
 after they have erupted; that the gums are rarely found in a 
 healthy condition ; that the peridental membrane is never in- 
 vaded by pus germs so long as it is in a perfectly normal state ; 
 that in phthisical patients and those with low vitality and pa- 
 tients who have been ill for any length of time, a low form of 
 inflammation of the gums extending to the peridental membrane 
 and alveolar process with pus infection takes place; that the 
 granular debris or calcic deposits in all cases are secondary con- 
 siderations in the breaking down of tissue. 
 
 Neurotics and degenerates, whether wealthy persons or those 
 confined in institutions, are mostly afflicted. Children as well as 
 grown people suffer with the disease. 
 
 In 1897 the author laid particular stress on the poisons cir- 
 culating in the blood causing interstitial gingivitis from auto- 
 intoxication. 
 
 In 1899 he ^° he spoke of the possibility of calcic deposits on 
 the roots of the teeth being "calcareous matter absorbed from 
 the alveolar process in the immediate vicinity of the root," etc. 
 This theory was later confirmed by researches on the alveolar 
 process and mentioned in a paper on "Interstitial Gingivitis," 
 published in The Dental Summary, 1903. 
 
 John Fitzgerald,'^ in 1899, claimed that "The production of 
 pyorrhoea depends upon two factors, a predisposing cause and 
 
 '^ The International Dental .Tonrnal, April, 1896. 
 
 ^° Interstitial Gingivitis or So-called Pyorrhoea Alveolaris, page 169. 
 
 *^ Clinical Journal, March 1, 1899. 
 
HISTOEY. 11 
 
 a local irritation. The predisposing cause may be tuberculosis, 
 syphilis, scurvy, the exhaustion of acute infectious diseases or 
 any other source of malnutrition. The exciting cause may be, 
 and most usually is, a gingivitis produced in one of the ways to 
 be presently described. There is also a pyorrhoea of gouty 
 origin, in which the local necrosis of the peridental membrane is 
 caused by gouty disease of one of the blood vessels in its sub- 
 stance." 
 
 The views on etiology of this condition have varied, it will 
 be observed, from purely constitutional causes to purely local 
 causes, inclusive of microbic affections. In the main it will 
 be ob\T-ous, however, that both constitutional causes, whether 
 inherited or acquired, have been regarded as of influence by the 
 majority of those who have written on the subject. There has, 
 however, been very little exact study of either the predisposing 
 or the exciting causes of the condition. Even the impetus given 
 the study of etiology by bacteriology and embryology has as yet 
 failed to make itself felt to any considerable degree in this 
 department of dental pathology. 
 
 In 1903 the author spoke of the alveolar process as being an 
 end organ ; he also laid stress upon inflammation of the alveolar 
 process as one of the first diagnostic symptoms in constitutional 
 diseases in the same year. 
 
 In 1904 he spoke of the pulp as being one of the most per- 
 fect end organs in the body. 
 
 In an article, '^ Endarteritis Obliterans and Arterial Hyper- 
 trophy in the Alveolar Process," ^- the author first called atten- 
 tion to the calcic deposits (not tartar) on the roots of the teeth 
 and stated that it was "the detritus from the alveolar process." 
 In this article, he lays emphasis on the fact that the alveolar 
 process is not only a transitory structure but is also an end 
 organ which makes it very susceptible to disease. The nerves 
 and blood vessels approach a blank Avail. The roots of the teeth, 
 so far as disease is concerned, are foreign bodies. 
 
 Examination of the alveolar process of animals or human 
 suffering from disease, in which the eliminating organs do not 
 
 The Dental Digest, October, 1903. 
 
12 INTERSTITIAL GINGIVITIS. 
 
 throw off the effete matter (autointoxication), especially in 
 syphilitic, tuberculous and scorbutic persons, easily reveals this 
 morbid state. 
 
 In "Pathology of Root Absorption and Alveolar Abscess" ^^ 
 absorption of the alveolar process is always resultant upon irri- 
 tation and inflammation. The strong point is emphasized that 
 the alveolar process is doubly transitory and also an end organ. 
 He also lays stress on the fact that in the constructive stage of 
 the alveolar process, at the third and fourth periods of stress, 
 the bone ^\ill reproduce itself but after the person has obtained 
 his growth, very little or no restoration can take place. He also 
 states that neuroses or degeneracy in the child has much to do 
 with the success of treatment and that autointoxication also 
 plays a great part in final results. 
 
 In a paper on "Peridental Abscess," ^* in some of the lower 
 vertebrates, there is a continuous succession of teeth called 
 polyphyodontia. When one tooth has performed its function 
 it disappears to give way to another. This continues through- 
 out life. In all vertebrates, including man, where only two sets 
 of teeth are developed, it is called dyphodontia. The alveolar 
 process and teeth of these vertebrates, including man, have re- 
 tained phylogenetic remnants of the physiologic processes of 
 removing transitory structures. Should man live long enough, 
 he would normally lose his second set of teeth by osteomalacia 
 or juvenile or senile absorption depending on the age of the 
 patient. This is a great factor in the transitory nature of the 
 alveolar process. 
 
 The author first mentioned autointoxication in an article, 
 "Autointoxication in Its Medical and Surgical Relations to the 
 Jaws and Teeth. " ^^ 
 
 3" The Dental Digest, 1904. 
 
 "^ The Dental Digest, June, 1903. 
 
 "^ Journal of the American Medical Association, 1897. 
 
CHAPTER 11. 
 
 INTEODUCTIOISr. 
 
 The attempt has been made in the present work to reduce to 
 order the chaotic notions as to etiology, pathology and treatment 
 which, during the present century, have gathered around the 
 morbid condition erroneously entitled Pyorrhoea Alveolaris. 
 While even erroneous titles may have their meaning so fixed by 
 usage that any danger from the error involved in the title may 
 be practically nil, still this is not the case with the title just 
 cited. It suggests erroneous etiology, since pyorrhoea implies 
 that there must always be a flow of pus, and hence that the dis- 
 ease must always result from infection with pus microbes. It 
 implies erroneous pathology and erroneous treatment for the 
 same reason. This being the case, such a title is so dangerously 
 misleading as to compel in the present stage of dental science its 
 modified use as a term for a disease. With a view of clearing up 
 this question at the outset by the use of a proper title, I have 
 adopted as a designation for the condition hitherto known as 
 pyorrhoea alveolaris, the term "Interstitial Gingivitis." To this 
 designation (as to all other attempts to express within a small 
 space an extended pathology, etiology, prognosis, and clinical 
 aspects) there are some objections. The term interstitial is 
 used by some pathologists in a limited obscure sense. By the 
 mass of dental pathologists, surgeons, physicians, and by med- 
 ical lexicographers, the term is employed in precisely the sense 
 in which it is used in the present work. The English surgeon 
 and lexicographer Quain defines interstitial as follows : "Inter- 
 stitial (inter, between; and sto, I stand) ; relating to the inter- 
 stices of an organ. The term is applied in physiology to the 
 tissue which exists between the proper elements of any 
 structure, namely, some form of connective tissue. In 
 pathology the word is used in connection with absorption 
 when a part is gradually removed without any obvious 
 breaking off, and also to indicate the implication of the intersti- 
 tial tissues in morbid processes or their infiltration with morbid 
 products, as interstitial pneumonia, interstitial hepatitis." 
 
14 INTERSTITIAL GINGIVITIS. 
 
 The Encyclopaedic Medical Dictionary of the American 
 Foster, states that interstitial has three signitications : First, it 
 is applied to a condition disseminated through the substance of 
 an organ or part, and to an inflammation affecting the connec- 
 tive tissue of an organ; second, it is also applied to that form of 
 growth which consists in the interposition of new elements be- 
 tween old ones, instead of in addition to the surfaces ; third, it 
 is applied to pathologic processes occupying the space between 
 the essential parts of an organ which constitute its proper tissue, 
 and is then employed in a sense opposed to that of parenchy- 
 matous. 
 
 A glance at the illustrations demonstrates the validity of the 
 application of the term interstitial (in the sense of Quain, Fos- 
 ter, and the other lexicographers) to the condition erroneously 
 called pyorrhoea alveolaris. 
 
 I have adopted the term gingivitis for reasons which will be 
 obvious at the first glance. The philologic objection may be 
 made that in it Greek and Latin are yoked together. Practically 
 this is no objection, since German, French, as well as English, 
 medical authorities employ such terms of mixed origin. Indeed 
 the French (Mailhol ^ for example) apply the term gingivitis to 
 the very condition to which I have applied it. In addition, they 
 add to it the specific term ''expulsive," to designate "a form of 
 recession of the gums, accompanied by alveolar osteoperiostitis, 
 and the gradual expulsion of the tooth from its socket." Fos- 
 ter ^ suggests the substitution of the term ulitis as more philo- 
 logically correct. The term gingivitis, however, has crept into 
 such wide use, that it would be futile to attempt to displace it 
 for merely philologic reasons. 
 
 The term ''gingivitis," however, conveys the idea that the 
 disease always begins at the margin and is confined to the gums 
 themselves. Here again we have an erroneous conception of 
 the pathology of the disease. Thus in the formation of an 
 alveolar or peridental abscess, there is an inflammation pre- 
 ceding the pyorrhoeic stage. This is an interstitial inflamma- 
 tion and the gum tissue is not involved. Again, in inflamma- 
 
 * Odontalgie. 
 " Foster, op. cit. 
 
INTRODUCTIOJv^. • 15 
 
 tion due to mercury, lead, copper, brass, drug, autointoxications 
 and other poisonings and irritations, there is an interstitial in- 
 flammation of the alveolar process and again the gums are not 
 involved until the disease proceeds to a later stage. 
 
 My researches have shown that inflammation may take place 
 from irritants or poisons circulating in the blood at any locality 
 between the gum margin "and the apical end of the root of the 
 tooth. This inflammation may terminate in healthy resolution or 
 it may go on to abscess with a discharge through a small fistula 
 upon the gum which afterwards may heal without pain to the 
 patient and the gingival margin may not be involved. 
 
 I have shown microscopic slides with these pathologic condi- 
 tions in almost every constitutional disease. An inflammation 
 may take place at the end of the root due to irritation or death 
 of the pulp. The gingival border is again not involved. Irrita- 
 tion with inflammation around the roots of teeth occur in gout, 
 rheumatism, syphilis and many other constitutional diseases 
 and the gum margin does not become diseased or the seat of the 
 inflammation may be at any point on the root and extend to the 
 gingival border. 
 
 In all these illustrations the parts are restored to health 
 without pyorrhoea alveolaris or even in many cases gingivitis. 
 It is in such pathologic conditions that the word ^'interstitial" 
 is added to "gingivitis." By this term, then, we know just 
 what is meant. In no other term now in use can we locate the 
 inflammatory area. 
 
 The two terms I have employed convey a fairly correct idea 
 of the pathologic process involved in both deep-seated and super- 
 ficial inflammation, and do not imply erroneous views as to 
 etiology, pathology, prognosis and treatment. 
 
 The pathologic conception adopted in the present work anent 
 interstitial gingivitis is that the disorder is a local inflammatory 
 condition of the gums, or alveolar process, or both, tending to 
 accelerate their normal tendency to disappearance at certain 
 periods of stress, or involution, of which involution the changes 
 produced by old age are a type. In this early senility of the 
 gums and alveolar process, for such it may be termed, two 
 great types of causes play a part; the exciting and the pre- 
 
16 INTERSTITIAL GINGIVITIS. 
 
 disposing causes. The exciting causes may be purely local, or 
 may be local expressions of constitutional states. Thus it will 
 be shown that the influence of uric acid when present is exerted 
 as a local irritant, and not as a constitutional factor — the theory 
 urged so strongly by Pierce. The uric acid hypothesis, once 
 very dominant in medicine, is now losing its force. The trend 
 of medical opinion is to consider it one of the danger signals of 
 autointoxication which assumes prominence because of its ten- 
 dency to excite local irritation. It is but one of a number of 
 local expressions of constitutional defect. This view of the in- 
 fluence of uric acid in etiology the present work will try to dem- 
 onstrate. Prominent among etiologic factors which have to be 
 reckoned with, are pathogenic germs. In the present work it will 
 be shown by all laws of bacteriology (under which investiga- 
 tions must be conducted) that there is no specific germ which 
 is capable of producing the disease itself, and furthermore, that 
 the pyorrhoea stage of the disease is merely a complication due 
 to pyogenic germ infection of the already diseased gums. The 
 views of Galippe as to a specific organism will be shown to have 
 failed of support by numerous control experiments described in 
 the present work. As these have been conducted by different 
 experimenters they are free from the personal elements of error 
 which vitiate the researches of Galippe, who violated that canon 
 of the laws of Koch which compels production of the disease by 
 the alleged specific germ. One predisposing factor will be 
 shown in the present work to be the nature of the structures 
 affected. This in pathology is called local predisposition. The 
 gums, alveolar process, etc., will be shown to be transitory 
 structures, as well as end organs, in themselves predestined (as 
 already stated) to certain changes at certain ages. By the in- 
 fluence of the disease, about to be discussed, these changes 
 occur prematurely. The influence of the toxic agents (mercury, 
 potassium iodide, etc.) will be shown to have been exerted con- 
 stitutionally through the central nervous system, their local ef- 
 fects being a secondary consequence of this. The same will be 
 shown to be the case with conditions like scurvy and autointoxi- 
 cation (where the constitutional factor is most prominent), and 
 with the great neuroses (paretic dementia, locomotor ataxi<'t, 
 
IXTRODUCTIOX. 17 
 
 etc.)- Here, as in the toxic conditions, one great element consid- 
 ered is the influence of the constitutional conditions upon the 
 nerves governing local blood supply and tissue waste and repair. 
 These influences are significantly illustrated in the various proc- 
 esses described later which tear down and build up. 
 
 The influence of morbid heredity as a direct factor ^\dll be 
 shown not to be great. The influence, however, of degeneracy 
 expressing itself along the lines of least resistance ^\ill appear 
 as an ominously important factor. Heredity here, as elsewhere, 
 is a warning rather than a destiny. 
 
 The influence of the nervous system on the processes of 
 growth and repair, which is called its trophic function, has been 
 shown to play a part in both the etiology of the disease and in 
 its progress. This function has received but little attention from 
 dentists, albeit its influence has been recognized in dental path- 
 ology in connection A\ith great neuroses like paretic dementia 
 and locomotor ataxia, in which gum disorders occur, followed by 
 loosening of the teeth. The pathology of the disease has been 
 discussed in the light of established facts of general pathology 
 which have been accepted by the leading dental investigators, 
 and not merely from a hypothetic standpoint. The disease has 
 been regarded as a local exaggeration of certain physiologic 
 processes, accompanied by diminution of the intensity of others. 
 In the study of this phase of the question, the latest researches 
 of dental pathologists as well as original observation and ex- 
 periment have been employed. 
 
 Among tbe many questions which the present treatise is 
 believed to settle (so far as experimentation can) is the follow- 
 ing: The question of the influence and nature of its etiology. 
 It is shown that here, as elsewhere in biology, the etiology of 
 morbid conditions has many phases ; that in it exciting and pre- 
 disposing causes have alike to be considered ; that while causes 
 may be constitutional in origin they very often exert their 
 action locally; that the disease is not a product of civilization 
 nor a product of any one etiologic factor ; that there is no ground 
 yet adduced for believing the disease to be specifically infectious 
 and due to a germ of a specific nature ; that in it the germ infec- 
 tion occurs as a consequence of existing disease, and is not the 
 
18 INTERSTITIAL GINGIVITIS. 
 
 cause of the morbid condition, but one of its stages : Pyorrhoea. 
 The experiments made, as well as the pathologic and chnical 
 data, have been obtained from many observers, so that as many 
 control observations should be had as were necessary to elim- 
 inate personal elements of error inevitable upon original obser- 
 vation and research. In the pathology no statement is made 
 which is not demonstrated by corroboratory data, including a 
 photograph of the condition. The treatment has been based upon 
 the pathology and etiology. Its central idea is that the human 
 being must be regarded as something more than his mouth and 
 teeth; hence the duty of the dental scientist is, like that of all 
 medical scientists, best shown in a prophylactic direction. 
 
CHAPTER III. 
 
 TRANSITORY STRUCTURES. 
 THE JAWS. 
 
 Because of man's advance in evolution and because of the 
 local degeneracies tliereon resultant, through the law of economy 
 of growth whereby one structure is sacrificed for the benefit of 
 the organism as a whole, the face, jaws, teeth, gums, alveolar 
 process and peridental membrane, being variable structures, are 
 predisposed to disease in their very order of evolution. 
 
 The jaws are growing smaller because large ones are not 
 required. The structures are changing their shapes to adapt 
 themselves to the new environment. Thus — instead of broad 
 large jaws with low vaults ; short, broad alveolar processes with 
 plenty of blood supply and vitality to resist mastication; teeth 
 short, ^vith large bell crowns to give plenty of room between the 
 roots for considerable thickness of the alveolar process for the 
 nourishment of the peridental membrane and support and pro- 
 tection of the gum tissue — small narrow jaws occur ^yith appar- 
 enth" high vaults; long, slender and thin alveolar processes, 
 which are not used in mastication with sufficient force to carry 
 the blood for the nourishment of the tissues. The teeth are 
 changing their shape, causing the roots to come closer together, 
 and thus lessening the area of the alveolar process. 
 
 That the jaws of man are growing smaller is easily demon- 
 strated. Scientists claim two types of heads as a starting point 
 in the study of head and face deviations, the brachycephalic 
 (round) head of the Teutonic race and the dolichocephalic 
 (long, narrow) head of the negro. These two primitive types 
 of heads possess two distinct types of jaws. The brachycephalic 
 head has a large round dental arch; the jaws and dental arches 
 may or may not protrude, while the dolichocephalic head has 
 large, long, protruding jaws and dental arches. The normal nat- 
 ural tendency in the evolution of man is to eventually (owing to 
 
20 
 
 INTERSTITIAL GINGIVITIS. 
 
 admixture of races and environment) harmonize these two types 
 and produce a mesaticephalic (medium) head, face and jaws. 
 The frontal development of the brain in phylogeny is gradually 
 causing the skull bones to project forward. Owing to disuse in 
 ontogeny the jaws are growing smaller and receding. 
 
 While these changes are gradually going on normally, cer- 
 tain factors are brought to bear upon the mother and child which 
 increase or diminish the nutrition of the child and bring about 
 arrest or excessive development of the face, jaws and teeth. 
 These factors are an unstable nervous system ^ either in parent 
 or child or both. 
 
 Fig. 1. — Illustrates thk Primitive Head with a Eeceding Forehead and Protrud- 
 ing Face and Jaw. The Second Illustration Shows an Advance in Evolu- 
 tion WITH the Head, Face and Jaavs on a Perpendicular Line, While the 
 Third Shows a Recession of the Face and Jaws. 
 
 That these views can be verified are easy of demonstration. 
 Drop a perpendicular line (Fig. 1) from the supraorbital ridge 
 below the lower jaw. It will be found that in most of the prim- 
 itive races the jaws will protrude outside the line and the fore- 
 head will remain inside the line. As a human face has advanced 
 in its phylogeny, the reverse has taken place. 
 
 Thus an examination of ten thousand people in the streets of 
 London revealed the fact that in only four and thirteen one-hun- 
 dredths per cent of people examined did the jaws extend outside 
 the perpendicular line ; twelve and eighty-seven one-hundredths 
 per cent on the line, and eighty-three per cent inside the line. 
 In an examination of three thousand English • school children 
 (about ten years of age) ninety-three per cent possessed jaws 
 
 * Talbot: Developmental Pathology: A Study in Degenerative Evolution. 
 
TEANSITOEY STRUCTURES, 21 
 
 inside the perpendicular line; six per cent on tlie line and one 
 per cent outside the line. An examination of eight thousand 
 people of Boston showed six per cent of jaws extending beyond 
 the perpendicular line ; fourteen per cent on the line and eighty 
 per cent inside the line. The examination of the people of Bos- 
 ton was made because they more nearly represent those of Eng- 
 land in this country in nationality, environment and influence 
 of marriage and disease. It has required more than one thou- 
 sand years to bring about these results. A more vivid illustra- 
 tion of this change and one that can be easily understood by 
 the reader is that which has taken place in the negro in the more 
 settled parts of America in two hundred and fifty years. 
 
 An examination of the lowest negro type in Mississippi was 
 made for me by Dr. William Ernest Walker of New Orleans. 
 His examinations of three hundred and fifty-seven showed the 
 facial angle protruded beyond the perpendicular line in ninety- 
 seven and five-tenths per cent of jaws, while two and five-tenths 
 per cent of jaws examined were on the line. An examination by 
 Dr. Arthur E. Dray of six hundred and eighty-six negroes in 
 Philadelphia, eighty-three and fifty-seven one-hundredths were 
 found outside the perpendicular line, fifteen and ninety-five one- 
 hundredths on the line and forty-two one-hundredths inside the 
 line. An examination of one thousand and eighty-five in Chi- 
 cago, fifty-one and six one-hundredths per cent protruded; thir- 
 ty-one and eight-tenths were on the line and sixteen and six- 
 tenths per cent were inside the line. An examination of one 
 thousand negroes in Boston by Dr. Eugene F. O'Neill showed 
 forty-five and four-tenths per cent outside the line; thirty-nine 
 and five-tenths per cent on the line and fifteen and one-tenth per 
 cent inside the line. It mil be seen, therefore, that in Northern 
 and in old negro families, from race admixture and environment, 
 there is less protrusion and more recession than in the Southern 
 pure negroes. Arrest of the bones of the face is as common in 
 old negro families in the North as among the Caucasic races. 
 
 To further substantiate this claim a comparison of the meas- 
 urement from the outside of the first molars of the upper jaws 
 of modern races with ancient skulls and ancient races may be 
 here given. Examinations made by the late Dr. Mummery, in 
 
22 
 
 INTERSTITIAL GINGIVITIS. 
 
 1860, of ancient British skulls measured 2.12 inches, maximum 
 2.62 inches, with an average of 2.37 inches. The modern Eng- 
 lish jaws measure minimum 1.88 inches, maximum 2.44 inches 
 with an average of 2.19 inches. The jaws of people living in 
 America measure minimum 1.75 inches, maximum 2.52 inches 
 with an average of 2.14 inches. The difference between the an- 
 cient Roman soldiers and modern Romans is the same as that of 
 the English.' The lateral measurements of the pure negro as 
 found in Mississippi are minimum 2.25 inches, maximum 2.75 
 inches, with an average of 2.51 inches. The lateral diameter of 
 modern negroes varies considerably owing to neurasthenia in 
 the parents and disease in the child. Some jaws measure as low 
 as 1.75 inches. The jaws of modern negroes residing in Boston 
 for many generations are not unlike those of the native whites. 
 
 A further demonstration that the jaws are becoming smaller 
 is shown by the disappearance of the third molar, or the irreg- 
 ularties resultant on its eruption because of want of room, or 
 its eruption with pain for like reason. In the primitive races 
 it is large and well developed. 
 
 Dr. Charles Ward says a ''point in which the jaws of aborig- 
 inal tribes, are, as a rule, superior to those of civilized races is 
 in the proportion of the horizontal ramus. As pointed out by 
 Harrison Allen, the alveolar and inferior border of the jaw tend 
 to parallelism in savages, while in civilized races the symphysial 
 height is usually greater than the height in the vicinity of the 
 molars. This may be due to gradual degeneration of the 
 platysma myoides muscle. Of the significance of the 'ante- 
 gonium' or 'pregonium' of the same author I am uncertain, 
 but incline to the belief that it is a 'stigma of degeneration.' 
 Finally, an as yet incompleted study of the relative proportion 
 of jaw to skull has convinced me that the jaws of savages are not 
 only proportionately but actually heavier than our own, and 
 that the ' cranio-mandibular index,' as I term it, which is the 
 ratio between the weight of jaw and weight of cranium, rises 
 steadily as we descend from semi-civilized to barbarous and 
 savage tribes." 
 
 "Thus, while the white males examined gave an index (pro- 
 
 Talbot: Irregularities of the Teeth. 
 
TRANSITORY STRUCTURES. 23 
 
 portion of jaw to skull) of 11.8, the male Australians presented 
 an index of 15.4. 
 
 '* Absolute size of the lower jaw is greater in savages: Of 
 nine aborigines, including seven North American Indians, one 
 African and one American negro, six Malays and five Austral- 
 ians, all with beautifully perfect teeth, the mean weight of the 
 jaw was 102.4 grams. Of eighteen white males the mean weight 
 of the jaw was only 83.4 grams. Yet the weight of the skull was 
 nearly alike in both classes, being 690.9 grams for the aborigines 
 as against 680.5 for the whites. The weight of the lower jaw 
 compared with that of the cranium, or the cranio-mandibular 
 Index is 15.6 for aboriginal men as against 12.16 for white men. 
 It is 46.2 for the anthropoid apes, our nearest living relatives 
 among mammals. ' ' 
 
 The change in the two extremes of heads, the brachycephalic 
 and the dolichocephalic to the mesaticephalic also produces 
 change in the shape of jaws in like manner. Instead of the large 
 round jaw of the brachycephalic and the long narrow jaw of the 
 dolichocephalic, a medium size jaw development also follows. 
 
CHAPTER IV. 
 
 TRANSITOKY STRUCTURES.^ 
 THE ALVEOLAE PROCESS. 
 
 The alveolar processes are situated upon the superior bor- 
 der of the inferior maxilla and upon the inferior border of the 
 superior maxilla. These bones, considered a part of the maxil- 
 lary bones often so described by anatomists, should, however, be 
 considered from a more careful study of their physiology and 
 pathology as practically distinct bones — their structure, func- 
 tions and embryology differ so completely from the structure 
 and functions of the maxillary bones. The superior and infe- 
 rior maxillae are (unlike the alveolar processes) composed of 
 hard, compact bone structure. The large, powerful muscles 
 attached to them indicate that powerful work is to be accom- 
 plished. When fully developed they retain their full size 
 through life. The alveolar processes are composed of soft, 
 spongy bone of a cancelloid structure. As early as the eleventh 
 week of intrauterine life, calcification of the deciduous teeth 
 commences, and by the twentieth week calcific material is 
 abundantly deposited. Ossification is also rapidly progress- 
 ing about the dental follicles. At birth, the sacs are nearly or 
 quite inclosed in their soft, bony crypts, and the crowns of the 
 teeth upon their outer surface are composed of enamel, which 
 is dense and hard. The embryologic phases of the dental shelf 
 elsewhere cited" indicate this development. 
 
 The alveolar process, being soft and spongy, molds itself 
 about the sacs containing the crowns of the teeth and about 
 their roots after their eruption, regardless of their position in 
 the jaw. While the alveolar processes have grown rapidly, they 
 have up to this time developed only sufficiently to cover and 
 
 ^Pyorrhoea Alveolaris. Paper No. 2. The International Dental Journal, April, 
 
 1896. 
 -Talbot: Irregularities of the Teeth, page 93. 
 
TRANSITORY STRUCTURES, 25 
 
 protect the follicles while calcification proceeds. When the 
 crowns have become calcified and the roots have begun to take 
 in their calcific material, absorption of the borders of the proc- 
 esses takes place in the order of the eruption of the teeth. 
 When the teeth have erupted, the alveolar processes develop 
 downward and upward with the teeth until they attain the 
 depth of the roots of the teeth, which extend in most instances 
 into the maxillary bones in the anterior part of the mouth at 
 least, and the upper and lower teeth rest at a point in har- 
 mony with the rami. The depth at which they penetrate the 
 bone differs in different mouths. This depends upon the 
 length of the roots and the alveolar process. This in turn de- 
 pends upon the length of the rami. The incisive fossa, the canine 
 eminence and the canine fossa give evidence of this externally. 
 These sockets are lined with extensions of the process, thus 
 making its upper border irregular. The crypts of the perma- 
 nent teeth are located at the apices of the roots of the tem- 
 porary teeth. The permanent teeth have large crowns which 
 touch each other, forming a line to the posterior part of the jaw. 
 These teeth, as they erupt, entirely absorb the alveolar process 
 which surrounded the temporary teeth, and as the new set 
 comes into place a new process is built up around them for 
 their support. 
 
 The process of absorption of the alveolar process and the 
 building up of new bone around the first and second set of 
 teeth is inflammatory. Tliis then is the beginning of intersti- 
 tial gingivitis in the life of every individual. Whether this 
 primitive inflammation continues through life or not, will de- 
 pend upon the general health of the person and his ability to 
 keep his gums and alveolar process in a normal, healthy con- 
 dition after the temporary teeth have erupted. 
 
 The permanent teeth require a deeper alveolar process to 
 support their roots, which are much longer than those of the 
 tem.porary teeth. Hence the difference in the depth of the 
 vault of the first and second sets of teeth. 
 
 The alveolar process of each superior maxilla includes the 
 tuberosity, and extends as far forward as the median line 
 of the bone, where it articulates with the process upon the 
 
26 
 
 INTERSTITIAL GINGIVITIS. 
 
 opposite side. It is narrow in front, and gradually enlarges 
 until it readies the tuberosity, where it becomes rounded. 
 
 The process is composed of two plates of bones (Fig. 2), an 
 outer and an inner, which are united at intervals by septa of 
 cancellous tissue. These form the alveoli for the reception of 
 the roots of the teeth. In some cases the buccal and labial sur- 
 faces of the roots of healthy teeth extend nearly or quite 
 through the outer bony plate and are covered by the peridental 
 and mucous membranes only. 
 
 This plate is continuous with the facial and zygomatic sur- 
 faces of the maxillary bone. The inner plate is thicker and 
 stronger than the outer, and is fortified by the palate bones. 
 The external plate is irregular upon the outer surface, promi- 
 
 FiG. 2. — Diagram op the Superior :m axillary Bone with the Teeth Removed. 
 
 nent over the roots of the teeth, and depressed between the 
 roots or interspaces. 
 
 With the change in the size of jaws there is also change in 
 the shape of the vault and alveolar processes. When the den- 
 tal arches are large, measuring from 2.25 to 2.50 inches, the 
 vaults are low and the alveolar processes are short and thick, 
 not only giving stability to the teeth, but also plenty of nour- 
 ishment. Now that the dental arches are growing smaller, with 
 an average of from 1.90 to 2.00 inches, the vaults are higher in 
 proportion, the alveolar processes long and thin. This renders 
 the teeth and jaws more susceptible to trophic changes and 
 hence to disease. The alveolar process in the anterior part of 
 the mouth, in which the incisors and cuspids are situated, is 
 much thinner than in the posterior parts. 
 
TKANSITORY STEUCTUEES. 27 
 
 The sockets for the incisors and cuspids are conical and 
 much larger than any of the other single sockets. The alveolar 
 process is longer and thinner than at any of the other teeth. 
 The sockets for the bicuspids are flattened upon their anterior 
 and posterior surfaces, and near the apices they are frequently 
 bifurcated. The sockets of the molars are large at the open- 
 ings. About the middle of their length, however, they are 
 divided into three smaller sockets for the reception of the roots. 
 In the case of the third molar the number of sockets ranges 
 from one large cavity to three or four of smaller size. When 
 disease attacks the tissues, destruction is, therefore, more rapid 
 in its progress in the anterior parts of the mouth than in the 
 posterior, where the processes are thicker and more nourish- 
 ment is required. 
 
 The septa are very thin at the margin and gradually increase 
 in width to the middle of the jaw, where they become thicker, 
 and are finally lost in the substance of the jaw. Some septa 
 are thicker than others, and where two teeth are mdely sepa- 
 rated, the width of the septa naturally corresponds to the space 
 between the teeth. 
 
 What is true in regard to a change in the size of the jaws is 
 also true in respect to the shape of the crowns of the teeth. 
 While they are not growing smaller in proportion to the size of 
 the jaws, they are changing shapes. Once they were quite bell- 
 shaped, giving considerable space between the roots for a thick 
 alveolar process, thus rendering support to the peridental and 
 mucous membranes, now the shape has changed. The proximal 
 surfaces are almost straight, lessening the width and thus allow- 
 ing only for a thin septum, with barely sufficient surface to sup- 
 port the tissues without material blood and nerve supply. 
 
 The sockets are lined with a thin plate of compact, bony 
 substance, extending from the outer and inner plates of the 
 alveolar process to the apex, where there are small openings 
 for the entrance of the nerve and blood vessels for the nour- 
 ishment of the teeth. 
 
 The bony plate has upon its inner surface the elastic peri- 
 dental membrane, which acts as a cushion for the teeth, while 
 it is surrounded by a spongy bone. 
 
28 
 
 INTEKSTITIAL GINGIVITIS. 
 
 The teeth are held firmly in their alveolar sockets by the 
 peridental membrane. Teeth with one conical root, and those 
 with two or more perpendicular roots, are retained in position 
 by an exact adaptation of the tissues. Teeth having more than 
 one root and those bent or irregular, receive support from all 
 sides by reason of their irregularity. Fig. 3 (a section of the 
 jaw of a cat) illustrates the relative position of the teeth, peri- 
 dental membrane and alveolar process to each other. 
 
 After the removal of the permanent teeth the alveolar 
 process is entirely absorbed. Fig. 4 shows how the absorption 
 takes place. The teeth have all been removed from the supe- 
 rior maxilla and the alveolar process has been entirely absorbedc 
 
 Fig. 3. — Ground Section of Jaav and Teeth of Cat. (Andrews.) 
 
 The molars on the lower jaw having been extracted, absorption 
 of the alveolar process has resulted in marked contrast with the 
 anterior alveolar process, which remains intact and holds the 
 teeth firmly in place. It is, hence, evident from the changes 
 which occur, from the first development of the teeth to their 
 final extraction, that the alveolar process exists solely to pro- 
 tect the teeth in their crypts during development and after 
 
TRANSITORY STRUCTURES. 
 
 29 
 
 eruption. After the temporary teeth are in place the alveolar 
 process remains unchanged (except by gradual enlargement in 
 harmony with the growth of the maxillary bones) until about 
 the sixth year, when the second set appears. The crowns of 
 the permanent teeth require more space than those of the tem- 
 
 FiG. 4. — Plaster Casts of the Superior and Inferior Jaws ix Position'. All the 
 Teeth Have Beex Eemoved ox the Upper Jaw, axd the Molars and Second 
 Bicuspids ox the Lower Jaav. Absorption of the Jaavs Where Teeth Have 
 Been Eemoved Well Advanced. 
 
 porary set; and the alveolar process must necessarily enlarge 
 to accommodate them. This enlargement of the alveolar proc- 
 ess is caused chiefly by formation of the crowns of the perma- 
 nent teeth before eruption, and to a limited extent only by 
 
 Fig. 5.- 
 
 -The Anterior Alveolar Process Excessively Developed, Carrying 
 the Teeth Upwards. 
 
 growth of the maxillary bones. These may cease development 
 at any period of the life of the individual, or continue as late 
 as the thirty-sixth j^ear. As diameter of the crowns of the per- 
 manent teeth form a larger circle than that of tlie maxillarv 
 
30 INTERSTITIAL GINGIVITIS. 
 
 bones, the alveolar process must necessarily increase its diam- 
 eter and present large spaces between the roots of the teeth 
 for the development of the alveolar process. 
 
 The process is solely for retaining the teeth, and if for any 
 reason the dental follicles should not be present, and the tooth 
 should not erupt, or if it should be extracted early, the process 
 would not be developed at that point. In my collection of mod- 
 els are cases of arrested development of the alveolar process, 
 caused by the lack of bicuspid and lateral incisor germs, and by 
 extraction of deciduous and permanent teeth. 
 
 If one or more teeth w^ere not to antagonize, the alveolar 
 process would extend beyond the natural border, carrying the 
 teeth with it. A marked illustration of this is seen where the 
 molars are decayed to the gum and the roots remain. The 
 vascularity of the process may be such that hypertrophy re- 
 sults. Excessive development of the alveolar process is fre- 
 quently observed by everj^ practitioner in connection with the 
 anterior inferior teeth. When the articulation is normal, occlu- 
 sion of these teeth never takes place. Frequently (especially 
 in patients from six to twelve years of age) these teeth extend 
 to and occlude with the mucous membrane of the hard palate. 
 Such a case is illustrated in Fig. 5. This model is taken from 
 the jaw of a person thirty-seven years of age, but this excessive 
 development took place between the ages of six and twelve 
 years, since at that period the vascularity of the tissues is more 
 vigorous, and the development of the process more formative 
 than at any period subsequent to the development of the first 
 permanent teeth. 
 
 In one patient under observation the incisors and cuspids, 
 together with their alveolar process, are situated upon the 
 external surface, while the bicuspids, molars and their alveolar 
 process are located upon the inner border of the jaw. In an- 
 other patient, the alveolar process failed to cover the roots of 
 the bicuspids and molars upon the outer surface, the teeth hav- 
 ing forced themselves into a larger circle through the alveolar 
 process by the contact of the crowns. The roots in this patient 
 
 Dental Surgery, page 44. 
 
TKANSITORY STRUCTURES. 31 
 
 can easily be outlined by the finger througli the mucous mem- 
 brane, the outer plate of the alveolar process barely, if at all, 
 covering them. Tomes' illustrates a patient of faultj" develop- 
 ment of the outer plate of the alveolar process, exposing the 
 crown of the temporary teeth. This occurred in a hydro- 
 cephalic. I have a number of models shomng the anterior alve- 
 olar process projecting beyond the normal position through the 
 forward movement of the molars. This may be due to a nat- 
 ural movement of the molars forward, or the process may be 
 forced forward by the -improper occlusion of the jaws. The 
 teeth are moved from one position to another simply by the 
 force consequent upon absorption and deposition of bone. This 
 is noticeable in the spaces between the centrals, when the alve- 
 olar process develops to a larger circle than is necessary to 
 accommodate the teeth. The alveolar processes are influenced 
 in one direction or the other by the pressure of articulation. 
 This results from inharmonious development of the jaws. The 
 teeth may come together in such a manner as to throw the 
 alveolar processes either to the right or the left, thus produc- 
 ing a full, round arch upon one side of the jaws, and a perfectly 
 flat or straight arch upon the other. Occasionally both upper 
 and lower alveolar processes are carried forward in the same 
 manner. The alveolar process upon the lower jaw is more 
 liable to be found upon the inner border of the jaw than is the 
 upper alveolar process, as the inferior maxilla is larger and 
 more dense than the superior, and when the teeth are once in 
 position upon the lower jaw they are not so liable to subse- 
 quent change. Owing to this the teeth of the superior maxilla 
 do not form so great a circle. This causes the teeth upon the 
 sides of the jaw to conflict, and the lower teeth and alveolar 
 processes to be carried in, while the anterior teeth of the lower 
 jaw are held inside of the superior anterior teeth, thus carry- 
 ing the alveolar processes inward. 
 
 The teeth are continually changing their positions in the 
 mouth. This is as often beneficial as it is detrimental. That 
 the teeth may perform their full function, they should not only 
 remain firmly in the alveolar process, but they should also 
 antagonize properly. The teeth may be compared to the bricks 
 
32 
 
 INTERSTITIAL GINGIVITIS. 
 
 in an arch. Eemove a brick and the arch falls to pieces. It is 
 frequently found that the teeth do not articulate properly; by 
 a slight movement, or by cutting away the grinding surfaces, a 
 better articulation may be secured. When this operation is per- 
 formed, the teeth move in their sockets by absorption and depo- 
 sition of bone, demonstrating the fact that the process changes 
 in shape and substance. Ziegler* says absence of functional use 
 is a frequent cause of premature lacunar absorption of the 
 bone. This form of atrophy from disuse occurs not only when 
 a limb or a part of a limb is deprived of its normal activity, 
 but also when portions of a single bone cease to perform their 
 function of support, and finally, like all the bones of the body, as 
 age advances, normal or physiologic absorption takes place, 
 while the teeth are still in the jaws. Unlike other bones of the 
 
 Fjg. 6. — Hypertrophy of the Entire Alveolar Process. 
 
 body, however, the absorption of the alveolus progresses to a 
 greater extent because of the unstable condition of the struc- 
 tures. 
 
 From what has already been said of the vascularity of the 
 alveolar process, it is evident that hypertrophy of the tissue may 
 ensue from an unbalanced nervous system and from simple irri- 
 tation of varying degree. This unbalanced nervous system may 
 act directly upon the pituitary body, producing hypophyseal 
 disorders which in turn aifect the growth of the jaws and alve- 
 
 * A Text-Book of Special Pathological Anatomy, page 145. 
 
TRANSITORY STRUCTURES. 
 
 33 
 
 olar process. The irritation consequent upon the eruption of 
 the teeth, together mth the excessive blood supply, are both 
 primal causes of overbuilding of tissue, i. e., hyperplasia. 
 
 The ragged roots of the temporary teeth, produced by ab- 
 sorption of the gases from the putrescent pulps, and the pres- 
 sure of the permanent crowns against the tissues, produce suf- 
 ficient stimulation to excite physiological action. Tissue-build- 
 ing generally is seen in connection with all the teeth, and the 
 process becomes unnaturally thick, the teeth frequently are 
 carried in one direction and another; cementosis of the roots 
 of the teeth and hypertrophy of the process result. 
 
 In cases of hypertrophy of the alveolar process, enlarge- 
 ment is associated with the inner plate of the alveolar process. 
 In patients coming under my observation the inner plate in 
 
 Fig. 7. — Hypertrophy of the Alveolar 1'rocess Around the Left 
 Superior Molar Teeth. 
 
 most is the part of the alveolar process affected (Fig. 6 case). 
 The outer plate, although quite irregular from the arrange- 
 ment of the teeth, is usually normal in thickness. This dis- 
 parity in the two plates of the alveolar process is due to the 
 fact that the inner plate of the alveolar process possesses a 
 large blood supply, the posterior or descending palatine arter- 
 ies furnishing the ossific material. I have observed but few 
 
34 INTERSTITIAL GINGIVITIS. 
 
 patients where hypertrophy has extended to and included the 
 outer plate. When the outer plate becomes involved the alve- 
 olar process assumes a very thick condition. Occasionally 
 hypertrophy will affect one side only or one distinct locality 
 (Fig. 7). In this patient the enlargement is upon the left side 
 and extends from the first bicuspid posterior to and including 
 the maxillary tuberosity. Instead of the force being directed 
 inward, as is generally the case, the process is forced outward 
 and backward. This enlargement occurred previously to the 
 development of the second and third molars. The alveolar 
 process extends downward and occludes with the teeth upon 
 the lower jaw, thus preventing the molars from erupting. 
 
 The causes which produce hypertrophy of the alveolar proc- 
 ess are those due to an unstable nervous system. This subject 
 is discussed in my work on "Developmental Pathology : A Study 
 in Degenerative Evolution." 
 
 (Late researches have shown that the hypophysis and its 
 disorders have much to do with arrest and excessive develop- 
 ment of the body as a whole or of particular organs or struc- 
 tures of the body. The author many years ago called the atten- 
 tion of the profession to the fact that an unstable nervous sj^s- 
 tem of the parent or disease in the child after birth produced 
 excessive or arrest of development of the tissues. It is possible 
 that the unstable nervous system of the parent or the diseases 
 of the child act first upon the pituitary body, which in turn 
 acts upon the tissues themselves or that they both act together.) 
 
CHAPTER V. 
 
 THE ALVEOLAR PROCESS UNDER THE MICROSCOPE. 
 
 Under the microscope, two systems of Haversian canals are 
 seen in the alveolar process. Kolliker^ describes these as fol- 
 lows : 
 
 "The Haversian canals are of two kinds. One with the 
 regnlar lamellae system surrounding it, and the other, the so- 
 called Volkmann's canals, containing the perforating vessels 
 from Von Ebner, which have no surrounding lamellae, but sim- 
 
 
 YiQ. 8. — Section of Bone Showing Blood A^essels of Vok Ebner (Kolliker). 
 
 ply penetrate through the layers of bone. Volkmann's canals 
 are present in all tubular bones in old and young. While espe- 
 cially present in the outer basal lamellae, they occur also in the 
 interstitial leaflets and in the inner chief lamellae as well as in 
 the periosteal layers of the skull bone. Here their number is 
 very variable (Fig. 8). They run partly transversely or 
 obliquely, and alsa partly longitudinally, through the lamellas. 
 
 ^ Handbuch der Gewebelehre, page 272. 
 
36 
 
 INTERSTITIAL GINGIVITIS. 
 
 Many of these canals open in the outer or inner surfaces of the 
 substantia (compact substance), and also here and there in the 
 Haversian canals, and form altogether usually a wide-meshed 
 irregular network. In their structure they are sometimes 
 smooth and sometimes furnished with dilatations and angles 
 projecting in and out in profile. The widest has a diameter of 
 100 micrometers or more, and the narrowest not more than 10 
 or 20 micrometers, and there are still narrower ones which are 
 altogether obliterated, appearing like rings or circular-formed 
 
 Fig. 9. — Section of Bone (Higher Magnification) Showing 
 Blood Vessels of Von Ebner. 
 
 structures without any lumen, or like those far from rare oblit- 
 erated true Haversian canals first described by Tomes and 
 de Morgan. The contents of the Volkmann canals are the same 
 as the Haversian canals." 
 
 Fig. 8 is a cross section of the medulla of a calcified human 
 humerus slightly changed. The outer lamellae contains a large 
 number of Volkmann 's canals running longitudinally and trans- 
 versely and extending through the outer plate of bone into the 
 periosteum. Fig. 9, the cross section of the section seen in 
 
THE ALVEOLAR PROCESS UNDER THE MICROSCOPE. 
 
 37 
 
 Fig. 8, shows these canals more highly magnified. The Haver- 
 sian canals are large romid spaces (Fig. 10), containing a sin- 
 gle artery and vein. The fine hair-like spaces running from 
 these large spaces are the canalicnli. The dark spots circulat- 
 ing each Haversian canal are the lacunae. The canalicnli run 
 from one lacunae to another or into a Haversian canal or they 
 anastomose with each other. The rings of bone about each 
 Haversian canal are called lamella. The lacuna' seem to be 
 about uniformly distributed throughout the bone. The spaces 
 
 
 
 -^ 
 
 
 -^■ 
 
 ^",^''*"* 
 
 ^/V^*' ■^ 
 
 
 
 
 
 Fjg. 10. — Transverse Section of the Diaphysis of the Humerus 
 
 Magnified 350 Times. 
 
 A, Haversian Canal. Dark Spaces, Lacunar. 
 
 Hair-like Spaces, Canaliculi. 
 
 Fig. 11. — Longitudinal Section of Bone Magnified 100 Times. 
 
 between the lacunae and canaliculi are filled with lime salts. 
 
 A longitudinal section of bone (Fig. 11) is similar in appear- 
 ance to the cross section. Instead of the lacunae being arranged 
 in rows around the Haversian canals they are parallel. It will 
 be noticed that the Haversian canals run in different directions 
 and communicate ^\ith each other at certain intervals. The 
 foregoing description, with illustrations from Kolliker, is essen- 
 tially that of the minute anatomy of the alveolar process. 
 
CHAPTER VL 
 
 THE GUMS. PERIOSTEUM, MUCOUS AND PERIDENTAL MEMBRANES 
 UNDER THE MICROSCOPE. 
 
 GUMS AND MUCOUS MEMBRANE. 
 
 The tooth, according to Minot/ is a papilla which projects 
 into the epidermis, and ossifying in a particular way, changes 
 into ivory around the soft core or pulp. To the papilla the epi- 
 dermis adds a layer of enamel. The tooth proper unites with 
 a small plate of dermal bone at its base. By a modification on 
 the jaw, the epidermis first grows into the dermis, and then 
 the dermal tooth papilla is developed. The teeth were primi- 
 tively organs of the skin and widely developed over the sur- 
 faces of the body. As the mucous membrane is practically a 
 continuation of the skin, it, in accordance Avith the law of indi- 
 viduation, became specialized and lost some of the functions 
 of the skin while developing the others to greater perfection. 
 
 The mucous membrane lines the cavity of the mouth, the 
 nose, and extends through the larynx into the lungs and through 
 the oesophagus into the stomach. It covers the tongue, jaws, 
 alveolar process, dipping down between the necks of the teeth 
 and the alveolar process as far as the peridental membrane, 
 leaving a free space between the membrane and the teeth 
 through its entire length. 
 
 It consists of two layers (Fig. 12), the epithelium (A) and 
 corium (B), separated by the basement membrane (C). The 
 epithelium is composed of the epitheUal cells : First, one row of 
 columnar cells (D) situated upon the basement membrane (C) ; 
 second, two rows of six-sided prickle shells (E) ; third, two rows 
 of six-sided cells (F) ; fourth, two or three rows of sciuamous 
 cells (G) ; and fifth, four or five rows of flattened dead cells (H), 
 which were originally the columnar cells upon the basement 
 
 ^ Embryology, page 481. 
 
GUMS AXD MUCOUS MEMBRANE. 
 
 39 
 
 membraue. The young new cells are the columnar cells which 
 pass from one stage to another, changing their shapes until they 
 eventually become dead cells and are exfoliated from the surface 
 of the tissue. The basement membrane (C) is made up of fibers 
 running longitudinally, from papillae, which allow the tunica 
 propria containing blood vessels and nerves to pass up into the 
 epithelium structure. w 
 
 --^-'•^■- -"-" 
 
 Fig. 12. — Diagrammatic Tt.t.ustbatiox of the Epithelium and SrsMrcors Layers 
 OF THE Mrcous Membrane. 
 
 A, Epithelium. B, Corium. C, Basement Membrane. D, Columna Cells. E. 
 Prickle CeUs. F, Six-sided CeUs. G. Squamous Cells. H. Flattened Dead Cells. 
 
 The corium (B) (which lies below the basement membrane) 
 is composed of alveolar comiective tissue, white yellow fibrous 
 connective tissue, muscular fibers, nerves, blood vessels and 
 lymphatics. It is inade up of the tunica propria and the sub- 
 mucosa. 
 
 The tunica propria (beautifully shown in Fig. 13) consists 
 
40 INTERSTITIAL GINGIVITIS. 
 
 of interlacing connecting fibers interspersed with nmcli elastic 
 fibrous tissue. This tissue penetrates the epithelial layer in the 
 form of cone-shaped papillae, varying in length with the thick- 
 ness of the epithelium. This layer being the thickest at the 
 gum margin (E), these papillae are the longest and largest at 
 this locality. The fibers of the tunica propria pass gradually 
 into the submucous membrane (G), and from there into the peri- 
 osteum and peridental membrane (M), so that it is difficult to 
 determine the mucous capacity line of demarcation separating 
 the ditferent structures. The submucosa is composed of fibrous 
 connective tissue of a much less compact variety. This struc- 
 ture is attached to the bones through the periosteum and peri- 
 dental membrane. In this structure the glands, blood vessels, 
 nerves, fat cells, etc., occur. 
 
 The larger blood vessels (K) are found in this structure. 
 From these large blood vessels small capillaries extend to the 
 tunica propria. It is here that inflammation commences in 
 interstitial gingivitis when due to local irritation. Numerous 
 veins accompany each artery, and lymphatics form a network 
 around them. Small nerve filaments are also in this structure, 
 which pass through the tunica propria and into each papilla in 
 connection with the capillaries. The terminal nerve fibers come 
 in contact with the muscular fibers, so that there is direct com- 
 munication by blood vessel and nerve throughout the muco^ip 
 membrane from the nose, stomach and lungs. The gum tissue 
 is very thick and made up of fibrous tissue running in three or 
 four directions, rendering it dense, tough and hard. The mem- 
 brane thus differs from the same structure in other parts of the 
 body. On account of these numerous fibers, this structure is 
 bound tightly to the alveolar process. The gum tissue acts as 
 a cushion and protection from irritation which may arise from 
 hard substances being taken into the mouth. As this membrane 
 passes and coalesces with the membrane of the lips and cheeks, 
 it becomes much thinner and less dense. In the center of the 
 tooth, the parallel fibers in the tunica propria are composed of 
 flattened fasciculi of connective tissue. There are three sets 
 of fibers — those which run vertically, those which radiate and 
 are fan-shaped, and those which are horizontal. 
 
X 75. A. A. obj. Zeiss. Micro-x>li"tographs, reduced one-third. 
 
 Fig. 13. — Lox&iTUDixAL Section of Tooth and Gum Tissue. Dog. 
 
 D. Dentine. E. Epithelial Tissue. G, Submucous Membrane. K, Capillaries. M, 
 Fibrous Tissue. V, Violent Inflammation. AA, Point of Union of Epithelial Tissue 
 and Peridental Membrane. EE, Space Pocket from Want of Union of the Epithelial 
 Fold. 
 
42 INTERSTITIAL GINGIVITIS. 
 
 The mucous membrane, like tlie alveolar process and peri- 
 dental membrane, is composed of very unstable tissue. It 
 changes its structure, blood vessels and nerve system as often 
 as the other structures. Its blood vessels and nerve system are 
 continually renewing connective tissue, periosteum and periden- 
 tal membrane. 
 
 A difference is noted in the structure of the papillary layer 
 in man and the lower animals, such as the dog, the sheep and 
 the calf. In man the gum tissue is not so thick, therefore the 
 papillae are broader and shorter, while in the lower animals the 
 papillae are narrow, long and more closely set together. Blood 
 vessels and nerves are not so numerous and close together in 
 man as in animals. 
 
 THE PERIOSTEUM AND PERIDENTAL MEMBRANE. 
 
 The periosteum is a fibrous tissue covering the outer surface 
 of the alveolus. The peridental membrane is composed of simi- 
 lar structures covering the roots of the teeth and lining the 
 inner wall of the alveolus. They are both derived from the 
 mesoblastic layer. For this reason there can be very little dif- 
 ference in the character of the structure of each, except so far 
 as function is concerned. The periosteum is made up of four 
 different kinds of fibers. An outer layer of coarse, w^hite fibrous 
 tissue, an inner layer of fine, white fibrous tissue, elastic fibers, 
 and penetrating fibers (fibers of Sharpey). 
 
 The fibers of the periosteum are coarser than those of the 
 peridental membrane. The coarser fibers run parallel with the 
 alveolar process (J) over the border and extend as far as the 
 union of the epithelial layer (E) and the periosteum (H), Fig. 
 14. (^'The dental ligament," Black.-) The finer fibers run in 
 all directions and enter the alveolar process at every point. If 
 a section of the alveolar process treated with acids or a section 
 affected by halisteresis or osteomalacia be placed under the 
 microscope, the fibers are seen to retain the original shape of 
 the bone. 
 
 American System of Dentistry, page 663. 
 
X 75. A. A. obj. Zeiss. Micro-photographs, reduced one-third. 
 
 Fig. 14. — Longitudinal Section of Tooth, Alveolar Process, Peridental Mem- 
 brane AND Periosteum. Normal Tissue. Sheep. 
 
 B, Dentine. C, Cementum. E, Epithelial Tissue. G, Submucous Membrane. 
 H, Periosteum. J, Alveolar Process. K, Capillaries. L, Haversian Canals. M, 
 Fibrous Tissue, AA, Point of Union of Epithelial Tissue and Peridental Membrane. 
 
X 75. A. A. obj. Zeiss. Micro-photographs, reduced one-third. 
 
 Fig. 15. — Cross Section of Tooth, Alveolar Process, Peridental Membrane 
 AND Periosteum. Normal Tissue. Dog. 
 
 B, Dentine. C, Cementum. D, Pnlp. H, Periosteum. J, Alveolar Process. 
 K, Capillaries. M, Fibrous Tissue. U, Nerve Tissue. CT, Connective Tissue. 
 
GUMS AND MUCOUS MEMBRANE. 45 
 
 The fibers of the periosteum, therefore, are continued 
 throughout the process from the periosteum on the one side to 
 the peridental memljrane on the other. This is also illustrated 
 in the mouths of persons, where (after wearing artificial den- 
 tures for a short time) heat produces absorption of the lime 
 salts, leaving the fibrous tissues intact. 
 
 The periosteum is abundantly supplied with blood vessels 
 which anastomose with each other and enter the alveolar proc- 
 ess at the Haversian canals. The plexus of blood vessels is much 
 larger proportionately in connection with the alveolar process 
 than with other bones of the body, owing to its transitory 
 nature. 
 
 The peridental meml)rane commences at the margin of the 
 epithelium at the neck of the tooth AA, Fig 14, and is attached 
 directly to the cementum. This membrane has various func- 
 tions : First, it fills the space between these two structures, 
 forming a cushion for the teeth to rest upon; second, like the 
 alveolar process, it is present only when the teeth are present, 
 and therefore develops with, the alveolar process when the first 
 teeth erupt, it is entirely lost when the temporary teeth are 
 shed, is restored with the eruption of the second set, and when 
 the permanent teeth are extracted it disappears with the alve- 
 olar process completely; third, it furnishes the nourishment for 
 the teeth while they are in position in the jaw, and holds them 
 in their sockets. 
 
 The fibrous tissue, in its earliest stages comprises nearly all 
 or quite all of that portion of the jaw which eventualh^ becomes 
 the alveolar process. Calcification begins at the center of the 
 jaws and gradually closes in upon the fibrous membrane until 
 it becomes the thickness of a sheet of paper. In young persons 
 the membrane is much thicker than in old age, since, as age 
 advances, the osteoblasts on the one hand and the cementoblasts 
 on the other send out new material and each wall closes in upon 
 the membrane, which becomes very thin in old age and almost 
 lost. 
 
 The fibers which compose this membrane extend in all direc- 
 tions; some crossT/ise penetrating the cementum, on the one 
 hand, and the alveolar process on the other. In a general way. 
 
46 INTERSTITIAL (ilNGIVITIS. 
 
 since the fibers extend tlirougii the alveolar wall, they are more 
 closely adherent to the bone than to the cenientum, and usually 
 cling to the latter when the tooth is removed. It will be observed 
 that these fibers do not enter the alveolar process uniformly as 
 claimed by Gray' and Pierce*, like tacks or nails driven regu- 
 larly into a board (the ''fibers of Sharpey" Fig. 14), but vary 
 as to quantity in different localities. In some localities they 
 penetrate in large quantities and almost surround a piece of 
 alveolar process, while a few fibers penetrate but a short dis- 
 tance. In some places, they can be traced almost through the 
 alveolar process. These fibers are much finer in man (Fig. 15) 
 than in the lower animals (Fig. 14, dog). In connection with 
 the fibers which pass into the alveolar process are numerous 
 blood vessels. Others run diagonally, and still others length- 
 wise, all making up a tissue which holds the tooth in position in 
 the jaw. The fibers enter the peridental membrane at all points 
 of the process, from its margin to the apex of the roots. The 
 elasticity of this membrane is so great that in correcting irregu- 
 larities a tooth may be turned from one-fourth to one-half 
 around without breaking the fibers. The elasticity is greatest 
 in youth. As age advances, the membrane grows thinner and 
 thinner until, late in life, there is almost a bony union between 
 the tooth and the alveolar process, thus preventing stretching 
 of the fibers. At the upper border, under the gum tissue, these 
 fibers extend over the edge of the alveolar border and unite 
 with the fibers of the periosteum on the outer border of the 
 process, forming the interstitial tissue. 
 
 If absorption of the inorganic substance of the alveolar 
 process occurs, the fibrous tissue retains the shape of the proc- 
 ess. The same results when inflammation of the peridental 
 membrane takes place at the gum margin or at the apex of the 
 root of the tooth. What was once alveolar process is now peri- 
 dental membrane or fibrous tissue. 
 
 Two kinds of structures are present in the alveolar process 
 — a dense, compact, hard structure (composed of lime salts), 
 
 ' Anatomy. 
 
 * American System of Dentistry, page 668. 
 
X 75. A. A. obj. Zeiss. Micro-pbotograplis, reduced one-third. 
 
 Fig. 16. — Cross Section of Tooth, Alveolar Process and Peridental Membrane. 
 Ir jECTED Blood Vessels. Normal. Dog. 
 
 B, Dentine. C, Cementum. I, Peridental Membrane. J, Alveolar Process. K, 
 Capillaries. L, Haversian Canals. 
 
X 75. A. A. obj. Zeiss. Micro-pliotographs, reduced one-third. 
 
 Fig. 17. — Cross Section of Tooth, Alveolar Process and Peridental Membrane. 
 Injected Blood Vessels. Normal. Dog. 
 
 B, Dentine. C, Cementum. I, Peridental Membrane. J, Alveolar Process. K, 
 Capillaries. L, Haversian Canals. 
 
GUMS AND MUCOUS MEMBRANE. 49 
 
 and a fibrous tissue; either alone will retain the shape of the 
 tissue. 
 
 Blood vessels permeate this membrane throughout from the 
 gum tissue at the neck of the tooth, through the alveolar walls 
 to the end of the roots. They are most abundant in youth. 
 Capillary blood vessels enter the Haversian canals through the 
 process and into the cementum. Many of these blood vessels 
 extend the entire length from the gum margin to the apex in 
 straight lines and vice versa. In many of the illustrations, the 
 blood vessels will be seen to follow the line of the alveolar 
 process (Fig. 14). A great supply of blood vessels penetrate 
 the membrane through the alveolar walls. These vessels unite 
 and anastomose with the arteries which traverse lengthwise, 
 forming a complicated plexus (Fig. 16). According to some 
 writers the vascular supply of the peridental membrane is situ- 
 ated in the center of the structure. This has not been my expe- 
 rience. All of my slides, as well as those here presented, show 
 the blood vessels to be situated nearest the alveolar process. It 
 is quite natural that this should be so, since very little blood is 
 required for the nourishment of the cementum, while the larg- 
 est amount is required to supply the alveolar process. The sys- 
 tem of blood vessels situated in the peridental membrane and 
 showing their relation to the surrounding tissue is well shown 
 in the injected specimen from healthy dogs (Figs. 16 and 17). 
 Pus pockets and abscesses are hence more liable to form near 
 and in the alveolar process than near the tooth structure. When 
 infection takes place, the products of inflammation are carried 
 through the blood vessel and the foci of round cell inflammation 
 are located near or in the alveolar process where abscesses form. 
 The vessels seen in the membrane anastomose very freely with 
 those at the gum margin, showing the membrane to be well 
 nourished in all its parts. Should one part become involved by 
 disease the other parts are overnourished in consequence. 
 
 These blood vessels enter the alveolar walls ^\ith the fibrous 
 tissue through the Haversian canals and these in turn permeate 
 the entire bone. As age advances, however, the bone becomes 
 more dense, and the Haversian canals become smaller and 
 (under certain conditions) cease to exist. When disease takes 
 
50 INTEESTITIAL GINGIVITIS. 
 
 place, either at the gingivus or at the apex of the root, the sup- 
 ply of hlood being thus cut off, the tissues receive sufficient 
 nourishment through the alveolar wall. Since the structures are 
 in a transitory state, being destroyed and repaired so fre- 
 quently, it is evident why the blood supply is so rich. 
 
 CALCOSPHERITES. 
 
 Small, hard bodies are frequently found in the peridental 
 membrane. These are sometimes in the form of concentric 
 rings of lime salts and are called calcospherites. They are not 
 always round, but may be of any shape and vary as well in size. 
 They bear the same relation to the peridental membrane that 
 pulp stones do to the dental pulp. Black^ says: "I have seen 
 more of them about the roots of the molars than elsewhere, 
 but have found them along the sides of the roots of the bicus- 
 pids. " When irritation and inflammation take place in the 
 peridental membrane, the cementol)lasts build up cement sub- 
 stance, just as the osteoblasts do in the alveolar process and 
 the odontoblasts do in the pulp chamber. Sometimes they are 
 attached to the root of tlie tooth, producing a condition called 
 exostosis or cementosis. They may remain unattached, float- 
 ing in the tibrous tissue. These are very common in connec- 
 tion with interstitial gingivitis. 
 
 DO GLANDS EXIST IN THE MUCOUS AND PERIDENTAL MEMBRANES? 
 
 A somewhat widespread opinion locates special glands in 
 the gingival tissues and the peridental membrane. This seems, 
 to a certain extent, to be in part due to the lack of definite 
 knowledge as to the etiology of interstitial gingivitis, and in 
 part to the fact that certain constitutional conditions, such as 
 mercurial and potassium iodid poisoning and scurvy, manifest 
 themselves in the gum tissue in a way similarly to their action 
 in the glandular structures of the body. Black*^ claims, for ex- 
 ample: ''That part of the gingival margin that lies in against 
 the neck to the tooth is of a different structure from its other 
 
 " Periosteum and Perirleiital Membrane, page 94. 
 ^ American System of Dentistry, pages 955-956. 
 
X 75. A. A. obj. Zeiss. Micro-photographs, reduced one-third. 
 
 Fig. 18. — Longitudinal Section of Gum. Normal Tissue. Sheep. 
 
 C, Cementum. E, Epithelial Tissue. G, Submucous Membrane. K, Capillaries. 
 M, Fibrous Tissue. AA, Point of Union of Epithelial Tissue and Peridental Mem- 
 brane. Nm, Nasmyth's Membrane. Sg, So-called Glands of Serres. 
 
52 INTEKSTITIAL GINGIVITIS. 
 
 parts. Here it is clothed with a very soft, round or polygonal 
 gland-like epithelium that suggests the formation of a gland, 
 but fails to assume the glandular structure, though it seems to 
 have been regarded as such by Serres. This — which I shall call 
 the gingival organ — emits a profusion of small rounded cells 
 which are always found in the saliva (Salter) and are usually 
 called mucous corpuscles. It is well known that certain glands 
 have the power of the selection and excretion of certain poi- 
 sons, and in this way of eliminating them from the system, and 
 that if the substance be in large amount, hyperemia, or even 
 inflammation, may result. It is also known that mercury and 
 potassium iodid will produce inflammation of the free margins 
 of the gums, and Salter has found these cells are in greater 
 abundance under these circumstances; also that the cells taken 
 from the gingival border and submitted to chemical tests after 
 the person has taken potassium iodid are found to yield and 
 are tinged with iodin." 
 
 Longitudinal sections of the tooth, alveolus and surrounding 
 tissues, under the microscope, exhibit a very peculiar formation 
 of the mucous membrane at its line of union mth the peridental 
 membrane at the neck of the tooth. Black^ (in an article beau- 
 tifully illustrated by Frederick Noyes) seems to identify these 
 with the so-called glands of Serres or gingival glands (Fig. 18). 
 He speaks of them as glands in various places throughout the 
 article; for example, ''But little can now be said of the func- 
 tion of the network of glands of the peridental membrane, be- 
 yond what is indicated by their form, location and histological 
 characters. With the knowledge of their position and general 
 character, clinical observation leads to the conclusion that they 
 are readily disturbed by certain drugs, notably by mercury and 
 iodin; and that they are often disturbed by substances poison- 
 ous to them floating in the blood streams. This is evidenced 
 by the appearance of marginal gingivitis, with soreness of the 
 peridental membrane. Such disturbances would not be likely 
 to occur without the presence of some specialized or secretory 
 tissue. ... It seems to me verv certain that the disease 
 
 ^Dental Cosmos, Fehniary, 1899. 
 
GUMS AND MUCOUS MEMBRANE. 53 
 
 which I have described as phagedenic pericementitis has its 
 seat in these glands." Black, however, does not seem quite cer- 
 tain of the validity of his position, since he further remarks, 
 ''Though definitely lobulated, this body does not seem to pos- 
 sess the characters of a gland, and I should not suppose from 
 an examination of its tissues that it had a glandular function. 
 It encircles but a portion of the neck of the tooth, usually only 
 the approximal portion, thinning away toward the buccal and 
 lingual, so that in many of the lengthwise sections it may be 
 very small, or does not appear at all." 
 
 In many slides of sections from canine jaws and human,^ the 
 same peculiar arrangement of structure was observed, although 
 not in so marked a degree. In the immature herbivora (calf and 
 lamb) these peculiar formations of structure are well marked, 
 albeit less so in the carnivora, and still less in man. 
 
 Were glands present in this locality it is logical to infer that 
 they would become involved in mercurialism, plumbism and 
 scurvy, and exhibit marked inflammation with broken-down 
 structures in a given locality, as at the union of the gum tissue 
 with the peridental membrane. Such a case is unknown. 
 
 The mucous membrane under the microscope appears at a 
 point between the teeth (and faintly so at the inner and outer 
 border as shown by Black) to double upon itself. When the 
 tooth erupts, absorption of the gums occurs at the highest point. 
 The gum tissue passing down to the neck of the tooth folds or 
 crowds upon itself between the teeth with a peculiar curve 
 downward, inward and then outward and upward. At the upper 
 border, about midway from the gingival margin to the neck of 
 the tooth, may be seen a space or pocket (never twice alike in 
 appearance) where the edge of the gum tissue comes in contact 
 with the original epithelium. Sometimes the space or pocket is 
 closed up (Figs. 48, 49, 57). Again it remains open (Figs. 13, 
 37, 56, 59). Frequently this peculiar type of structure is absent, 
 showing that the fold of gum tissue either has been absorbed in 
 
 * The material obtained for making slides from man, other than the scur\'y cases, 
 was obtained through the kindness of surgeons from jaws removed from hospital 
 patients, as a result of disease; the surgeons placing them into alcohol or Miiller's 
 solution as soon as removed. 
 
■^*p 
 
 
 \:h^ 
 
 W. 
 
 
 %• 
 
 X 75. A. A. obj. Zeiss. Alicro-pbotugraphs, ru<luecd one-third. 
 
 D 
 
 Fig. 19. Cross Section of Tooth and Peridental Membrane. 
 Normal Tissue. Sheep. 
 C, Cementum. D, Dentine. I, Peridental Membrane. W, Epithelial Debris 
 
I 
 
 I 
 
 3*^ 
 
 .?-' 
 
 
 
 V. 
 
 
 •;• 
 
 X 300. No. 2 projection ocular. D. D. obj. Zeiss. Micro-photographs, 
 reduced one-third. 
 
 Fig. 20. — Cross Section of Tooth and Peridental Membrane. 
 Normal Tissue. Sheep. 
 
 C, Cementuni. D, Dentine. I, Peridental Membrane. W, Epithelial Debris. 
 
56 
 
 INTERSTITIAL GINGIVITIS. 
 
 the eruption of the tooth or did not form. This peculiar form 
 encircles only a portion of the neck of the tooth (according to 
 Black's examination of the structure in sheep). This in itself 
 seems to offset the glandular theory, since gingivitis almost in- 
 variably starts on tlie lingual or palatine and labial surfaces 
 
 X 560. No. 2 projector ocular. One-twelfth obj. Zeiss. 
 
 Fig. 21. — Cross Section of Tooth and Peridental Membrane. 
 Normal Tissue. Sheep. 
 
 C, Cementum. D, Dentine. I, Peridental Membrane. W, Epithelial Debris. 
 
 where this structure does not appear. In the slides of the scurvy 
 case there does not appear the slightest evidence of anything 
 resembling glandular structure. Hence it would seem safe to 
 conclude that the glandular structure does not occur in this 
 
GUMS AND MUCOUS MEMBEANE. 57 
 
 locality. It is by no means impossible that in the peculiar epi- 
 thelium in this locaUty, epithelial cells undergo changes which 
 to some observers simulate glandular structure, but on histo- 
 logic analysis are distinguishable from it, resembling in this 
 the crypts of the head of the penis. 
 
 In cross sections of the peridental membrane, with a low 
 power may be seen dark bodies arranged along the margin of 
 the cementum in the peridental membrane (Fig. 19). They are 
 more numerous, however, near the gingival border than at the 
 root extremity. These bodies are more numerous and better 
 defined in the sheep than in the calf, and more apparent in the 
 canine jaw than in the human. Under higher power (Fig. 20) 
 they may be distinctly demarcated as epithelial cells arranged 
 in single rows of loops, again in double rows, again in rows of 
 three and sometimes in round or oblong groups, with clusters of 
 cells without shape or form. With a still higher magnifying 
 power (Fig. 21) it will be seen that these masses of cells are 
 polygonous, never prismatic. They hence are similar in shape 
 to the epithelial cells situated above the columnar colls. They 
 also resemble the cells which are situated inside of the epithelial 
 lamina. In the larger amplification the nucleus can be readily 
 observed. 
 
 Black® has attempted to demonstrate that glands exist in 
 the structure and that the cells last mentioned are glands. 
 Black lays down as a sine qua non of a gland that there should 
 be an opening to the surface. He has made an attempt (Fig. 15) 
 to demonstrate such an outlet, but this figure does not show 
 clearly that the glands empty into the duct or have an exit at 
 the surface. These bodies, however, not only fail (like the 
 ductless glands) in this particular, but in more important char- 
 acteristics of glands. They do not have (as Robin and Magitot 
 remark) a columnar or prismatic cell wall. It is not difficult 
 to understand how epithelial cells are scattered in different 
 shapes and sizes throughout the peridental membrane. Epi- 
 
 » Dental Cosmos, February, 1899, pages 112-118. 
 1" Dental Follicle, page 116. 
 " Embryology, pages 581-90. 
 
58 INTERSTITIAL GINGIVITIS. 
 
 thelial cells have the property of multiplying and developing 
 in structures wherever located." 
 
 If epithelial cells should migrate within the submucous mem- 
 brane and fibrous tissue, proliferation will occur under certain 
 circumstances. The tooth, according to Minot," is a papilla 
 which projects into the epidermis and, ossifying (calcifying) in 
 a particular way, changes into ivory around the soft core or 
 pulp; to the papilla the epidermis adds a layer of enamel. The 
 tooth proper unites with a small plate of dermal bones at its 
 base. By a modification in the jaws the epidermis first growls 
 into the dermis and then the dermal tooth papilla is developed. 
 The first indication of the development of tooth germs in mam- 
 mals is a thickening of the epithelium covering the jaw. This 
 thickening, which appears as a ridge during the sixth week of 
 embryonic life, forms on the under side of the epithelium. This 
 curving ridge expands into an outer portion (the outline of the 
 groove between the lip and the gum) and an inner portion, 
 the dental shelf which grows obliquely inward. The papillae 
 for the milk teeth are formed on the under side of the shelf, and 
 it is thus possible for the shelf to continue growing toward the 
 lingual side, so that the second set of germs is developed for 
 the permanent teeth. The end of the shelf, toward the articula- 
 tion of the jaws, is prolonged without retaining the direct con- 
 nection with the epithelium and from this prolongation arise 
 the enamel organs for the three permanent molars. Wherever 
 a tooth-germ arises the dental shelf is locally enlarged, and the 
 local enlargement constitutes an enamel organ which projects 
 from the under side of the shelf. The portions of the shelf 
 between the enamel organs gradually break up, forming first 
 an irregular network, and later separate fragments^- which 
 may persist throughout life and lead to various pathological 
 structures. While the permanent germs are forming, the shelf is 
 solid between them, although it has assumed the reticulate 
 structure between the germs of the milk teeth. In consequence 
 of the reticular formation, the fully developed enamel organs 
 
 " Including the epithelial debris of Eobin and Magitot. 
 
GUMS AND MUCOUS MEMBRANE. 59 
 
 have several bands or threads by which they are connected with 
 the dental shelf proper. 
 
 After the shelf has developed somew^hat, its line of connec- 
 tion with the epithelium of the gum becomes marked by a super- 
 ficial groove, as may been seen in the human embryo of eight 
 to ten weeks. This groove was formerly supposed to be the 
 first trace of the dental shelf, but Rose's observations correct 
 the supposition. 
 
 The second step in mammals is the formation of outgrowths 
 (in man ten in each jaw) from the under side of the dental shelf ; 
 each outgrowth is the outline of an enamel organ for a milk 
 tooth. The outgrowth is covered toward the mesoderm by a 
 layer of the epidermis, w^hile the core is filled with polygonal 
 cells which resemble those of the middle part of the Malpighian 
 layer of the skin. The outgrowths, after penetrating a short 
 distance, expand at the low^er ends, but remain each connected 
 by a narrow neck with the overlying epidermis. The expanded 
 end is the enamel germ proper; it very soon assumes a tri- 
 angular outline, as seen in sections, owing to the flattening of 
 its under side, and at the same time it moves somewhat toward 
 the lips. Meanwhile the shelf continues growing on the lingual 
 side of each ingrowth to produce the enamel organs destined for 
 the second or permanent teeth. 
 
 At this stage it is noticed that the mesenchyma under the 
 flattened end of the enamel organ has become more dense, to 
 form the outline of the dental papilla, and is beginning to de- 
 velop fibrillae around both the enamel germ and the papillary 
 outline. The fibrillar envelope is the future dental follicle. 
 
 The third step is a final differentiation of the enamel organ 
 and the accompanying shaping of the papilla. The enamel organ 
 continues growing and becomes concave on its under side so 
 that the mesoderm underneath acquires the shape of the papilla. 
 It is now that the form of the tooth is determined by the form 
 assumed by the papilla, which in its turn is probably deter- 
 mined by the growth of the enamel organ. 
 
 The follicle is merely an envelope of connective tissue in 
 which can be distinguished an outer dense and inner looser 
 layer; in the latter the cells are more distinct and the fibrillar 
 
60 INTERSTITIAL GINGIVITIS. 
 
 are less numerous than in the former. A rich network of capil- 
 lary vessels is developed in the follicle and appears in part as a 
 series of villous-like growth into the enamel organ. The folli- 
 cle develops first over the lower part of the papilla, then over 
 the enamel organ, the neck of which aborts and the follicle 
 closes over, completely separating the enamel organ from its 
 parent epidermis. The enamel organ changes greatly in appear- 
 
 FiG. 22. — Section through the Incisive Portion or the Lower Jaw of an Ovine 
 Embryo, Measuring 82 Millim. (3 1/3 Inches) in Length. Magnified 260 
 DiAM., after Drs. Ch. Legros and E. Magitot. 
 
 D, Oral Epithelium. C, Lowest Layer of Cells in the Stratum Malpighii. F, 
 Epithelial Cord. K, Bourgeon of the Secondary Cord. I, Follicular Wall. H, Dental 
 Bulb. 
 
 ance. The layer of cylinder cells is well preserved over the 
 concave surface, but only where the epithelium is in contact 
 with the dental papilla. In the neck the cells become irregular 
 in form. Over the convex surface the cells become lower and 
 cuboidal. They ultimately atrophy and flatten out. The cells in 
 the center of the enamel organs undergo a peculiar metamor- 
 phosis. They remain united together by a few thread-like 
 processes. 
 
 It is obvious from these changes in the embryo how what 
 Robin calls the epithelial debris is derived from the epithelial 
 
GUMS AND MUCOUS MEMBRANE, 
 
 61 
 
 cord, the follicular wall and the round bodies of lamina epithe- 
 lium debris. According to Ch. Robin and Magitot/^ who were 
 the first to describe these bodies, "The phenomena of budding 
 commences, namely, when the epithelial cord has finished its 
 course, having conducted the primary enamel organ to that point 
 whence its subsequent evolution will be effected and soon after 
 the formation of the secondary follicle, immediately after the 
 rupture of the cord of the primitive follicle." Robin leans to 
 the opinion that these bodies disappear soon after they are 
 formed, "The time of their disappearance varies, they remark, 
 in different species of animals. In the human embryo the 
 
 :Mu,^?^?;^?9^ ?p:tr^:v. K. 
 
 Fig. 23. — Vertical Transverse Section through the Incisive Eeqion of the 
 Lower Jaw op Human Foetus Measuring 38 Centimetres (15^^ Inches), 
 Magnified 80 Diam., after Drs. Ch. Legros and E. Magitot. 
 
 b, Bony Formation, d, Oral Epithelium, g, Enamel Organs. H, Dental Bulb. 
 I, Cord of the Permanent Follicle. K, Debris on the Follicular Wall of the Primitive 
 Follicle and from its Cord. K, Epithelial Globule. L, Enamel Organ of the Permanent 
 Tooth. 
 
 remains of the cord of the primitive follicles may be found, even 
 after the formation of the follicles of the permanent teeth, and 
 it is probably during the process of eruption that these bud- 
 dings become atrophied; in the canine embryo the facts are 
 nearly the same; in the bovine and ovine embryos (calf and 
 lamb) it has seemed to us that these proliferations disappear at 
 
 " See their Memoir on the Genesis and Development of the Dental Follicle in Jour, 
 de Physiologic de Brown-Sequard, 1860. 
 
62 INTERSTITIAL GINGIVITIS. 
 
 a correspondingly earlier stage ; and we think it safe to say that, 
 as a general rule, the complete absorption occurs toward the 
 period of eruption. ' ' 
 
 The embryology of the dental shelf, which has been sum- 
 marized by Minot from Waldeyer, Kolliker, Von Ebner" and 
 0. Hertwig, indicates the source of the structures which have 
 been mistaken by Black for the limiting walls of glands. 
 
 After the epithelial cords of the temporary and permanent 
 sets of teeth have been demarcated from their folUcles, the proc- 
 
 
 asxcrnxivv 
 
 Fjg. 24. — From the Lower Jaw of an Ovine Embryo, Magnified 80 Diameters, 
 Showing the Completed Dental Follicle and the Surrounding Tissues, 
 
 AFTER DrS. Ch. LeGROS AND E. MaGITOT. 
 
 a, Meckel's Cartilage, b, Traces of Ossification, c, Lowest Layer of Epithelial 
 
 Cells, d, Oral Epithelium. F, Ameloblastic Layer. F, (Lower) External Layer of 
 the Enamel Organ — a continuation of the Layer of Ameloblasts. g, Stellate reticu- 
 lum of the Enamel Organ. H, Bulb. I, Follicular Wall. K, Buddings from the 
 Cord. 
 
 ess of cell building proceeds like the process of cord building. 
 These buds, according to Charles Robin and Magitot,'' are given 
 off at tlie upper border of the follicle and below the epithelium 
 of the gum. "In fact, as soon as the epithelial lamina loses its 
 connection with the foUicle, by the rupture of the cord, the epi- 
 
 "Handbuch der Zahnheilkunde, 1890, pages 209-262. 
 «Loc. cit., 1860. 
 
GUMS AND MUCOUS MEMBRANE. 
 
 63 
 
 thelial cells composing it become greatly increased in number at 
 the severed point. The multiplication of cell-elements results 
 in the formation of irregular buddings, which wander in differ- 
 ent directions into the deeper portions of the embryonal tissue. 
 These buddings vary greatly in form ; sometimes they are sim- 
 ple cylinders, retaining their connection with the primitive 
 lamina by pedicles of various lengths, and sometimes this slight 
 
 X 50. One-half -in. obj. No, Oc. 
 
 Fig. 25. — Cross Section of Epithelial Cord. Man. 
 
 T, Peridental Membrane. W, Epithelial Debris or Cord. EO, Endarteritis Obliterans. 
 
 connection is absorbed, thus isolating an epithelial mass." 
 
 This budding occurs at different points along the cord (Fig. 
 22) at the end and upon the outer surface of the follicular wall 
 (Figs. 23 and 24) at the point where the cord is severed from the 
 enamel organ. These gradually diminish as they descend upon 
 its sides. Doubtless the epithelial cord remains in the periosteal 
 
64 INTEESTITIAL GINGIVITIS. 
 
 and submucous tissue tliroughout life. Fig. 25 represents evi- 
 dent sections of epithelial cord in a man sixty-eight years of age, 
 and Fig. 26 in a dog eight years. In the photographs of the 
 scurvy cases and of dogs will be seen evidences of the persist- 
 ence of epithelial debris late in life. The position already cited 
 from Eobin and Magitot as to its early disappearance would 
 hence appear to be too strongly taken. 
 
 Robin and Magitot claim that this budding process occurs at 
 or about the time of the rupture of the cord. Up to this period 
 ossification has not taken place, but then deposits of bone appear 
 in the fibrous tissue of the middle and outer surfaces. The bone 
 deposit gradually takes the form of the jaw, filling in and 
 encroaching upon the fibrous tissue, forming a bony wall on the 
 one hand, and the crown and root of the tooth on the other. 
 When the tooth is ready to erupt, the crown pushes the soft tis- 
 sue laterally, while the root develops, forms a defined wall with 
 the peridental membrane between them. The epithelial debris 
 (to use their term) which before was scattered over the entire 
 surface of the dental follicle, is now crowded into the very nar- 
 row space of the peridental membrane, and owing to the position 
 of the debris at the upper part of the follicle, it would be nat- 
 ural to find most of it at the peridental membrane. 
 
 BONE BUILDING AND ABSORPTION. 
 
 Development of the alveolar process is relegated to a series 
 of cells situated in the fibers of the peridental membrane or 
 fibrous tissue, and close to the margin of the bone tissue, and 
 throughout the Haversian canals. These cells are called the 
 osteoblasts. They perform the function of building up the bone 
 tissue. Even after the alveolar process has developed its normal 
 shape, so unstable is the nervous system which presides over 
 these cells at this locality, that at the slightest provocation, 
 either local or constitutional, they will continue their process of 
 construction. Hence, the frequency of hypertrophy of the proc- 
 ess, and in disease the calcification of the peridental membrane. 
 
 On the other side of the membrane, next the root surfaces, 
 may be seen other cells which build up and destroy the cemen- 
 
BONE BUILDING' AND ABSORPTION, 
 
 65 
 
 tiiin; these are called cementoblasts and cementoclasts. These 
 are of little importance in this connection with the study of this 
 disease, although they are frequently present and at work when 
 inflammation of the membrane occurs. 
 
 There is, however, another class of cells found in the peri- 
 
 X 560. No. 2 projection ocular. One-twelfth obj. Zeiss. 
 
 Fig. 26. — Cross Section Epithelial Cord. Dog. 
 
 I, Peridental Membrane. W, Epithelial Debris or Cord. U, Nerve Tissue. 
 
 dental membrane of the utmost importance in this connection, 
 the osteoclasts, located in the fibers, and in close proximity to 
 the alveolar wall, and around the inner border of the Haversian 
 canals. The function of these cells is to tear down irregular 
 
66 INTERSTITIAL GINGIVITIS. 
 
 bone and tootli strncture due to unstable nervous tissue, and 
 from tlie slightest irritation. 
 
 The gums, mucous membrane, alveolar process and peri- 
 dental membrane, owing to their transient nature, are influenced 
 by the slightest irritation. This influence is the result of both 
 constitutional and local causes. It consists of an irritation in 
 the peripheral nerves which sets the osteoblasts and osteoclasts 
 at work to l)uild up or tear down the alveolar process. This in- 
 fluence may be only sufficient to stinuilate these cells to action 
 without inflammation. This is noticed in the advance toward old 
 age, in long, lingering debility, in the development of bone, espe- 
 cially the tearing down and the building up of the inferior max- 
 illary backward. It may be noted in mild or intense inflamma- 
 tion of the peridental membrane, due to more acute forms of 
 disease, to scurvy, mercurial, lead and iodide poisoning, or to 
 local irritation. So sensitive are these structures that in neu- 
 rotics and degenerates the slightest irritation produced in the 
 physiologic development of the permanent teeth is sufficient to 
 start the osteoblasts to building up bone structure, thus pro- 
 ducing that pathologic condition called hypertrophy of the alve- 
 olar process ; one of the most marked evidences of an unstable 
 nervous system. 
 
 The breaking down of the tissues by the osteoclasts may be 
 induced by as slight a cause. The alveolar process being so thin 
 about the teeth, destruction of the entire walls is accomplished 
 without difficulty, and in a very short time, thus loosening the 
 teeth, which eventually drop out. 
 
 According to Kaufmann ^''' the following processes take part 
 in the absorption of bone : (a) Lacunar Absorption, (b) Forma- 
 tion of Perforating Canals, (c) Disappearance after Prior 
 Absorption of Lime (Halisteresis) (Bony Waste) and Osteo- 
 malacia. 
 
 "By far the connnonest form of bone destruction is by 
 lacunar absorption. This process occurs not only under physio- 
 logic conditions, but is extraordinarily frequent in pathologic 
 states, e. g., in the various types of atrophy. They form on the 
 
 "Pathologische Anatomie. 
 
BONE BUILDING AND ABSORPTION, 
 
 67 
 
 smooth, superficial surfaces of the bone deep grooves (so-called 
 Howship's lacunae) in which lie smaller or greater polynuclear 
 cells (osteoclasts, Kolliker) which evidently blend together (Fig. 
 27). There are no alterations of the bone substance that would 
 indicate a primary line of absorption (Plummer). The con- 
 fluence of these lacunae form larger cavities. 
 
 ''The second form of bone absorption, which is occasionally 
 met under physiologic conditions, is by means of perforating 
 canals (so-called Volkmann canals). Under physiologic condi- 
 tions canals occur in varying numbers in tlie lamellae (general 
 
 
 
 Fig. 27. 
 
 a, Bone Trabeevila'. h, Tubercle with Granulation Tissue, c. Broken-down Tissue. 
 
 d, Blood Vessel, e, Osteoclasts. /, Fat Cells. (Kaufmann.) 
 
 lamellae) which contain vessels (perforating vessels). These are 
 often associated with the Haversian canals and gradually pass 
 into them, but unlike them, are surrounded with circular lam- 
 ellae. Under pathologic conditions the conception of these per- 
 forating canals is somewhat widened. On the one hand 
 Volkmann 's canals are spoken of when reference is made to the 
 vessels or vascular connective tissue penetrating from one 
 medullary space in the spongy substance, or from one Haversian 
 canal in the compact substance, to another, in such a way that a 
 passage is made from one part of the bone to the other; Volk- 
 
68 
 
 INTERSTITIAL GINGIVITIS. 
 
 mann's canals also include irregular ampula-formed dilations 
 or cavities (Fig. 28). By confluence of these are produced cav- 
 ities or irregularly outlined canals penetrating tlie bone sub- 
 stance. These, if they empty into the medullary space, become 
 filled witli cells. 
 
 I 
 
 
 e b a e ^ 
 
 Fig. 28. 
 
 a, Large Spaces Eesulting from Absorption of the Trabeculse. h, Decalcified Bone. 
 c and d, Decalcified Bone and Atrophied Trabecular, c, Haversian Canals. (Kauf- 
 mann.) 
 
 "Under much rarer conditions, especially in senile marasmic 
 osteomalacia and also in that occurring in pregnancy, bone 
 absorption takes place after a prior abstraction of lime (haliste- 
 resis) and the remaining substance (bone cartilage) is then fur- 
 
BONE BUILDING AND ABSORPTION. 69 
 
 tlier dissoh^ed, passing through a temporary fibroid stage. This 
 destruction of the decalcified and interfibrillae decomposed bone 
 is produced as a rule without osteoclasts. The decalcified border 
 zones of the trabeculse appear with simple carmine (coloring) or 
 by double stains. ' ' 
 
 Viewing the alveolar process, including the gums, peridental 
 membrane and periosteum in man's ontogeny as a whole, it will 
 be seen that the changes which are going on in apparently nor- 
 mal individuals make it an exceedingly transitory structure. 
 
 In connection with what has already been said in regard to 
 the transitory nature of the alveolar process, there is another 
 factor to be considered which makes it a doubly transitory 
 structure. 
 
 In man's phylogeny, in some of the lower vertebrates ^'^ there 
 is a continuous succession of teeth throughout life. In man's 
 ontogeny, it would be strange if he did not retain still further 
 evidences of phylogenetic peculiarities in tooth development in 
 relation to the alveolar process. 
 
 Man and some of the lower vertebrates have only two sets of 
 teeth. When the first set comes into place, the alveolar process 
 builds itself up about the roots to hold the teeth in place. When 
 these are to be lost, a low form of inflammation sets up absorp- 
 tion of the bone and the teeth are lost. When the second set 
 erupt new bone is developed about the roots to hold the second 
 set in place. Should man live long enough the second set would 
 drop out even though he possessed a normal healthy body. 
 This process is atavistic. With all these changes going on in 
 man's ontogeny, we again have an exceedingly transitory struc- 
 ture. With the phylogenetic and ontogenetic changes, man has 
 a doubly transitory structure in the alveolar process. I have 
 called this process of bone absorption, osteomalacia or juvenile 
 or senile absorption according to the age of the patient.^® 
 
 Transitory structures are more easily involved in disease 
 than other structures. How much more quickly then will a 
 structure which is doubly transitory become involved in disease? 
 
 "Talbot. Developmental Pathology: A Study in Degenerative Evolution. 
 " Talbot. Pathogeny of Osteomalacia or Senile Atrophy. The Dental Digest, 
 August, 1903. 
 
70 INTERSTITIAL GINGI\'ITIS. 
 
 Mammals (upon whom researches have been conducted by the 
 author) demonstrate they are phylogenetically subject to this 
 disease and perhaps lower vertebrates, including the reptiles 
 under similar circumstances or environment., 
 
 The Al\teolae Process as an End Organ/''- — I have called the 
 alveolar process an end organ. My reason for doing this is that 
 the tooth, so far as the process and its diseases are concerned, is 
 a foreign body.-° The arteries, vessels of Von Ebner and espe- 
 cially the nerves pass through the bony process, in a wavy man- 
 ner and stop at the root of the tooth. 
 
 There are other end organs in the body, chief of which are 
 the kidneys, the eye and the brain. Physicians claim, and 
 rightly, that because these are end organs they are more easily 
 involved in disease and are often the determining factors of 
 kidney lesions. Alfred C. Croftan says, "It is not surprising 
 to find that particularly those organs that are supplied by end 
 arteries are chiefly involved, for in them vascular disturbances 
 must first produce nutritional derangement. Chief among the 
 organs supplied by end arteries are, precisely, the kidneys, the 
 retina and the brain, and I think this explains the frequent in- 
 volvement of the kidneys, eyes and brain in Bright 's disease. 
 The fact that the retina and the brain are often found injured 
 before the kidneys, that cases of Bright 's disease run their fatal 
 course occasionally with practically no renal changes, but with 
 serious apoplectiform brain lesions and retinitis, bears out this 
 conception and constitutes a valid argument against the com- 
 mon belief that the nephritis is the primary event and the de- 
 termining phenomenon of the disease." 
 
 A marked difference exists between the kidney, eye and brain 
 as end organs and the alveolar process as an end organ. This 
 difference is the important point in the study of interstitial gin- 
 givitis. End arteries running into the kidney, eye and brain, 
 owing to the soft nature of these tissues, are given a chance to 
 expand and recover, permitting, in a measure, the blood to flow 
 more easily, thus prolonging the tendency to disease, or allow- 
 
 " Endarteritis Obliterans. The Dental Digest, October, 1903. 
 
 ^'' Interstitial Gingivitis or So-called Pyorrhoea Alveolaris. The Dental Sum- 
 mary, 19t)3. 
 
ALVEOLAR PROCESS AS AN END ORGAN. 71 
 
 ing the tissues, under favorable conditions to recover. On the 
 other hand, blood vessels extending throughout the alveolar 
 process in a tortuous manner cannot expand, and as a result, 
 blood charged with toxins and subject to cardio-vascular changes 
 immediately sets up irritation and inflammation which results in 
 dilatation, bone absorption and arterial degeneration. These 
 changes, therefore, will occur much earlier in the alveolar proc- 
 ess than in other end organs. 
 
 The transitory nature of the alveolar process, especially as 
 an end organ, makes it exceedingly sensitive to systemic 
 changes and disease. The sensitiveness of this structure to auto- 
 toxic states is easily demonstrated as people advance in years. 
 At the fifth period of stress (about forty-five and beyond) the 
 excretory organs weaken. The toxic elements of the body are 
 not carried off as freely as formerly. These circulate in the 
 blood and accumulate in the alveolar process, setting up irrita- 
 tion and inflammation. Absorption of the alveolar process grad- 
 ually takes place. People enjoying apparently good health -will, 
 as they advance in years, note the absorption of the alveolar 
 process and the exposure of the roots of the teeth. How much 
 more readily will absorption take place when the function of 
 any one of the eliminating organs be involved, such as constipa- 
 tion, asthma, skin affections or kidney lesions. 
 
 In addition to the alveolar process being a doubly transitory 
 structure it is also an end organ, of a bony nature and the most 
 sensitive structure of the human organism, hence any constitu- 
 tional disturbance due to disease, drug poisoning or autointoxi- 
 cation would more quickly affect it. Sudden changes in temper- 
 ature from heat to cold and vice versa, where the organism is 
 unable to adjust itself readily, also leave their mark upon the 
 very susceptible tissue. 
 
 The study of interstitial gingivitis and its treatment must be 
 based upon the phylogeny, ontogeny and peculiar anatomy of 
 the structures involved. There are no other structures in the 
 human body associated like the jaws, alveolar process and teeth. 
 The pathology, therefore, is unique in itself. 
 
 Transitory structures in the body as well as end organs are 
 known to be very susceptible to disease and are, as a rule, the 
 
72 INTERSTITIAL GINGIVITIS. 
 
 first to be involved. The alveolar process, being classed as a 
 doubly transitory structure as well as an end organ consisting 
 of bone, is one of the first, if not the first, structure to register 
 systemic changes. 
 
CHAPTER VIL 
 
 INOEGAXIC SALTS AXD INTERSTITIAL GIXOn^ITIS. 
 
 The foods wliicli enable the body to repair its waste, to bnikl 
 up new tissue and to supply the energy, are divisible into four 
 classes : the inorganic substances, the fats or hydrocarbons, 
 and the starches and sugars, or carbohydrates, and the proteid 
 compounds. These divisions are, however, relative, since the 
 proteids may contain both hydrocarbons and carbohydrates. 
 The inorganic substances, such as water, phosphates, chlorides, 
 carbonates, sulphates, etc., enter the body, as a rule, under their 
 own form, either alone or in combination with other classes. 
 They are not oxidized or split up within the system to enter into 
 the chemical formations of other compounds, but are united 
 mechanically with the proteid group. These bodies act, as a rule, 
 in a purely mechanical manner. After ha\dng served their pur- 
 pose, they pass out of the system with the excretions, compara- 
 tively unchanged in their composition. They are the only 
 member of the group of foods which are of a special interest in 
 the present research. The inorganic salts have not received the 
 attention from physiologic chemists that their importance de- 
 mands. They are, as a rule, found in greater or lesser quanti- 
 ties in all foods taken into the body. They do not serve as a 
 source of energy, but as the other foods are needed for the de- 
 velopment of the tissues, so the inorganic salts are needed for 
 the building of bone tissue and the repair of waste. This is ac- 
 complished b}^ the soluble salts in the blood. Human blood has 
 the follo"s^dng composition : 
 
 ANALYSIS OF HUMAN BLOOD (c. SCHMIDT). HOWELL 's PHYSIOLOGY. 
 
 Man. Woman. 
 
 25 Years. 30 Years. 
 
 Water 788.71 .... 82-4.55 
 
 SoHds 211.29 .... 175.45 
 
 Proteids and Extractives 191.78 .... 157.93 
 
 Fibrin 3.93 .... 1.91 
 
 Hfematin (and iron) 7.70 6.99 
 
 Salts 7.88 .... 8.62 
 
74 INTERSTITIAL GINGIVITIS. 
 
 INORGANIC SALTS OF HUMAN BLOOD, 1,000 PARTS (c. SCHMIDT). 
 
 Blood Corpuscles. 
 Blood Plasma. 
 
 CI 1.75 CI 3.53G 
 
 K,o 3.091 K20 0.311 
 
 NA., 0.470 NA.o 3.410 
 
 SO3' O.OGl SO3 r 0.129 
 
 P205 1-355 P.O. 0-145 
 
 CaO CaO 
 
 ^'^no ^'^90 
 
 These acids and bases exist, of course, in the plasma and the 
 corpuscles as salts. It is not possible to determine exactly how 
 they are combined as salts, but Schmidt suggests the following 
 combination : 
 
 PROBABLE SALTS IN THE CORPUSCLE. 
 
 Potassium Sulphate 0.132 
 
 Potassium Chloride 3.679 
 
 Potassium Phosphate 2.343 
 
 Sodium Phospate 0.633 
 
 Sodium Car])ouate 0.341 
 
 Calcium Phosphate 0.094 
 
 Magnesium Plio_sphate 0.060 
 
 PROBABLE SALTS IN THE PLASMA. 
 
 Potassium Sulphate 0.281 
 
 Potassium Chloride 0.359 
 
 Sodium Chloride 5.546 
 
 Sodium Phosphate 0.271 
 
 Sodium Carbonate 1.532 
 
 Calcium Phosphate 0.298 
 
 Magnesium Phosphate 0.218 
 
 It will be seen that the corpuscle contains an excess of 
 potassium salts, and the plasma contains an excess of sodium 
 salts. All parts of the blood contain salts, however. 
 
 Throughout the entire body, there is a rich supply of blood 
 vessels penetrating every tissue. The plasma of the blood pass- 
 ing by exosmosis through the walls of the capillaries is thus 
 brought in immediate contact with the tissues to which it brings 
 nourishment and oxygen of the blood, and from which it 
 removes the waste products of metabolism. Other usable prod- 
 ucts or lymph are collected in small capillary spaces, which in 
 
INORGANIC SALTS AND INTERSTITIAL GINGIVITIS. iO 
 
 turn open into definite lymphatic vessels. These vessels unite 
 into larger and larger ones, which eventually pour this usable 
 waste product into the great thoracic or left lymphatic ducts, and 
 a second smaller right lymphatic duct. These in turn empty 
 into blood vessels, each upon its own side. The lymph contains 
 essentially the same constituents as the blood plasma, and the 
 salts are found in the same proportion as in it. They are then 
 eliminated through the sweat glands, tonsils, mucous glands, 
 kidneys, large intestines and salivary glands. 
 
 The composition of the deposits in the various parts of the 
 body vary according to the locality and the character of the 
 excreta eliminated in connection vdth them. 
 
 The chemical composition of the human bile, according to 
 Jacobson,^ is as follows : 
 
 Water 977 .40 
 
 Sodium Glyeoeholato 9 . 94 
 
 Cholesteriii 0.54 
 
 Free Fat 0.10 
 
 Sodium pahnitate and sterrate 1.26 
 
 Lecitine . 04 
 
 Other organic matter 2.26 
 
 Sodium chloride 5.45 
 
 Potassium chloride . 28 
 
 Sodium phosphate 1-33 
 
 Lime phosphate 0.37 
 
 Sodium carbonate . 93 
 
 Of this analysis the solid ingredients constitute 22.5 parts per 
 thousand, of which two-thirds are organic and one-third inor- 
 ganic. The inorganic salts of the bile are in most cases returned 
 to the blood, where they are redistributed to the tissues. Occa- 
 sionally, however, gall stones occur, which are composed of 
 (analysis H. D. Geddings -) : 
 
 Moisture 3 . 32 
 
 Biliary matter 32 . 182 
 
 Cholesterin 54.952 
 
 Matter soluble in ether 7.77 
 
 Iron traces 
 
 Phosphoric acid traces 
 
 Lime traces 
 
 Magnesium traces 
 
 ^ American System of Dentistry. 
 
 " Transactions South Carolina Medical Association, 1880. 
 
76 INTERSTITIAL GINGIVITIS. 
 
 Secretions of tlie pancreatic juice (dog) by C. Schmidt are as 
 follows : 
 
 Water 900.76 
 
 Solids 99 . 24 
 
 Organic substances 90 . 44 
 
 Ash 8 . 80 
 
 Sodium carbonate . 58 
 
 Sodium chloride 7 . 35 
 
 Calcium magnesium and sodium phosphate 0.53 
 
 The composition of the normal human pancreatic juice has 
 not been determined completely owing to the difficulty of obtain- 
 ing the secretion. According to Zawadsky the composition of 
 the secretion of a young woman was as follows : 
 
 Water in 1,000 parts 864.05 
 
 Organic substance in 1,000 parts 132.51 
 
 Proteids in 1,000 parts 92 . 05 
 
 Salts in 1,000 parts 3 . 44 
 
 INORGANIC SALTS IN THE SWEAT. 
 
 ''Of the inorganic salts, NaCl is by far the most abundant; 
 it occurs in quantities varjdng from 2 to 3.5 parts per thousand. 
 The elements of the sweat which are of importance from an 
 excretory standpoint are water, inorganic salts and urea or re- 
 lated nitrogenous compounds, ' ' 
 
 Inorganic salts from the faeces are made up of the salts of 
 sodium, potassium, calcium, magnesium and iron. According to 
 Enderlin ^ the following represent the composition of the ma- 
 terial matter in the faeces : 
 
 S.A.LTS SOLUBLE IN WATER. 
 
 Sodium phosphate 2 . 63 
 
 Sodium chloride and sulphate 1.37 
 
 S.\LTS INSOLUBLE IN WATER. 
 
 Earth phosphate 80 . 37 
 
 Ferric phosphate 2 . 09 
 
 Calcium sulphate 4.53 
 
 Silicic acid 7.94 
 
 Like other constituents of the lymph, the salts vary consider- 
 ably in proportion, according as the fluid is more or less rich in 
 
 "Gamgee, Physiological Chemistry of the Animal Body. 
 * American Text-Book of Physiology. 
 
INORGANIC SALTS AND INTERSTITIAL GINGIVITIS. i I 
 
 water. The salts are much more abundant than the organic 
 sohds. 
 
 Inorganic salts in the urine consist, according to Howell,* 
 chiefly of chlorides, phosphates and sulphates of the alkalies and 
 the alkaline earths. As a rule they arise partly from the salts 
 ingested with the food, which salts are eliminated from the blood 
 by the kidney in the water secretion, and in part they are formed 
 in the destructive metabolism which takes place in the body, 
 particularly that involving the proteids. Sodium chloride occurs 
 in the largest quantities (about 15 grams per day), of which the 
 greater part is derived directly from the salt taken in the food. 
 The phosphates occur in combination with Ga and Mg, but chiefly 
 as acid phosphates, of Na or K, The acid reaction of the urine 
 is caused by these latter. The phosphates are produced in part 
 from destruction of phosphorous-containing tissues in the body, 
 but chiefly proceed from phosphates in the food. Following are 
 the average quantities in grams of the chief substances normally 
 excreted in the urine in six hours : ' 
 
 Water 1440 — 1500 
 
 Sohds 57 — 68 
 
 Organic : 
 
 Urea 28 — 68 
 
 Uric acid 7 
 
 Hippuric acid 3 — 2 
 
 Kreatinin 1.7-^— 2.1 
 
 Inorganic : 
 
 Sodium chloride 15 — 20 
 
 Phosphoric acid 2.5 — 3 
 
 Sulphuric acid 2 — 2.5 
 
 Sodium 5 — 7 
 
 IMagnesium .04 
 
 Potassium 3 — 4 
 
 Calcium .03 
 
 Urinary calculi (classified according to their principal ingre- 
 dients), are divided into: 
 
 1. Uric stone, composed of uric acid and acid urates. 
 
 2. Oxalic stone, composed of lime oxalate. 
 
 3. Phosphoric stone, which are composed of magnesium 
 phosphate and carbonate with urate of ammonia. 
 
 • Landolt, Physiology. 
 
78 INTERSTITIAL GINGIVITIS. 
 
 Each oiie of these compounds is nearly in a pure state. A 
 stone may be composed entirely of one salt or it may be com- 
 posed of two, three or four, each compound forming separate 
 consecutive layers through the stone. One examination made by 
 Howship Dickinson '^ showed eighty-nine per cent lime carbonate 
 and the rest lime oxalate and phosphate of lime. 
 
 The deposits upon the teeth are derived partly from the salts 
 ingested with foods, which salts are eliminated from the blood in 
 water secretion, and in part they are found in the waste of tissue 
 which takes place in the body. 
 
 The saliva, according to Schmidt, is made up of the following: 
 
 Water 991.45 
 
 Organic material 2 . 89 
 
 Inorganic : 
 
 Calcic chloride 4 . 50 
 
 Sodium chloride • • • -^ 
 
 Calcic phosphate 1-16 
 
 Magnesium • • • • 
 
 1,000.00 
 
 This material floating in the saliva, together with the epithe- 
 lial scales and other extraneous matters, contribute to form what 
 is known as tartar. This material collects upon the teeth, and 
 according to examinations by Stevenson consists of : 
 
 Soft tartar Hard tartar 
 
 on molars. on lower incisors. 
 
 Water and organic matter 21.48 17.51 
 
 Magnesium phosphate 1.31 1.31 
 
 Calcium phosphate with a litte carbon- 
 ate and trace of flourine 77.21 81.18 
 
 100.00 100.00 
 
 Another analysis made by Scheheoetskey resulted thus : 
 
 Water and organic matter 22.07 
 
 Magnesium phosphate 1.07 
 
 Calcium phosphate 67 . 18 
 
 Calcium carbonate 8 . 13 
 
 Calcium flouride 1 . 55 
 
 100.00 
 
 • Renal and Urinary Affections. 
 
INORGANIC SALTS AND INTERSTITIAL GINGIVITIS. 
 
 79 
 
 Malenfant found that salivary calculi (located in Wharton's 
 duet) was composed of: 
 
 Lime phosphate 27 
 
 Magnesium phosphate 1 
 
 Basic lime phosphate 60 
 
 Alcohol and muriatic acid 4 
 
 Ptyalin . 2 
 
 Loss 6 
 
 100 
 
 The following are results of analysis of salivary calculi by 
 various observers : 
 
 Calcium carbonate 
 
 Calcium phosjihate 
 
 Magnesium phosphate. 
 
 Soluble solids 
 
 Organic matter 
 
 Water and loss 
 
 81.2 
 
 79.4 
 
 80.7 
 
 13.9 
 
 30 
 
 15 
 
 4.1 
 
 5.0 
 
 4.2 
 
 38.2 
 5.1 
 
 75 
 
 55 
 1 
 
 6.2 
 7.1 
 
 4.8 
 8.5 
 
 5.1 
 
 8.3 
 
 38.1 
 
 5 
 
 25 
 
 1.3 
 
 2.3 
 
 1.7 
 
 6.3 
 
 
 
 2 
 75 
 
 23 
 
 Deposits in the tissues in gout are made up of soda and lime 
 urates. In order to compare the calcic deposits in other parts of 
 the body with the so-called serumal deposits upon the teeth af- 
 fected with interstitial gingivitis, thousands of teeth were ob- 
 tained from three dental offices which make a practice of extract- 
 ing teeth. From these one thousand were selected at two differ- 
 ent times, making two thousand teeth containing deposits direct 
 from the tissues. These were submitted to a chemical analysis 
 by J. H. Salisbury, at Rush Medical College, who reports as 
 follows : 
 
 ''The method which I employed in analysis of calcic deposits 
 was as follows : The material was so selected as to be free as 
 possible from salivary tartar and a weighed portion was dried at 
 100° C. This was then carefully incinerated and again weighed, 
 and the difference calculated as organic matter. The residue 
 after incineration was divided into two portions, A and B. 
 
 "A was used for the estimation of phosphates as follows: 
 The ash was dis&clved in nitric acid and the solution precipitated 
 
80 INTERSTITIAL GINGIVITIS. 
 
 with ammonium molybdate. The precipitate was washed, dis- 
 solved in ammonia precipitated by magnesia mixture and the 
 precipitate of ammonia magnesium x)hosphate, washed, dried, 
 ignited and weighed. 
 
 "In B, calcium and magnesium were estimated as follows: 
 The ash was dissolved in hydrochloric acid and the acid just 
 neutralized with ammonia water and sodium acetate added. It 
 was then made slightly acid with a drop of hydrochloric acid 
 and precipitated with ammonium oxalate. The precipitate of 
 calcium oxalate was filtered off, washed, converted into calcium 
 oxide and weighed. The filtrate was made alkaline, sodium 
 phosphate added, and the precipitate of magnesium-ammonium 
 phosphate collected, washed, dried, ignited and weighed. In 
 case the phosphoric acid determined in A did not saturate the 
 calcium and magnesium obtained in B, the excess of base was 
 calculated as carbonate. 
 
 ''The following is the composition of the calcic deposits on 
 the roots of the teeth, according to analysis of April 18, 1898 : 
 
 "Water and organic matter 32.24 
 
 Magnesium phosphate -98 
 
 Calcium phosphate 63 . 08 
 
 Calcium carbonate 3 . 70 
 
 100.00 
 
 ''Analysis of the calcic deposits on the roots of the teeth 
 October 24, 1898, shows it to have the following composition: 
 
 Water 4.48 
 
 Organic matter 27 . 00 
 
 Calcium phosphate 72 . 73 
 
 Magnesium phosphate 4. 91 
 
 99.12 
 
 The composition of the alveolar process is as follows : 
 
 Organic matter: Gelatine and blood vessels 33.30 
 
 Inorganic matter: 
 
 Calcium phosphate 51 . 04 
 
 Calcium carbonate 11 . 30 
 
 Calcium fiouride 2 . 00 
 
 Magnesium phosphate 1 . 10 
 
 Sodium oxide and sodium chloride 1.26 
 
 100.00 
 
INOKGANIC SALTS AND IXTEESTITIAL (ilNUlVITIS. 81 
 
 By comparing the tables of the composition of calcic deposits 
 upon the roots of teeth with that of the alveolar process, it will 
 be observed that there is very little difference. Tartar deposited 
 from the salivary glands and calcic deposits upon the roots of 
 the teeth must not be confounded since there is little in common 
 between them, Tartar is the principal cause of local interstitial 
 gingivitis commencing at the gum margin, while calcic deposits 
 are the result of interstitial gingivitis and are always located 
 upon the root of the tooth at the point of absorption of the 
 alveolar process. The amount of calcic salts in the blood is very 
 small as compared with the amount deposited upon the roots of 
 the teeth and what is lost in the fluids around the teeth. The 
 author ' has stated that the calcic deposit upon the roots of the 
 teeth was the absorbed alveolar process and not derived direct 
 from the blood as has been suggested. 
 
 While nearly every kind of food taken into the stomach con- 
 tains inorganic salts, every excretory organ of the body throws 
 out a certain amount of these salts. Some of these organs 
 excrete the salts in a pure state, while in others the salts are 
 combined with acids or fluids peculiar to that organ. These salts 
 differ in composition and quantity on different days, at different 
 hours of the same day; differ at different ages of the same per- 
 son and differ in persons of like age, on the same diet. No mat- 
 ter how careful the chemist may be in analysis, no two results 
 will be exactly alike. For this reason, in tartar and calcic deposit 
 upon the roots of teeth, two different analyses of the same de- 
 posits are cited. It is evident that while slight differences occur 
 in the table, these are due chiefly to the character of the secre- 
 tions. The kidneys and salivary glands clearly excrete most of 
 the waste inorganic salts. 
 
 Since each excretory organ has its part in elimination of 
 waste inorganic salts, it is clear that if one organ becomes tired 
 or diseased, other organs have an extra amount of material to 
 excrete. In any event, the blood becomes surcharged with waste 
 inorganic salts. There is a class of patients with deformed jaws 
 and irregular teeth, tonsil hypertrophy, mucous membrane, 
 nasal bone and post-nasal space disorder, adenoids, arrest of the 
 
 ' Endarteritis Obliterans. The Dental Digest, 1903. 
 
82 INTERSTITIAL GINGIVITIS. 
 
 facial bones. They are neurotics and possess degenerate struc- 
 tures. This class comprehends those whose nervous system is 
 unstable and whose physical development is a departure from 
 the race type. This unstable or tired condition may affect but 
 one excretory organ. In most cases it affects all organs as well 
 as the entire body. In these patients, especially in youth, does 
 hypertrophy of the alveolar process take place and large de- 
 posits are observed upon the teeth. In this class may be placed 
 rachitic children. 
 
 Inorganic salts taken in food are generally utilized until the 
 osseous system has attained its growth. This usually occurs at 
 about the twenty-sixth year, but full growth may not be attained 
 until the thirty-sixth year. When this period has been reached, 
 although the body still has the sam^e supply of inorganic salts, 
 the system can assimilate only what it needs. The remainder 
 becomes waste. Under such conditions the blood is overcharged 
 with these salts. 
 
 A condition of the system, which has received too little atten- 
 tion, occurs in a class of children ranging from six to eight 
 years, who excrete larger quantities of inorganic salts through 
 the kidneys and salivary glands. In such cases the teeth 
 become coated with tartar. The gums become inflamed from 
 irritation. Interstitial gingivitis is developed in youth. These 
 children may be rachitic, or border upon the disease. They are 
 neurotics, with degenerate structures, suffer from rachitis, rapid 
 decay of the teeth and irregularities. They occur in American 
 and European schools of idiocy and for dependent and defective 
 children. From seventy-five to ninety per cent of these children 
 have interstitial gingivitis, ranging from simple inflammation of 
 the gums to absorption of the gums and alveolar process with 
 pus exudate. Miller noticed in an examination of twenty-six 
 cases of rachitic children under twelve years of age that seven 
 manifested pronounced symptoms of interstitial gingivitis. 
 This was no doubt due to accumulation of calcic salts upon the 
 teeth, producing irritation and absorption of the alveolar proc- 
 ess and contraction of the gums. 
 
 In cases where large collections of tartar are deposited upon 
 the teeth of children there is also an excess of excreta through 
 
INOEGANIC SALTS AND INTERSTITIAL GINGIVITIS. oS 
 
 the kidneys. Examination of urine in such cases will reveal 
 always from four to eight times more deposit than the normal 
 for the age of the patient. Defective nutrition is the result, the 
 bones are small, and the jaws and teeth are irregular. The teeth 
 decay early in life and it is with difficulty that the decay can be 
 arrested. What is true of children is also true of people at 
 advanced age. 
 
 After the skeleton had attained its growth (even in those 
 cases where no deposits were before observed) the blood became 
 overcharged with lime salts and the teeth became a nidus for the 
 deposit from the salivary glands. It is, therefore, clear why 
 deposits and inflammation of the gums are so common after the 
 twenty-sixth year, and more common later in life. Defective 
 children and people who have obtained their growth are more 
 susceptible to trophic disorders of nutrition and the tissues take 
 on disease more readily than healthy individuals earlier in life. 
 When inflammation takes place in connective tissue in all parts 
 of the body (especially if the blood be surcharged with inorganic 
 salts) deposits take place in that tissue through the capillary 
 system. On the other hand, when inflammation of the connective 
 tissue takes place, if inorganic salts be scarce in the blood, de- 
 posits do not take place. As is elsewhere sliown,^ calcic deposits 
 on the roots of teeth are a result of inflammation and pus infec- 
 tion and not the cause. 
 
 International Dental Journal, April, 1896. 
 
CHAPTER VIIL 
 
 THEORIES OF INTERSTITIAL GINGIVITIS. 
 
 The etiology of interstitial gingivitis, according to the views 
 summarized previously, is divisible into local and constitutional. 
 While one school leans largely to the local etiology, another ad- 
 vocates as strongly the constitutional theory, and a third be- 
 lieves in both the constitutional and local theories as causes. 
 The author, from his elaborate researches which began in 1886, 
 is an exponent of the latter class. In a general way, etiology may 
 be divided into exciting and predisposing. Etiology may also 
 depend upon an element dependent on the exciting cause, 
 an element dependent on the constitution of the individual at- 
 tacked, and finally an element dependent on his condition 
 when attacked, both as regards his general system or any one 
 of his organs. The chief constitutional causes to which the 
 disease has been ascribed are general conditions of the 
 health, heredity, constitutional disorders, excessive lime salt 
 secretion, meat-eating, nervous exhaustion, scorbutus and uric 
 acid states, as well as environment. To these may be added 
 drug and metal poisoning such as mercury, lead, brass, 
 arsenic, bromides, etc., as well as autointoxication. The local 
 causes assigned are acute inflammation of the mucous mem- 
 branes, catarrhal states, germs or fungi, irregular teeth, 
 lactic acid, pocket disease, hemorrhagic deposits, serumal 
 calculi and uncleanliness. That all these factors exercise an 
 influence is undeniable, but the enormous etiologic role which 
 has been assigned to some of them is the result of generalization 
 from too few causes. Many of the assigned causes could be com- 
 pressed into fewer etiologic influences. Thus meat-eating, the 
 uric acid states, arthritis or gout are too intimately connected to 
 be regarded as different causes, from a constitutional stand- 
 point. As has been already pointed out, uric acid acts, when it 
 acts at all, like lactic and other acids, as a local irritant rather 
 
THEORIES OF INTERSTITLVL GINGIVITIS. 85 
 
 than as the constitutional condition (as many suppose) which 
 underlies its production and of which it serves as an index. 
 
 Scorbutus is an expression of a nutritional disorder due very 
 frequently in the adult to an excess of meat or a monotom^ of 
 diet. It is a constitutional disorder, peculiarly apt to have its 
 local expression in the gums long ere the general constitutional 
 symptoms are manifest. The germs and fungi etiologists, on the 
 other hand, tend to ignore the constitutional state behind the 
 local culture medium, which must be furnished before growth of 
 the germ or fungus can occur. In order, therefore, to determine 
 whether an alleged cause be exciting or predisposing and what 
 is the influence of the etiologic moment, as the union at one time 
 of the two constitutional factors already cited is called, analysis 
 is required of all the varied factors charged with producing the 
 disease. The influence of heredity is generally left out of con- 
 sideration unless it be direct, which it rarely is, since heredity, 
 as has been well remarked, is usually a prophecy rather than a 
 destiny. It hence constitutes, as a rule, a predisposition. 
 
 The chief tissues concerned in the elimination of waste prod- 
 ucts are the skin, the lungs and air passages, including the 
 mouth and nose, the kidneys, liver and intestines. Interference 
 with the eliminatory powers of the kidneys, liver and intestines 
 causes autointoxication and is especially apt to throw extra work 
 on the skin, lungs and air passages. Of this a sour-winey odor 
 of the breath in diabetes is an excellent illustration. What is 
 true of such a marked form of suboxidation, resulting in auto- 
 intoxication, is true of less pronounced forms. The peculiarly 
 foul odor of the breath and skin in faecal intoxication indicates 
 that the mucous membranes of the nose, throat, mouth and gums 
 are doing the work of elimination which should have been done 
 by the intestines. The failure of the kidney to perform its share 
 of eliminatory work is most apt, however, to find expression in 
 the skin, lungs, nose, mouth and gums. 
 
 The influence of the nervous system on the growth and 
 repair of any tissue is admitted by every physiologist. This 
 influence is entitled the trophic function of nerves. It is not, 
 however, exactly settled whether it be exerted through the 
 nerves themselves or secondarily through their control of the 
 
86 INTERSTITIAL GINGIVITIS. 
 
 vaso-motor (blood vessel) system. Many trophic distnrbances, 
 as J. Collins ^ remarks, are probably due to vaso-motor changes, 
 and it is not possible to separate by any sharply defined line the 
 vaso-motor from the tropho-neuroses. At the same time, it 
 should be distinctly remembered that there exist tropho-neuroses 
 in which there are no apxjreciable vaso-motor changes as in many 
 cases of acromegaly and hypertrophies. On the other hand, 
 there are any amount of vaso-motor disturbance which are by 
 no means trophic in character. Trophic disturbance, which may 
 play a very important part at the onset of interstitial gingivitis, 
 is neurotic cedema due to nerve irritation. While this is most 
 frequent on the face, lips, tongue, pharynx, forehead and genital 
 organs, it also appears on the gums. The cedema reaches its full 
 development in from one-half to two hours. There is a feeling 
 of stiffness and unyieldingness, but no sensation of inflammatory 
 swelling. This type of trophic disorder often initiates changes 
 in the mucous membrane which may readily form the basis of 
 interstitial gingivitis. This condition may not be only due to 
 ordinary nervous causes, but may arise from constitutional con- 
 ditions, gout, etc., and toxic influences. 
 
 * Nervous Diseases, by Dr. F. X. Dercum. 
 
CHAPTER IX. 
 
 URIC ACID AND INTERSTITIAL GINGIVITIS. 
 
 Uric acid was first isolated by Sclieele in 1776. It consists of 
 a white spongy powder. It is devoid of taste and odor. Under 
 the microscope it is seen as rhombic tables or as elongated plates 
 resembling sheaves or rozettes. As deposited in the urine, it has 
 a more or less reddish tinge due to the presence of urinary color- 
 ing matter. 
 
 The nitrogenous constituents of urinary excretion consist 
 chiefly of urea or uric acid in certain animals and other nitro- 
 genous urinary constituents.^ 
 
 Uric acid is found abundanth^ in the urine of the lower ver- 
 tebrates, such as reptiles, birds and mammals. It would be 
 strange if it were not found in the fish tribe. It is more abun- 
 dant in birds than in reptiles. It seems to be a normal constit- 
 uent in both. Uric acid occurs more frequently in the urine of 
 carniverous mammals, although frequently absent. While found 
 in the urine of the herbivora, the quantity is often small and 
 variable. Traces of uric acid are found in the organs of these 
 animals such as the brain, heart, lungs, spleen, pancreas, while 
 it is always found in the blood of birds. In birds, the uric acid 
 is partly formed from the purin bases. It would be strange, 
 tlierefore, if it did not develop in man since he has retained 
 many of the phylogenetic peculiarities of his precursors. In 
 human urine, uric acid is observed in variable amounts. It has 
 been observed in healthy human blood. According to Hammar- 
 sten,^ the amount of uric acid eliminated with human urine varies 
 considerable but amounts on an average to 0.7 grams per day. 
 
 Hammarsten says, ''We used to ascribe an increasing action 
 upon the elimination of uric acid to proteid food, but the investi- 
 gations of Hirschfeld, Rosenfeld and Orgler, Silven, Burian and 
 Schur and others have positively proven that a diet rich in pro- 
 
 ^ Hammarsten, Physiological Chemistry, page 485. 
 
88 INTERSTITIAL GINGIVITIS. 
 
 teid does not itself increase the elimination of uric acid but only 
 according to the amount of nucleins or purin bodies contained 
 therein. The common statement that the elimination of uric acid 
 is smaller with a vegetable diet than with an animal diet, when 
 the quantity may be two grams or more per twenty-four hours, 
 is explained by this." We would naturally expect to find uric 
 acid in patients who live on a strictly vegetable diet as well as 
 in those who live on a meat diet, since uric acid is found in herbi- 
 vora as well as carnivora. 
 
 The uric acid, in so far as it is produced from nuclein bases, 
 is, in part, derived from the nucleins of the destroyed cells of the 
 body and in part from the nucleins of free purin bases intro- 
 duced with the food. 
 
 Belonging to the same group as uric acid are hypoxanthin, 
 xanthin, guanin and adenin. These are called purin bodies and 
 are liberated during the digestion of nucleo-proteids contained 
 in food. It has been found that a diet of meat, especially veal, 
 liver, pancreas and sweetbreads containing a large amount of 
 nucleo-proteid, leads to an increase in the excretion of purin 
 bodies in the urine as compared with a diet of eggs, butter, milk, 
 fruit, vegetables, cheese and bread. The amount of uric acid ex- 
 creted in new born infants is in excess as compared with the 
 adult. 
 
 The morbid conditions, in which the uric acid passed in the 
 urine is increased, are leucocytosis and leukaemia. This increase 
 may be attributed to the degeneration of the excess of leucocytes 
 in the blood. Certain drugs increase the amount of uric acid, 
 e. g., pilocarpin and salicylates. 
 
 Luxury and modern degeneracy are generally charged with 
 the production of diseases which were later found to have at- 
 tacked man in prehistoric periods. This has been the case with 
 interstitial gingivitis. 
 
 E. E. Andrews expresses the following opinion as to modes 
 of life: ''I have been led to believe from my own experience 
 that this trouble exists largely in the mouths of people accus- 
 tomed to luxury — good livers, people about middle age who 
 over-eat and under-work. ' ' 
 
URIC ACID AXD INTERSTITIAL CxIXOrV^ITIS. 89 
 
 No method of Ihdng can be regarded as a cause of interstitial 
 gingivitis except so far as it affects the general system, thus 
 producing trophic changes. There is probably a slight differ- 
 ence in liability to interstitial gingivitis between people of seden- 
 tary habits and active outdoor workers, as well as between ani- 
 mals domesticated or in captivity and those which run at large. 
 
 It is, however, obvious from the data of the chapter upon 
 ''History" that all races and stations, regardless of time, cli- 
 mate, or mode of Hfe, have suffered with the disease. Examina- 
 tions of animals in the American and European zoological gar- 
 dens show that it is not confined to any class of animals. Dogs, 
 cats, horses, cows, whether housed or running at large, suffer 
 with it as age advances. 
 
 Uric acid formation is not confined to large eaters. Spare 
 eaters may have considerable quantities since they may be unable 
 to take care of the uric acid derived from the moderate amount 
 of uric acid forming substances (purin bodies) in a normal diet. 
 
 To summarize then, it will be seen that the age of the patient, 
 the condition, of his system, the character and quantity of food 
 eaten and certain drugs must always be considered in relation to 
 the quantit}^ of uric acid excreted. 
 
 Since the discovery of uric acid in the urine by Scheele in 
 1776, the alleged influence of this factor was steadily advanced 
 to the time of Haig, of London, the most prominent exponent of 
 this theory. Since his time, a better knowledge of uric acid for- 
 mation and its influence upon the system has revealed the usual 
 exaggeration of the influence of this particular etiologic ele- 
 ment. Researches have shown that uric acid poisoning, in a 
 greater or lesser degree, is dependent upon the state of the sys- 
 tem, the nature and strength of the exciting cause. All three 
 play a part in the digestion, assimilation and elimination of the 
 purin bodies which underlie the condition of health formerly at- 
 tributed exclusively to uric acid. 
 
 The uric acid theory of disease having been so strongly advo- 
 cated by certain physicians, a number of dentists have applied 
 the same theory as a cause of interstitial gingivitis and pyor 
 rhoea alveolaris. 
 
90 INTERSTITIAL GINGIVITIS. 
 
 What John Fitzgerald - calls the gingival organs, possess, as 
 he remarks, in common with some other tissues of the body, the 
 power of selecting and excreting poisonous substances from the 
 blood. Some of these cause hyperaemia, or even inflammation, in 
 their passage. Uric acid has been found to play a part in so 
 many excretions that it has naturally attracted attention here. 
 The trend of medical opinion has set strongly in this direction, 
 but of late this trend is changing. 
 
 During the past two decades uric acid has assumed again the 
 prominence in pathogeny which it once had when called sup- 
 pressed gout. It is not surprising, therefore, to find that Reeves, 
 Pierce, Rhein and others claim a uric acid etiology for inter- 
 stitial gingivitis. In support of this claim are advanced the 
 results of three experiments which Pierce has had made on 
 tooth deposits. These deposits were examined chemically by 
 Ernst Congdon, of the Drexel Institute." The first specimen 
 contained a number of needle crystals of calcium urate, a few 
 crystals of free uric acid and crystals of calcium phosphate. 
 Destructive distillation gave a strong amnionic reaction. The 
 murexid test for uric acid and its compounds gave faint results, 
 although its characteristic color was evident in several places. 
 The second specimen presented the same crystals. The reaction 
 to the murexid test was strong and resulted in a number of 
 purplish-red spots. Similar results were obtained from the third 
 specimen. A. B. Brubaker examined six or eight specimens 
 in Pierce's presence, with like results to those obtained in the 
 previous examination. In three an abundance of sodium urate 
 crystals were present. 
 
 The great deficiency in the experiments thus described is the 
 small number of cases examined and the lack of proper control 
 experiments. These elements have so frequently led to errors in 
 dental pathology that I determined upon a series of investiga- 
 tions in two different laboratories, whose results were reported 
 some years ago.* The Columbus Medical Laboratory was se- 
 lected for one series of experiments in special cases. The labora- 
 
 2 The Clinical Journal, March 1, 1899. 
 
 ^International Dental Journal, Vol. XV, pages 1, 217, 501. 
 
 * Dental Cosmos, April, 1896. page 310. Journal of the American Medical Asso- 
 ciation, January 16, 1897. 
 
"URIC ACID AND IXTERSTITIAL GINGIVITIS. 91 
 
 tory of tlie Northwestern University Woman's Medical School 
 was selected for the other series of experiments, to which teeth 
 were sent as soon as they were obtained. One hundred and fifteen 
 teeth VN'^ere sent to the laboratory last named from three institu- 
 tions in Chicago Avhicli make a specialty of extraction. These 
 teeth had no history other than the fact that the cases were well- 
 marked instances of interstitial gingivitis with plenty of calcic 
 deposits, and that the teeth were loose in the sockets when ex- 
 tracted. Of the one hundred examinations made in the Columbus 
 Medical Laboratory, fifty were upon specimens of calcic deposits 
 from my patients and fifty were upon specimens obtained from 
 the institutions just mentioned, and were therefore ^\ithout his- 
 tory. The tests employed were the hydrochloric acid, the dry 
 distillation, and the murexid, these being the tests recommended 
 by Pierce. The examinations in the Columbus Medical Labora- 
 tory were made by J. A. Wesener, and those in the laboratory of 
 the Xorthwestern University Woman's Medical School by J. H. 
 Salisbury. 
 
 Of the one hundred and fifteen examinations made at the 
 Northwestern University Woman's Medical School by the first 
 test, in only two cases were found the needle-shaped crystals, 
 and one in which there was a slight resemblance of uric-acid 
 crystals. By the dry distillation test, thirteen gave no reaction 
 from ammonia, and in seven the reaction was slight. The re- 
 maining eighty gave a decided reaction. By the murexid test, 
 four gave a slight murexid color, but remainder gave no reac- 
 tion. Special examinations was made of twelve of these teeth by 
 the addition of strong hydrochloric acid, warming, decanting the 
 acid, and washing with water. These gave no reaction by the 
 dry distillation for ammonia. Two gave a slight reaction by the 
 murexid test. Li examination of the teeth of three uric-acid 
 diathetic women, over forty years of age, uric acid was not 
 detectible either by the murexid test or microscopically. The 
 examinations made in the Columbus Medical Laboratory were 
 still more interesting, since among them were specimens from 
 patients whose history could be obtained. Of the fifty obtained 
 outside, eight gave positive results from all three tests. The 
 other forty-two were positive by dry distillation, and negative by 
 
92 INTERSTITIAL GINGIVITIS. 
 
 the murexid and microscopical tests. Of the fifty patients, 
 thirty-eight females and twelve males, thirty-two were over forty 
 years of age, twelve over thirty years, and six over fifteen years. 
 Twenty-six have uric acid to a greater or less extent, nine 
 suffer with indigestion, seven of which are subject to sick head- 
 ache, thirty-four have rheumatism. Six are English, and four of 
 these have the true gout; the other two have rheumatism. 
 
 All are positive with the dry distillation test. All are nega- 
 tive with the murexid test. Forty-nine are negative with the 
 microscopical test. One shows needle-shaped crystals, but not 
 uric acid. It is a singular fact that in both laboratories, the 
 cases in which there were uric acid and gouty histories gave neg- 
 ative results. By the dry distillation test, out of two hundred 
 and fifteen cases, all but twelve cases (which have been treated 
 to remove nitrogenous material) responded. The twelve cases so 
 treated did not respond, since nitrogenous compounds in and 
 about teeth (even the saliva) burned to an ash will produce 
 ammonia. By the murexid test only twelve out of the two 
 hundred and fifteen gave a positive reaction. By the micro- 
 scopic examination but ten showed crystals. One of the chemists 
 who made the examination is positive that they were uric acid 
 crystals. The other is not, since lime-phosphate crystals resem- 
 ble uric acid crystals too minutely to be distinguished positively. 
 For three years Wesener made further examinations as to the 
 relative value of the three tests employed. According to his 
 experiments the murexid test is the most valuable, the crystal 
 test second, and the dry distillation third. The murexid test is 
 the most reliable in testing tartar for uric acid, since its red color 
 is easily distinguished from other colors and the test is simple in 
 application. The test for crystallized uric acid is very unsatis- 
 factory, since here must be dealt with a complex mass which not 
 only contains crystals of calcium phosphate (very similar to 
 those of uric acid) but a great mass of detritus obscuring the 
 crystals of uric acid. If crystals be present they by no means 
 settle the existence of uric acid. When the faintest quantity pos- 
 sible of uric acid is mixed with tartar from teeth and subjected 
 to crystallization, the results are always negative. If subjected 
 
UEIC ACID AND INTERSTITIAL OIXOIVITIS. 93 
 
 to the murexid test, the results are always positive. The dry 
 distillation test is so inaccurate as to be unworthy consideration. 
 
 Since these results were published, seven hundred and thirty- 
 five cases have been examined. These examinations were con- 
 ducted by Jerome H. Salisbury, now of Eush Medical College. 
 The teeth procured from institutions which make a specialty of 
 extracting contained the dark calcic deposit above the pus line. 
 By the murexid test, six out of the three hundred gave a distinct 
 reaction; eighteen showed crystals under the microscope. The 
 murexid test was performed as follows: The deposit was se- 
 lected as carefully as possible, removed from the tooth, and 
 placed in a small porcelain crucible. A drop of pure nitric acid 
 was added and the mixture evaporated on the water bath. When 
 dry, the evaporation was repeated with another drop of nitric 
 acid, and the crucible allowed to cool. When cool, the color pro- 
 duced by the nitric acid was observed, and then a glass rod, wet 
 mtli ammonia water, was brought near the deposit, and any color 
 produced was noted. If no color was observed, the ammonia was 
 allowed to flow over the residue. A yellow color was produced 
 in many cases by the nitric acid, which was deepened by the 
 addition of ammonia. The microscopic examination was made 
 by scraping off the deposit and evaporating it with a drop of 
 hydrochloric acid. The residue was moistened ^^ith water, and 
 the insoluble material placed on a slide and covered with a 
 cover-glass. It was examined with a No. 7 objective. Uric 
 acid, therefore, occurred in a certain very small proportion of 
 cases of calcic deposit on the teeth. 
 
 Four hundred and thirty-five cases w^ere later examined, mak- 
 ing in all nine hundred and fifty. Out of these four hundred 
 and thirty-five cases only four per cent showed uric acid by the 
 murexid test and eight per cent by the crystal test. Since the 
 crystal test is not so accurate as the murexid test, it is safe to say 
 that six per cent was the actual per cent of uric acid. As a 
 result of the different experiments, in the first two hundred and 
 fifteen cases fi.ve per cent uric acid was found. In the second 
 three hundred cases, four per cent, and in the third four hundred 
 and thirty-five cases, six per cent w^as found. In an examination 
 of nine hundred and fifty cases by different chemists at different 
 
94 INTERSTITIAL (ilNGIVITIS. 
 
 periods, five to six per cent give positive results as to uric acid by 
 the cliemic and microscopic examination. These results demon- 
 strate conclusively that interstitial gingivitis is not due solely to 
 uric acid ; that uric acid when found is merely an expression of 
 the uric acid diathesis and a coincidence, since it is not always 
 present in the gums and tartar of patients attacked either by 
 gout or the uric acid diathesis. In the six per cent of cases there 
 was nothing to show that uric acid was the cause of interstitial 
 gingivitis, since the deposits were examined after the teeth had 
 been removed. Any other irritation may have been the exciting 
 cause. Uric acid acts, when at all, solely as a local irritant, like 
 other acids and poisons. A microscopic examination of the tis- 
 sues involved occasionally reveals uric acid crystals. The fact, 
 however, that they are found in a small number of patients suf- 
 fering with interstitial gingivitis shows that they cannot be de- 
 pended upon as a general cause of the disease. 
 
CHAPTER X. 
 
 HEREDITY AND ENVIRONMENT IN INTERSTITIAL GINGIVITIS. 
 
 The relations of heredity are far more intricate than is usu- 
 ally assumed to be the case in the average discussion of the sub- 
 ject. The problem consequent on impregnation is not that 
 involved in the mere carrying of the mixture of parents in a fully 
 developed form through intra-uterine life. As all vertebrate 
 organs pass through the same stages before definitely differen- 
 tiating, the later types have to gain at the expense of the earlier 
 and hence must receive greater energy from the direct ancestors. 
 The want of this energy is shown in the various defects and de- 
 partures from types which occur in the different degeneracies 
 and congenital defects. The types of heredity ordinarily con- 
 sidered are direct heredity where the individual takes after im- 
 mediate ancestry, and type heredity where he takes after the 
 type to which he belongs. 
 
 The influence of heredity in interstitial gingivitis, as in other 
 morbid conditions, is still a mooted question. Morbid heredity, 
 as I have elsewhere shown,' is practically divisible into direct 
 and indirect. The first is the direct inheritance of the weakened 
 organism of the mother; the second is a condition of intra-uter- 
 ine infection. Heredity further should be distinguished from 
 congenital states which result from the operation of germs or 
 toxins during a particular pregnancy wherein these pass through 
 the placenta to the foetus. A child may be born of a tuberculous 
 mother with a tendency to tuberculosis but may not develop it; 
 on the other hand the tubercle bacilli may infect it through the 
 placenta so that it is born with tuberculosis. 
 
 The weakened organs of the mother (due to an unstable nerv- 
 ous system) may cause the child to inherit an unstable nervous 
 system. This, in turn, may cause an arrested or excessive devel- 
 opment of the jaw and alveolar process in the child at the periods 
 
 ^Talbot. Degeneracy: Its Signs, Causes and Effects. 
 
96 INTERSTITIAL GINGIVITIS. 
 
 of stress. Under such conditions the jaw is most frequently 
 arrested. An arrested jaw and alveolar process usually mean an 
 irregular dental arch in which the teeth are so closely packed 
 (owing to the crowns being straight, not bell-shaped) that the 
 alveolar process is almost entirely destroyed between the teeth. 
 To keep the gum margins clean and in a healthy condition in such 
 a mouth is almost impossible. The slightest inflammation, due 
 to irritation, of the gums, peridental membrane or alveolar proc- 
 ess, whether local or constitutional, will cause its destruction 
 sooner or later in the life of the individual. 
 
 Again, because the alveolar process is a transitory structure 
 as well as an end organ, and because of its thinness around the 
 teeth, the inheritance of a lowered vitality, both in the individual 
 or in the immediate structure under discussion, or both, will fur- 
 nish a predisposing cause for interstitial gingivitis. This is why 
 so many neurotic and degenerate children possess irregular jaws 
 and teeth, and why these children early develop interstitial gin- 
 givitis.- Hence heredity may well be the indirect cause of inter- 
 stitial gingivitis. 
 
 The reported cases of direct heredity in the pyorrhoeic stage 
 of interstitial gingivitis may belong in one or the other of these 
 categories, but such a theory can hardly be considered tenable. 
 Researches of many able investigators have failed to demon- 
 strate the germ theory, local or inherited, in causal relation to 
 interstitial gingivitis, as practiced by specialists, as we shall 
 see in Chapter XII. It is known, however, to every specialist 
 that the secondary condition of this disease (pyorrhoea alveola- 
 ris) is due to germ infection. Pus germs producing the sec- 
 ondary stage of the disease, are local in nearly every mouth and 
 are not supposed to be inherited. Pus germs in the mouth do 
 not, apparently, produce the first stage of the disease (intersti- 
 tial gingivitis), which is simple inflammation. We could hardly 
 expect to find directly inherited germs from the mother to the 
 child causing infection of the gums, peridental membrane or 
 alveolar process later in the child's life, since there is a period 
 between birth and the eruption of the temporary teeth where 
 no alveolar process is present and no infection takes place. 
 
 Talbot. Developmental Pathology: A Study in Degenerative Evolution. 
 
HEREDITY AND ENVIRONMENT. 
 
 97 
 
 Transitory organs are bound to be weakened by heredity, 
 both in their structure and in their resistance to morbific germs 
 and agencies. These weaknesses are especially apt to be empha- 
 sized during the second and third periods of stress'', when the 
 temporary and permanent teeth are erupting. Such weaknesses 
 may be the outcome of general nerve exhaustion on the part of 
 the parents (the mother especially) or of the child itself, and 
 they represent a changed (transformed) heredity far more com- 
 monly than a direct. This heredity may be more intense than the 
 constitutional lack of health in the parents. On the other hand, 
 the influence of intermarriage of several healthy generations 
 may so offset the evil results of the defects in the parents that 
 the inheritance of disease or the tendency to disease is slight, 
 if at all existing in the child. The last type of heredity, called 
 atavism (or *' throw-back" by breeders), is more likely to work 
 for good than for evil, although disease effects are more gener- 
 ally looked for. Concerned in this latter, where the individual 
 throws back to immediate remote ancestors, this element of 
 atavism tends, through preserving the type, to offset the defects 
 of immediate heredity and, indeed, often underlies the apparent 
 diiference between children of the same parents. It like^\^Lse 
 prevents equal inheritance from both parents, and sometimes 
 favors inheritance of strength or defect from either. It under- 
 lies also so-called collateral or indirect heredity and the trans- 
 mutation of heredity. By virtue of this atavism, a serious nerv- 
 ous defect in a parent or parents might express itself only in 
 an increased tendency to disease on the part of the child's tran- 
 sitory structures and end organs. 
 
 The periods of stress are times in the life of man when cer- 
 tain great life functions are developing or undergoing retrogres- 
 sion. These periods of stress are, during development in utero, 
 during the first dentition, during the second dentition (often 
 as late as the thirteenth year), during puberty and adolescence 
 (fourteen to twenty-five), during the climacteric (forty to sixty), 
 when uterine involution occurs in woman and prostatic involu- 
 tion in man, and finally, during senility (about sixty and up- 
 wards). These p.eriods often constitute a cause for the produc- 
 
 Talbot. Developmental Pathology: A Study in Degenerative Evolution. 
 
98 INTERSTITIAL GINGIVITIS. 
 
 tion of disease even thoiigli liereditary defect itself be absent 
 until tliis time when it first makes it appearance. 
 
 Another factor to be considered in this connection as compli- 
 cating the diagnosis of heredity in interstitial gingivitis is envi- 
 ronment, nnderstanding by this term all the external conditions 
 that can favor the development of the disorder. Family hab- 
 its and surroundings are apt to be alike for every member, so 
 that if anything in the environment especially favors the break- 
 ing out of a disease in one member, the same cause or causes 
 are equally likely to favor the occurrence of the disorder in sev- 
 eral members or even generations of the family, and this may 
 give rise to a suspicion of heredity. This consideration applies 
 to interstitial gingivitis, since the disease has been known to 
 develop in different members of the same family at similar 
 periods of life and under the same conditions. 
 
 That constitutional conditions of hereditary origin favor the 
 occurrence of interstitial gingivitis is undeniable, but this does 
 not mean that interstitial gingivitis itself is hereditary. They 
 favor its occurrence just as they favor any other morbid con- 
 dition, by lessening resistance or by preparing the way. The 
 interstitial gingivitis is only one of the many accidents that are 
 thus facilitated. 
 
 So far as salivary concretions are to be regarded as an excit- 
 ing cause, heredity may be put out of court, since these (though 
 varying widely in different individuals in the amount of the 
 deposits, and consequently in the irritation produced) are de- 
 pendent upon more remote constitutional or local conditions 
 and have no direct connection mth the heredity. Thus the vari- 
 ous deposits attributed to litha^mia or arthritic conditions (noto- 
 riously hereditary), are merely incidental to those conditions 
 and not essentially connected with their constitutional origin. 
 The constitutional conditions merely happen to furnish the irri- 
 tant. 
 
 Local uric acid poisoning* is, as I have elsewhere shown, 
 occasionally associated "v\ith interstitial gingivitis. The coexist- 
 ence signifies the lowered vitality of the system and autointoxi- 
 cation, rather than the etiolgy. 
 
 * The Dental Cosmos, 1896, page 312. 
 
HEREDITY AXD ENVIRON MEXT. 99 
 
 The same is true of all the other neurotic, rachitic and degen- 
 erative conditions, hereditary or otherwise, that are met ^^^.th, 
 associated with gingival inflammation. They favor the occur- 
 rence of the disease by causing a w^eakened capacity of resist- 
 ance, thus predisposing to the attack of any irritation. The 
 mouth, resistant as it ordinarily is, is at all times open to irri- 
 tation and infection. AYhen resistance is impaired it gives way 
 at its most vulnerable points, and the gingival margin because 
 of its transitory and end organ nature is one of these points. 
 Interstitial gingivitis is favored or hindered, like other disor- 
 ders, by constitutional conditions which may or may not be in- 
 herited, and which bear toward it the relations only of predis- 
 posing and accessory causes. 
 
 To summarize, therefore, it is reasonable to suggest that 
 interstitial gingivitis and pyorrhoea alveolaris are not inherited. 
 
 Interstitial gingivitis is the primary condition and represents 
 the reaction of a weakened transitory end organ to constitu- 
 tional or local irritation. 
 
 Heredity, direct and indirect, may of course weaken resist- 
 ance and predispose to the disease, particularly in a structure 
 so transitory as the alveolar process, but no direct transmission 
 of infection is either demonstrable or even tenable. 
 
 Pyorrhoea alveolaris is a secondary infection grafted on the 
 original inflammation by the agency of local pyorrhceic germs 
 such as are prone to invade any exposed membrane, and have 
 no relation whatever to hereditv. 
 
CHAPTER XI. 
 
 DEGENERATE TISSUES IN INTERSTITIAL GINGIVITIS. 
 
 One important factor of predisposition to interstitial gingi- 
 vitis is degeneracy, either local or general. Three possibilities 
 of life await each living being. The individual may remain 
 primitive and unchanged, progress toward a higher type or 
 retrogress to a lower type. In these three conditions, the fact- 
 ors underlying the stable state force the structures to remain 
 as they are; those underlying the progressive tendency make 
 them more elaborate, while the third tends to simplify structure. 
 Degeneracy is a gradual change of structure by which the organ- 
 ism becomes adapted to less varied and less complex conditions 
 of life. It is a reverse of development which proceeds from the 
 indefinite and homogeneous to the definite and heterogeneous 
 with a loss of explosive force due to the acquirement of inhibi- 
 tions or checks. In proportion to the depth of degeneracy does 
 it affect the early simpler or late complicated acquisitions. The 
 opposite process of progression is a gradual change of struc- 
 tures by which the organism becomes adapted to more varied 
 and more complex conditions of life. In progression there is a 
 new expression of form corresponding to new perfection of 
 work in the animal machine. In degeneracy, there is suppres- 
 sion of form corresponding to cessation of work. Elaboration 
 of some one organ may be the necessary accompaniment of 
 degeneracy in all the others. On the other hand, degeneracy in 
 one organ may be the necessary accompaniment to elaboration 
 in all the other organs. During any of the periods of stress 
 defects due to degeneracy are apt to appear and affect the line 
 of least resistance, determined by the depth of degeneracy, as 
 well as the variability of the structures concerned. This is the 
 reason certain individuals develop disease or become suscepti- 
 ble to disease since at these periods the entire organism under- 
 goes change, and the organs most affected by degeneracy are the 
 
DEGENERATE TISSUES IN INTERSTITIAL GINGIVITIS. 101 
 
 first involved. This is particularly true of transitory structures 
 like the alveolar proccess and it, in addition to being doubly 
 transitory and the most sensitive structure in the body is also 
 an end organ like the brain, eye and kidney. The teeth and jaws 
 are among the most variable structures in the body, and they 
 are peculiarly apt to be affected by either general degeneracy, 
 which affects the body as a whole, of local degeneracy, which 
 may aif ect one organ or structure or part of them. Degeneracy 
 factors causing nervous exhaustion in the parents leave their 
 stamp on the tonicity of the child's organs to combat disease. 
 Every nerve cell has two functions, namely: sensation or 
 motion and growth which are dependent upon each other, that is, 
 if the cell be tired by excessive work along the line of sensation 
 or motion, growth later becomes impaired. The cell then not 
 only ceases to continue in strength, but becomes self-poisoned. 
 Each of the organs (heart, liver, kidneys, etc.) has its own sys- 
 tem of nerves (the sympathetic ganglia) which while under the 
 control of the spinal cord and brain, act independently. If these 
 nerve centers become tired, the organ fails to perform its func- 
 tions, the general system becomes both poisoned and ill-fed, and 
 nervous exhaustion results. In most cases, however, the brain 
 and spinal cord are first exhausted. The nerves of the other 
 organs are thus allowed too free play, and exhaust themselves 
 later. This systemic nerve exhaustion particularly affects the 
 testicle in the male and the uterus and ovaries in the female, 
 hence an unstable nervous system in the offspring results. 
 Through this, the body is imperfectly supplied with natural 
 tonics (antitoxins) formed by these structures, and the general 
 nervous exhaustion becomes still more complete. All the organs 
 of the body are thus weakened in their function. Practically 
 the neurasthenic's organs have taken on degenerative functions 
 though not degenerate in structure. Through the influence of 
 these various nerve exhaustion agencies, the spinal cord and 
 brain lose their phylogenetic gains and the neurasthenic is no 
 longer adjusted to environment. Since the reproductive organs 
 suffer particularly, children, born after the nervous exhaustion 
 in the parents, are more or less checked in development owing 
 to the depth of degeneracy and the influence of healthy atavism. 
 
102 INTERSTITIAL GINGIVITIS. 
 
 Tlioy have degenerations in the structure of their organs which, 
 in the parents were represented by neurasthenic disorder in 
 function. As the ovaries of the neurasthenic female generally 
 exhibit prominently the effects of nervous exhaustion, the off- 
 spring does not retain enough vigor to pass through the normal 
 process of growth or should it survive, it is usually affected by 
 the profound neuroses. In these instances in connection with 
 irregular dental arches, there is always interstitial gingivitis 
 and pyorrhoea alveolaris. 
 
 The action of degeneracy, considered as a local factor of con- 
 stitutional origin, may be exerted to preserve embryonic con- 
 ditions in adult life. Such preservation may result in the break- 
 dow^n of tissues which would otherwise withstand germs, toxins 
 and poisons, or other causes of disease external to the tissues. 
 Given this condition of local degeneracy, a local predisposing 
 factor is added to both the exciting causes and the constitu- 
 tional predisposing factors. So long as the teeth and transi- 
 tory structures remain in the comparatively stable condition of 
 primitive races, this factor is, to a great extent, in abeyance. 
 When, however, the jaw begins to evolve (grow smaller), the 
 degenerate types find this factor adding dangers in their pliylo- 
 geny. In the degenerate, the struggle for existence between 
 organs (the brain and skull on the one hand, and the face, jaws 
 and teeth on the other) is not properly balanced, whence the 
 dangers from these local states of degeneracy that in the higher 
 types are expressions of advance undergone without danger. 
 This is excellently illustrated in the embryology of the mucous 
 membrane. This, in degenerate children, often fails so to de- 
 velop that the bactericidal function of mucus does not appear. 
 This hereditary feebleness of the mucous membrane is pecu- 
 liarly apt to occur in the nose, throat and gums, but other mu- 
 cous membranes are not exempt. 
 
 Miller, as elsewhere stated, found a little over thirty-three 
 and one-third per cent on examination of tw^enty-six rachitic 
 children under twelve years wdio manifested interstitial gingi- 
 vitis. Considering that most of these manifested symptoms 
 of inherited congenital or acquired constitutional defect, such 
 a small proportion is rather remarkable. The fact suggests one 
 
DEGENERATE TISSUES IN INTERSTITIAL GINGIVITIS. 103 
 
 of two explanations — either the children in the institution vis- 
 ited by Doctor Miller took better care of their teeth and gums 
 than is usual ">\itli this class, or the cases in which pus existed 
 only were classed as pyorrhoea. I have examined the mouths 
 of deaf mutes, blind, idiotic, feeble-minded and rachitic children 
 in the institutions in America and Europe. Interstitial gingivi- 
 tis was found in all its stages, from simple inflammation of the 
 gums to loosening of the teeth, in from twenty-five to seventy- 
 five per cent. In these cases not only are there constitutional 
 factors, but also uncleanliness of the mouth and gum tissues. 
 The degenerate children of even the best families encountered 
 in office practice usually have jaw deformities and teeth irregu- 
 larities as well as interstitial gingivitis. Patterson has had 
 under observation thirty-eight cases of well-marked pyorrhoea, 
 thirty-three of w^hich co-existed with nasal catarrh. These 
 cases were, no doubt, those of degenerate patients. The nasal 
 catarrh was a coincidence dependent on the general deficiency 
 of the mucous membrane. 
 
CHAPTER XII. 
 
 BACTEKIOl.OGIC RESEARCHES IN INTERSTITIAL GINClVITIS. 
 
 The causes which in'oduce interstitial gingivitis may be 
 divided into those producing infections and those producing irri- 
 tations from intoxication. 
 
 The infections may be divided into local and constitutional. 
 The constitutional infections are those which infect the gums, 
 alveolar process and peridental membrane, through the blood, 
 such as tuberculosis, syphilis, scurvy and similar diseases. 
 
 The local infections are those in wliich the germs infect the 
 tissues directly producing anthrax, actinomycosis, gonorrhoea, 
 syphilis, apthae,^ dead pulps and many other diseases for which 
 no name has yet been applied. 
 
 All these diseases have constitutional symptoms which are 
 associated and which must be understood in making a diagnosis. 
 Since most of these infections, whether constitutional or local, 
 are special diseases of the gums and alveolar process, they re- 
 quire special constitutional treatment according to the general 
 s3^mptoms as they arise and are therefore to be placed in a spe- 
 cial class by themselves. They are not considered again in this 
 work. 
 
 Experiments with bacteric infection upon animals and human 
 to produce interstitial gingivitis have been made by Galippe, 
 Miller, Rhein, Carpenter and Talbot. 
 
 Galippe " was probably among the first to make analj^tic 
 experimentation in the bacteriology of this disease. He claims 
 that there is found in the pus of pyorrhoea a parasite, resembling 
 in shape the Greek letter N. Injecting this into the belly of a 
 guinea pig, abscesses resulted, which had a special tendency to 
 affect bone tissue. Injections into the space between the teeth 
 and gums were negative in result. Galippe regards his experi- 
 
 ^ Talbot. Some Bacterial and Non-bacterial Diseases. Journal of the American 
 Medical Association, February 10, 1912. 
 
 'Die Infectiose ArthroDentaire Gingivitis, 1888. 
 
BACTEKIOLOGIC RESEARCHES IX INTERSTITIAL GINGIVITIS. 105 
 
 ments as suggestions for fiirtlier research, but not demon- 
 strative. 
 
 Miller,^ after explaining liis own methods, made a series of 
 culture experiments on agar-agar at blood temperature. Twelve 
 cases of pyorrhoea in human beings, and six in dogs, were exam- 
 ined. He isolated twenty different bacteria from human beings, 
 and nine from dogs. Among the twenty kinds, staphylococcus 
 pyogenes aureus was found twice, staphylococcus pyogenes 
 albus once, streptococcus pyogenes once. Of the other sixteen, 
 nine subcutaneously injected produced no particular reaction, 
 four a slight, three a severe suppuration in the subcutaneous 
 connective tissue. . . . Among the nine species found in 
 dogs, staphylococcus pyogenes albus occurred once. Of the 
 other eight, two subcutaneously injected caused no reaction, and 
 five but slight. One caused very profuse suppuration, by which 
 large portions of skin exfoliated. . . . Microscopic exami- 
 nation of stained sections revealed masses of different bacteria, 
 cocci and bacilli. Leptothrix occurred infrequently, and then 
 only on the surface of the cement, and where there were micro- 
 scopical cavities in it. . . . Miller succeeded consequently 
 in cultivating a large number of bacteria from pyorrhoea alveo- 
 laris which possessed pyogenic properties, but was not able to 
 determine the constant occurrence of any one which might be 
 regarded as the specific micro-organism of pyorrhoea alveolaris. 
 Miller remarks that it is not evident from Galippe's communica- 
 tion whether he found the N or B bacterium in all cases exam- 
 ined, or but once. 
 
 Sudduth, after repeated examinations, arrived at the same 
 conclusion as Miller. 
 
 Dr. M. L. Rhein's* investigations are here given. He says, 
 ''The results of my investigations made at the Pediatric Labora- 
 tory in New York some eleven years ago are given here for the 
 first time as corroborative e\'idence that in healthy bodies it is 
 impossible to produce this disease. Four guinea pigs, proven 
 . later at the autopsy to be absolutely free from any taint of dis- 
 ease or abnormality, were chosen. Their food was carefully re- 
 
 ' Micro-Organisms of the Human Month. 
 
 * Pyorrhcea Alveolaris. The Items of Interest, June, 1910. 
 
106 INTERSTITIAL GINGIVITIS. 
 
 duced day by day until they died at the end of ten weeks. Con- 
 trol pigs were kept in a cage alongside of these and fed with 
 the usual quantities of food. About the beginning of the tenth 
 week when the pigs were w^eakened from lack of food, all eight 
 of them were inoculated in the pericemental regions with injec- 
 tions of liquid cultures developed in bouillon, from pus taken 
 from the pockets of pyorrhoeal patients. On the third day all 
 evidence of the trauma produced by the injections had disap- 
 peared. At no time had there been the slightest evidence of 
 even a resulting gingivitis. As stated before, the autopsies 
 showed all four pigs to have absolutely normal organs, although 
 they were practically skeletons. Of the control pigs, while three 
 of them showed the same immunity to infection, the fourth one 
 showed evidence of inflammation, and at the end of the fifth day 
 there was a distinctive serus exudate coming from the neck of 
 the front tooth around which the injections had been made. I 
 have always regretted the fact that this pig was not killed and 
 an autopsy held. 
 
 ''Before this time I had examined the mouths of many hun- 
 dreds of guinea pigs inoculated by the Board of Health with 
 tuberculosis. Every one of these showed the most marked evi- 
 dence of pyorrhoeal conditions. In the same manner a visit to 
 any sanatorium for tuberculosis cases will show on examination 
 of the mouths, pyorrhoea alveolaris in a degree of severity 
 exactly conforming to the inroads which the disease has made. 
 A like examination of the medical wards of any hospital con- 
 taining cases of diseases of the heart, kidneys, liver, lungs, etc., 
 will, if no attention has been paid to prophylaxis of the mouth, 
 show conditions of pyorrhoea. Even when the most strenuous 
 efforts in this direction of mouth care are taken, if the form of 
 the malnutrition has passed to a certain stage, no care of the 
 mouth is sufficient to prevent the marked development of pyor- 
 rhoea alveolaris." 
 
 The results obtained in the Columbus Memorial Laboratory 
 of Chicago, by W. A. Evans for the author, were as follows : 
 
 In order to determine whether a specific bacterium existed in 
 the pyorrhoeic stage of interstitial gingivitis in man (necessary 
 to constitute this stage a special disease), pus from more than 
 
BACTERIOLOGIC EESEARCHES IX INTERSTITIAL GINGIVITIS, 107 
 
 fifty cases was examined. In all, the pus was obtained from the 
 gums by a platinum needle under proper methods of steriliza- 
 tion. The pus from some cases was smeared on a slide. This 
 was stained and such determination made as was possible with 
 this procedure. With the pus from fifteen cases, agar was inocu- 
 lated and placed in Petrie's dishes. The individual colonies 
 were grown on gelatin, agar, bouillon, potato and blood serum. 
 The results were as follows: In fifteen cases in which the 
 organisms were plated out, fifty-five organisms w^ere found. In 
 two there was no grow^th. Two had but one species of germs, 
 two had six, one had seven, and one had ten. The germs found 
 are divisible into three classes: Those usually pathogenic to 
 man, those exceptionally pathogenic to man, and those never 
 pathogenic to man. The first class was found thirty times, the 
 second twelve, and the third thirteen. Class third is, no doubt, 
 seemingly smaller than it should be, since many members of it 
 probably do not grow on ordinary culture media. Of the germs 
 most frequent and important, staphylococcus pyogenes aureus 
 occurred nine times, staphylococcus pyogenes albus six times, 
 and staphylococcus pyogenes citreus once. A lanceolate diplo- 
 coccus, growing like pneumonococcus, was found six times. 
 Streptococcus pyogenes w^as found twice. Bacillus coli com- 
 mune was found twice. A bacillus growing like the diphtheria 
 bacillus occurred twice. This last bacillus had the appearance 
 of the Klebs-Loeffler l)acillus. It lay on the slide like it and it 
 stained irregularly. Of the less important organisms, bacillus 
 P3^ocyaneus was found three times, micrococcus tetragenus seven 
 times, leptothrix seven times, bacillus mesentericus twice, bacil- 
 lus subtilis three times. There was also present a peculiar large 
 club-shaped fungus somewhat resembling the degenerative 
 forms of actinomycosis. 
 
 Did these examinations stand alone, definite conclusions 
 could not be drawn from them. These, however, are admissible 
 since all observations on this subject tend in the same direction. 
 While, as already stated, Galippe believed that he had isolated 
 two bacteria capable of causing pyorrhoea alveolaris, still he 
 failed with both to produce the disease. This failure, according 
 to the laws of Koch, is fatal to the position taken. 
 
108 INTERSTITIAIi GINGIVITIS. 
 
 M. Herzog, of the Cliicago Polyclinic, on examination of 
 cases of interstitial gingivitis, wliicli had not readied the pyor- 
 rhoeic stage, had the following results: Pieces from the gum 
 margin which had been fixed and hardened in a formalin solu- 
 tion, were partly imbedded in celloidin, partly in paraffin. The 
 sections were stained according to various methods, including 
 Gramm's, eosin (Unna's) and alkaline methylblue stain. The 
 examination of the tissue shows an unchanged lining of stratified 
 squamous epithelium, and, in the connective tissue below the 
 former, well-marked evidences of an inflammatory process. The 
 round-cell infiltration is best marked in the deeper layers toward 
 the periosteum, while the layers of connective tissue fibers nearer 
 to the lining epithelium show less evidences of inflammation and 
 are partly entirely free from any round-cell infiltration. The 
 infiltrating round cells are of the type of lymphocytes, plasma 
 cells and plasma mast cells. Very large and typical mast cells 
 are frequently found in the neighborhood of small vessels. 
 Many of the vessels seen are quite tortuous, and the vascular 
 supply of the connective tissue appears to be considerably in- 
 creased beyond the normal. Bacteria could not be demonstrated 
 in the inflamed areas. 
 
 M. Herzog 's examination of the interstitial gingivitis, pro- 
 duced by mercury in dogs, failed to reveal any bacteria. He was 
 of opinion that the histologic changes of inflammatory type 
 found, were due to the chemotactic influence of mercury and not 
 to microbic action. 
 
 In a paper ^ read before the Section on Stomatology of the 
 American Medical Association, at Columbus, Ohio, George T. 
 Carpenter mentioned some very interesting experiments in this 
 connection. By infecting a fresh wound in the gums of rabbits 
 with pyorrhoea and other pus he found the parts will remain 
 infected only from two to five days. In other rabbits a rubber 
 band was placed around teeth and pressed under the gums until 
 inflammation resulted, when the parts were infected with pyor- 
 rhoea and pus from a chronic ulcer; pus infection resulted. 
 
 Like experiments were made in the human mouth on gums 
 
 ^Some Points on the Etiology, Pathology and Treatment of Persistent Pyorrhcea 
 Alveolaris. 
 
BACTERIOLOGIC EESEAECHES IJ^ INTERSTITIAL GINGIVITIS. 109 
 
 which had been neglected as well as on healthy gums, and with 
 similar results. His experiments tend to show that, when ani- 
 mals and man are healthy, the tissues resist infection ; but when 
 diseased, infection results. All yield to treatment. 
 
 On examination of pus taken from pyorrhoea pockets pro- 
 ceeding from acute infection, two competent bacteriologists were 
 unable to find a micro-organism not found in pus from other 
 infected tissues. 
 
 These results, in Carpenter's opinion, tend to show that a 
 specific germ, to which pyorrhoea alveolaris is attributable, has 
 not yet been found. 
 
 The disease being so prevalent among dogs, it occurred to me 
 that they would be of great value for experimental inoculation. 
 The prevalence of the disease in dogs suggests that if it were a 
 specific infection, these must be inoculable. Miller '^ had made a 
 few inoculations of pus as well as of the deposits around the 
 teeth. Slight inflammation, and, in one case, a little suppuration 
 alone resulted. He afterward isolated twenty different bacteria 
 from the human mouth and nine from dogs. Some of the 
 uncommon varieties were infective, l)ut without marked results. 
 Isolated varieties would probably not produce results that could 
 be attained by inoculating animals with the fresh secretion (pus 
 and other deposits) from dogs already affected with the disease. 
 A dog was procured from the Veterinary Hospital whose gums 
 and outer alveolar process were almost entirely absorbed with 
 pus exudate. Street dogs selected for inoculation were forty-six 
 in number, ranging in age from one year to seven. They w^ere 
 of all breeds and conditions. Some were well fed, others very 
 thin. Many had sound, healthy gums ; others had slight inflam- 
 mation at different localities. No dog was used whose gums 
 and alveolar process had become infected or whose tissues were 
 absorbed. Two dogs were operated upon at a time. The gum 
 was separated from the necks of the teeth down to the alveolar 
 process and peridental membrane — one half at the canine, the 
 other at the second pre-molar, since in a majority of cases the 
 disease began at the canine tooth, probably on account of its 
 prominence and the thinness of the alveolar process. The sec- 
 
 Mifro-Organisnis of the Human Mouth, page 329. 
 
110 INTERSTITIAL GINGIVITIS. 
 
 Olid pre-molar was selected because it is the least prominent. 
 The secretions about the teeth and gnnis of the diseased dog 
 were collected upon a platinum wire (previously sterilized) and 
 conveyed to the injured parts. Thirty-nine healed in eight days. 
 In these the gum tissues were healthy. The pus had no effect. 
 The wounds healed as rapidly as any wounds possibly could. 
 In seven the gums were inflamed and infection occurred. Sup- 
 puration was slight in four and considerable in three. The path- 
 ologic findings in these cases were not unlike inflamiuation and 
 infection in other tissues. Similar results would, no doubt, have 
 taken place if inoculation had been performed with pus from an 
 abscess. The last three dogs were allowed to depart at the end 
 of four weeks with slight pus infection. 
 
 Since these researches were concluded, another series of ex- 
 periments was undertaken upon the lines conducted by Dr. 
 Carpenter, extending over a period of twelve years. These ex- 
 periments were performed upon dogs, guinea pigs, rabbits, white 
 Qiice, and humans. One hundred and seventy-six experiments 
 were made. They consisted of the application of pus from 
 pyorrhea patients direct to healthy and diseased gums with a 
 view of producing interstitial gingivitis or pyorrhoea alveolaris 
 or both. Applications were made to fifty-six humans, twenty-six 
 had slightly inflamed gums and thirty comparatively healthy 
 gums. Forty-eight dogs were treated in like manner; twenty- 
 nine young dogs had healthy gums and nineteen older dogs 
 slightly diseased gums ; thirty-two guinea pigs ; eighteen rabbits 
 and twenty-two white mice. While a slight inflammation was 
 produced in a part of those cases where inflammation already 
 existed, no extended chronic inflammation resulted. We would 
 naturally expect to obtain some results in the white mice since 
 they are of the degenerate type and very susceptible to disease 
 but the results were similar to those of other animals. These 
 experiments may later seem crude and with improved methods 
 better results may be obtained. 
 
 Outside of a few specific diseases of the gums and alveolar 
 process some of which have already been enumerated, no one 
 has demonstrated that specific pathogenic bacterial infection 
 is a cause of interstitial gingivitis although the mouth is known 
 
BACTERIOLOGIC RESEARCHES IX INTERSTITIAL GINGIVITIS. Ill 
 
 to be the breeding ground of an extensive variety of germs. 
 Teetli are extracted, irregular teeth are corrected, healthy gums 
 are injured in filling teeth and finishing fillings many times each 
 day but we seldom see local infection of the gums and alveolar 
 process, producing interstitial gingivitis which comes to us every 
 day for treatment. 
 
 In these diseased conditions, mechanical specialists spend 
 hours on the surgical treatment of the gums, peridental mem- 
 brane and alveolar process surrounding the tooth without first 
 destro}T-ng the pus germs about the teeth, injuring the parts 
 and carrying the pathogenic bacteria into the wounds. If infec- 
 tion were a cause, such rash treatment surely would intensify the 
 disease. Some of the lower vertebrates, such as the carnivora 
 live upon putrid food containing all forms of pathogenic bac- 
 teria but gum infection rarely, if ever, takes place. 
 
 Within the past year a machine has been placed upon the 
 market for the supposed purpose of forcing oxygen through the 
 tissues in the treatment of this disease. I have watched this 
 process of treatment "with fear and trembling" since the 
 method of application forces the pus germs through the inflamed 
 alveolar process. Why infection does not occur is a mystery. 
 This method of applying drugs and forcing pus germs into the 
 tissues without infection is a strong point in favor of the non- 
 infectious theory of interstitial gingivitis. 
 
 From our knowledge based upon original researches at the 
 present time, interstitial gingi\atis, from the viewpoint of the 
 specialist, cannot be classed as an infectious disease. It may be 
 possible in the future with more improved methods of research 
 to throw a clearer light on the nature of the process. 
 
CHAPTER XIII. 
 
 INTERSTITIAL GINGIVITIS, 
 
 Interstitial gingivitis is an inflammation wliicli ma}^ take 
 place in the gums, peridental membrane and alveolar process at 
 any point from the gingival border to the apex of the root or 
 roots of the tooth. This inflammation may be confined to a very 
 small area at any one of these locahties and progress to abscess 
 and be restored to health without other parts becoming involved 
 or the entire structure may become diseased resulting in the 
 exfoliation of the tooth. 
 
 To illustrate, among the local causes tartar or other irritants 
 at the gum margin will set up a gingi\itis. Remove the irritant 
 and by local treatment the gums are restored to health. The 
 interstitial structures have not been involved. In autointoxica- 
 tion, poisons circulating in the blood may and do collect in the 
 arteries midway between the gum margin and the apical end of 
 the root, set up inflammation and a peridental abscess forms 
 discharging directly upon the gum. The parts heal with very 
 little or no pain to the patient. The gum margin or the apical 
 end of the root or even the opposite side of the alveolar process 
 is not involved. Here we have an interstitial inflammation. 
 Again the pulp in a tooth dies, inflammation takes place at the 
 apical end of the root and proceeds to abscess. Here again we 
 have an interstitial inflammation without gingivitis. It is im- 
 possible, in many patients, to state just when the inflammation 
 begins and in most patients it is both gingival as well as deep- 
 seated. The term "interstitial gingivitis" is used to cover all 
 the inflammation of the gums, peridental membrane and alveolar 
 process. 
 
 Before discussing interstitial gingivitis we must first famil- 
 iarize ourselves with the nature of the structures involved since 
 there are no other structures in the human l)ody like them by 
 which the pathology can be compared. The structures and their 
 functions are unicpie in themselves. We must, therefore, re- 
 
INTERSTITIAL (ilXGIVITIS. 113 
 
 capitulate briefly the main points already In'ouglit out in pre- 
 vious chapters in regard to the structures involved. 
 
 In the evolution of the face, jaws and teeth the tendency is 
 for these structures to grow smaller, hence the jaws and alveolar 
 process are transitory organs. In this natural evolution the 
 influences of the parents, owing to excesses tend to produce tired 
 out reproductive organs; these fagged out reproductive organs 
 in turn tend to produce an unstable nervous system in both 
 mother and child. The most intense effect is on structures 
 which are transitory and always tend toward the least 
 resistance. 
 
 After birth, the child is subjected to one or all the children's 
 diseases which also tend to produce an unstable nervous system 
 in the child. The effect of an unstable nervous system upon the 
 child is to produce an arrest of development of transitory struc- 
 tures and acts also towards the line of least resistance. In both 
 conditions, that of the parents and that of the child, the ten- 
 dency is to produce a still smaller jaw and alveolar process. 
 
 Again, in some of the lower vertebrates, there is a succession 
 of teeth throughout life. In the higher vertebrates, including 
 man, there are only two sets ; one is shed as soon as it has served 
 its usefulness by absorption of the alveolar process and a second 
 set takes its place. As soon as the alveolar process has built 
 itself about the teethj the phylogenetic influence is ready to 
 remove the second teeth. In other words, the alveolar process 
 is only waiting for some irritant to set up a low form of inflam- 
 mation to produce absorption of the bone. AVe, therefore, have 
 in the alveolar process a doubly transitory structure. We have 
 also in the alveolar process an exceedingly sensitive end organ. 
 The tooth to all intents and purposes, so far as this disease is 
 concerned, is a foreign body. The arteries and nerves pass 
 through the bone in a tortuous manner as far as the root of the 
 tooth. Poisons circulating in the blood pass to the end of the 
 arteries and stop setting up irritation and inflammation. 
 
 There are otlier end organs in the body but tlie.y are all com- 
 posed of soft tissues. These tissues can and do expand when in- 
 flammation is set lip and in many instances recover health. Not 
 so with the alveolar process. When inflammation takes place in 
 
114 INTERSTITIAL GINGIVITIS. 
 
 tliis tissue, expansion of the arteries cannot take place and de- 
 struction occurs. The process rarely if ever recovers its lost 
 tissue. Because the alveolar process is a transitory structure 
 and end organ, it is the first structure in the body to respond to 
 poisons and toxins. Two illustrations are only necessary to 
 prove this statement. When a patient who has been working in 
 metals or drugs visits his physician for any ailment, the first 
 thing the physician does is to examine the gums to ascertain if 
 the patient is poisoned by the drugs or metals, this structure 
 being the first to become diseased and register the poisons. 
 
 Again, when the physician administers mercury or potassium 
 iodid in the treatment of a specific disease, he continues the 
 treatment until the gums are ''touched" (inflamed), this symp- 
 tom being the first and only sign that the system is under the 
 influence of the drug. In lead poisoning Ave have the blue gum ; 
 in mercury, red ; brass, green ; scurvy, red, etc. The colors are 
 due to the kinds of poisons collected in the ends of the capillaries 
 next to the root of the tooth. These indications are sufficient 
 proof of the statement that the alveolar process is the first 
 structure involved. 
 
 INFLAMMATION. 
 
 It is not my intention to enter into a minute description of 
 the phenomenon of inflammation but to simply state as briefly 
 as possible how it is produced and the changes which take place 
 in the tissues involved in the disease under discussion. 
 
 The most simple illustration of active inflammation in a 
 highly vascular tissue is that of an injury to the fairly trans- 
 parent web of the hind foot, tongue or mesentery of the frog. 
 The web of the foot of a small frog is so thin that the changes 
 occurring in and around the vessels of the part injured can be 
 readily found with the microscope. 
 
 With slight modifications due to local conditions in the tis- 
 sues under examination, the process of inflammation is the 
 same throughout the entire vertebrate series from the reptilia 
 upwards. 
 
 The frog is prepared by destroying the central nervous sys- 
 tem or spinal cord by passing a wire through the vertebral col- 
 
INTERSTITIAL GINGIVITIS. 115 
 
 umn after first being curarised. The web of the foot is then 
 placed under the microscope and a wound is made with a needle. 
 The first change noticed in the surrounding tissue of the injured 
 membrane is a dilatation of the vessels first of the arteries and 
 then of the veins. In the arteries, there is a very noticeable 
 acceleration of the flow of blood. At this early period, there is 
 very little evidence of dilatation of the capillaries. In the course 
 of an hour, however, expansion can be readily observed and the 
 former invisible capillaries now fill with blood and are quite 
 easily observed. In the course of an hour or two there is a slow- 
 ing of the blood current. Before the wound was made, there was 
 a well-marked central stream of corpuscles with an outer zone of 
 plasma devoid of corpuscles. Now the central stream of cor- 
 puscles broadens out and the center zone of plasma becomes 
 smaller and smaller. As it narrows, there is an increasing num- 
 ber of clear round blood leucocytes observed traveling at a 
 slower rate than the central stream and occasionally stopping 
 beside the walls of the vessels and after a short detention con- 
 tinue their course. The leucocytes act as though they wish to 
 attach themselves to the walls of the vessels. The current be- 
 comes slower and slower until there is a vast distinction between 
 the central and the peripheral streams. The corpuscles are now 
 closely packed together and fill the whole surface of the blood 
 vessel. The leucocytes now approach the vessel walls in large 
 quantities and adhere more firmly. While the current is 
 recognizable the action of the stream causes the leucocytes to 
 assume a pear-shaped appearance the larger round end pointing 
 in the direction of the current. As the blood stream gradually 
 slows the corpuscles may at last move in a series of movements 
 with the beats of the heart, while frequently in the veins and cap- 
 illaries the mass of blood may be seen moving in one direction 
 or the other. Frequently one or the other of these stages is 
 followed by complete stasis of blood in the vessels of the injured 
 area for occasionally little or no arrest is seen in the vessels. 
 Accompanying this stage, there is already considerable exuda- 
 tion of clear fluid from the wound; there is an out-pouring of 
 lymph from the* distended vessels. AVith the slomng of the 
 stream^ the leucocytes collect next to the walls of the small veins 
 
116 
 
 INTEESTITIAL GINGIVITIS. 
 
 and within the capillaries and pass from the interior to the ex- 
 terior of the vessels. (Fig. 29.) These leucocytes after passing 
 through the walls of the vessels collect in the lymph spaces be- 
 tween the vessel walls. There may also be found a small number 
 of red corpuscles distributed among them. The leucocytes do 
 not stop near the vessels but by an active ama3boid movement 
 they pass on to the point of injury. Then by the end of about six 
 hours the surrounding area of the injury may be covered by a 
 serum filled with leucocytes. Here then we trace the first step 
 towards the provisional protection of the wound. 
 
 Fig. 29. — Inflamed Human Mesentery (O.smic-acid Preparation) ; a, Normal 
 Trabecula; ft, Normal Epithelium (Endothelium); c, Small Artery; rf, 
 Vein with Leucocytes Arranged Peripherally; c, White Blood-Cells, 
 Which Have Emigrated or are Emigrating; /, Desquamating Endothelium; 
 /, Multinuclear Cells; g, Extravasated Red Blood-Cells. x180. (Ziegler.) 
 
 If, in producing this wound irritating substances have not 
 entered, the process may be arrested at this point. The stasis 
 of blood in the distended vessels may now be followed by a 
 restoration of the current and slow return of the vessels to their 
 former caliber will take place. 
 
 On the other hand, if irritants of a microbic nature enter the 
 wound the process may extend to abscess. If the irritants, in- 
 
INTERSTITIAL GINGIVITIS. 117 
 
 fections or poisons are too abundant, migration of quantities of 
 leucocytes takes place and they collect between the bundles of 
 connective tissue fibers. The cocci collect in the lymph spaces 
 and the massing of leucocytes corresponds to the accumulation 
 of the microbes. At the end of about forty-eight hours a com- 
 plete abscess forms, separated sharply from the surrounding 
 healthy tissue. In the center all traces of previous blood vessels 
 are lost, while in the periphery they are easily traceable ; in the 
 center of the abscess the original tissue has wholly disappeared, 
 while near the outer surface, sheaths and bundles of disinte- 
 grating fibers are seen ; about the tenth day new growth of tis- 
 sue begins to show itself. Numerous capillaries and newly- 
 formed connective tissue are seen and the process of restoration 
 takes place. 
 
 We have shown, in a general way, the different stages of 
 inflammation in soft tissues of all vertebrates, including the 
 gums and peridental membrane in man. The inflammatory proc- 
 ess which takes place in the alveolar process, however, is quite 
 different in its procedure. Instead of the traumatic injury to 
 the frog just cited, the injury to the alveolar process is brought 
 about by the poisons and toxins circulating in the blood and 
 which I have called constitutional causes. These poisons and 
 toxins take the form of local disturbance, of innervation, poor 
 circulation and tissue metabolism. Generally the action of 
 poisons is to contaminate all the blood which circulates to the 
 remote organs. This general action of the poisons and toxins in 
 the blood is added to the local action of irritants. These poisons 
 act upon the nerve sheaths, decompose the blood but mainly 
 affect the vessel walls. They also tend to accumulate in certain 
 organs ^vithin which they frequently develop their chief action 
 and often cause remarkable tissue change. 
 
 The principal structures affected by these poisons are the 
 end organs, namely, the eye, the brain, the kidney recognized by 
 every physician, while the dental pulp and alveolar process, 
 which I have previously mentioned, are the most complete end 
 organs in the human body and usually first involved. Because 
 of the nature of their structures and surroundings, symptoms of 
 disease are observed in these structures long before the other 
 end organs are affected. 
 
118 
 
 INTERSTITIAL GINGIVITIS. 
 
 The dental pulp (as before stated) is the most complete end 
 organ for the reason that the blood enters the tooth by a single 
 artery. It then multiplies until the pulp is composed of myriads 
 of minute arteries confined within bony walls. The return blood 
 again passes through the apical end of the tooth by a single 
 vein. It is not uncommon, therefore, for the arteries, filled with 
 poisons, to expand and prevent the return to circulation, thus 
 causing numerous diseases and frequently spontaneous death of 
 the pulp. 
 
 The second most complete end organ is the alveolar process. 
 It is the only bony end organ in the human body. The arteries 
 
 o fr 
 
 Fig. 30. — Is Similar to Tig. 10. The Haversian Canal Shows a Dark Line 
 Around the Inner Border Representing the Arterial Wall. — The Space 
 Between the Dark Line and the Bone is Filled with Fibrous Tissue. 
 
 penetrate the bone in a wavy manner as far as the root of the 
 tooth, which, so far as the disease is concerned, is a foreign body, 
 when circulation ceases to any great extent. 
 
 The simplest illustration of the action of these poisons is 
 that of a healthy individual at the sixth period of stress or 
 about sixty years of age. This senile period, however, may take 
 place at a much earlier time in life. The excretory organs be- 
 come weakened and the poisons formerly excreted by the lungs, 
 kidneys, bowels and skin are not eliminated but circulate in the 
 blood. Odor from the breatli, skin faeces, an abnormal urinary 
 
INTEESTITIAL GINGIVITIS. 
 
 119 
 
 acidity degree, indican and other poisons in the urine indicate 
 these changes. These poisons are retained in the peripheral 
 organs but more especially in the dental pulp and alveolar proc- 
 ess. Those receiving the greatest quantity and retaining it are 
 the ones so constructed as to prevent a return of the irritants or 
 poisons to the circulation. 
 
 The irritants cause a dilatation of the vessels, first of the 
 arteries and then of the veins. This dilatation of the arteries 
 presses against the bony walls of the alveolar process which 
 sets up absorption. (Fig. 30.) Since the poison is a general one 
 
 Fig. 31. — Bone Absorption ky ILalisteresis: In the Middle Space the Bone is 
 Just Beginning to Absorb Around the Artery. — The Space to the Left 
 Shows a Large Portion of Bone Absorbed, Leaving the Fibrous Tissue in 
 Place; While the Two Spaces at the Right and Bottom of the Illustration 
 Show the Lime Salts and Fibrous Tissue Entirely Destroyed. 
 
 many arteries act in like manner. Chemical changes also take 
 place around the arteries which assist greatly in producing bone 
 absorption. Halisteresis is produced and the bone quickly dis- 
 appears. Sometimes, especially when only a small area is in- 
 volved lacunar absorption only occurs. The vessels of Von 
 Ebner (capillaries) being much smaller, the irritation is not so 
 intense nor is the effect of pressure or chemical changes upon 
 the surrounding bone so great. The area of absorption, there- 
 
120 INTERSTITIAL GINGIVITIS, 
 
 fore, is limited, resulting in small canals from one Haversian 
 canal to another or from one absorbed area by halisteresis to 
 another. The tissue around the artery now is not unlike the 
 soft tissue previously under consideration and the natural proc- 
 esses of inflannnation continue. In many patients the process of 
 inflammation stops with the absorption of bone. The tooth or 
 teeth now are simply attached to normal fibrous tissue. In many, 
 the inflammatory process proceeds a little further. There is 
 now acceleration of the blood stream which later slows consid- 
 erably. The central stream of corpuscles broadens and the outer 
 zone of plasma grows smaller and smaller. The same process 
 takes place in reference to leucocytes, red l)lood corpuscles and 
 exudate as before (Fig. 31) and if there is sufficient irritation 
 and infection, an abscess will form in the matrix or fibrous tissue 
 which originally contained bony tissue. It will be seen, there- 
 fore, that the rigid bony framework of tissue prevents great 
 vascular dilatation without bone absorption. It may, however, 
 be the seat of great pain, due to pressure of the confined exudate 
 upon nerve endings. 
 
 Local changes in function such as want of proper articula- 
 tion; too great pressure in mastication on one or more teeth: 
 slight change in position of teeth after they have once become 
 solid in the jaw; destroying pulps and filling roots so that the 
 peridental membrane is required to do more work ; hypertrophies 
 of roots ; teeth that have once been abscessed and were appar- 
 ently restored to health, etc., are a few of the local causes which 
 earlier set up inflammation in the alveolar process by the irri- 
 tants and poisons in the blood stream than in the normal adjoin- 
 ing teeth. 
 
 Local irritations such as wedging of teeth for filling; correct- 
 ing irregularities of the teeth, etc., which have already set up 
 local inflammation are fruitful sources and weak localities for 
 the irritations in the blood stream to quickly renew inflamma- 
 tion and destruction of the alveolar process. 
 
 One of the best illustrations of the eifect of poisons in the 
 blood acting upon weak abnormal structures in the jaw is that 
 of phosphorus poisoning. It is known that persons working in 
 phosphorus, such as match-making, are liable to phosphor ne- 
 
INTEESTITIAL GINGIVITIS. 121 
 
 crosis of the jaws. When it occurs, it is usually associated with 
 a carious or diseased tooth. It is supposed that the phosphorus 
 enters the jaw through or around the tooth. This, however, is 
 not the case. The poisons circulating in the air are taken into 
 the system through the lungs or if handled by the hands through 
 the skin. It thus enters the blood and causes a general disturb- 
 ance of nutrition. The blood vessels become charged with the 
 poison and the taking in of oxygen is considerably diminished. 
 In consequence, degeneration of tissues results. The red blood 
 corpuscles change their color and break down. The nervous sys- 
 tem, especially the peripheral nerves degenerate. The arteries 
 in the alveolar process are the first to become diseased. The 
 parts of the jaw which first feel the effect of the poison are those 
 parts where the teeth have lost their normal function, more 
 particularly teeth with dead pulps whose roots may or may not 
 be filled, with or without slight inflammation, teeth which have 
 abscessed or been wedged or are doing more work than normal. 
 
 When absorption has taken place, the bone is not restored 
 after the person has obtained his growth, the transitory nature 
 of the process and only two sets of teeth being natural to man. 
 If the process be removed from any cause (even if the perma- 
 nent teeth be still in the jaw) it is not restored. 
 
 The absorption of the alveolar process, under constitutional 
 causes, usually begins at the gingival border because of its thin- 
 ness of structure. The gum tissue does not change but follows 
 the bone, in its absorption, until the tooth is exfoliated or until, 
 under treatment, the alveolar process is restored to health, when 
 the gum attaches itself firmly to the bone and is restored to its 
 normal condition. 
 
 We have shown the simple process of inflammation to the for- 
 mation of abscess and the absorption of bone in relation thereto 
 in the milder forms due to traumatism, toxins and poisons, but 
 the procedure under severe constitutional conditions is much 
 more intense. 
 
 The transitoiy nature of the alveolar process, its sensitive- 
 ness as an end organ, when inflammation is once set up in the 
 gums, alveolar process or peridental membrane, due to either 
 local or constitutional causes, compels it to become chronic with 
 
122 INTERSTITIAL GINGIVITIS. 
 
 disastrous results which are difficult of treatment and of restora- 
 tion to health, especially if the vitality of the patient is low. 
 This inflammatory process is along the line of least resistance. 
 
 THE NERVOUS SYSTEM IN INFLAMMATION. 
 
 There is much discussion by certain writers in regard to the 
 action the nervous system plays in inflammation. Some take 
 the stand that the central nervous system does act upon the 
 blood vessels in a given locality while others claim that it must 
 be a peripheral nervous mechanism which controls the blood ves- 
 sels. Experiments have shown that the vascular changes con- 
 nected with inflammation can occur independently of the central 
 nervous system. It follows then that there may be a peripheral 
 nervous mechanism controlling the vessels. 
 
 It has been demonstrated by Klebs ^ that the endothelial walls 
 of the capillaries do contract. The conclusion then is that the 
 endothelium of the capillaries is, to some extent, self regulating. 
 It is quite possible that the muscular coats of the smaller ar- 
 teries and capillaries act to stimuli. 
 
 Thoma - says, ''It is evident, however, that the local circula- 
 tory reaction after injury depends upon the condition of the 
 cerebro-spinal vasomotor centers and that the peripheral vaso- 
 motor nerve apparatus may also act independently. From what 
 has been said it appears that among the direct action of trau- 
 matism, injury to the nerves is of great importance. This injury 
 to the nerves at the site of the lesion is either a change in the 
 invisible molecular structure of the nerve fibers, or one which 
 can be recognized under the microscope. Each change in the 
 molecular structure of the nerve causes a change in its excitabil- 
 ity which is termed,' nerve irritation' by physiologists. This irri- 
 tation is frequently more or less painful, and is perceived sub- 
 jectively as pain. The disturbance of the innervation of the 
 vessel wall, however, is to be clearly distinguished from the sen- 
 sation of pain. The former also is partly caused by the direct 
 action of the injury to the vasomotor nerv apparatus contained 
 
 1 Klebs. AUg. Pathologie. 
 
 " Thoma. Pathology and Pathological Anatomy. 
 
THE NERVOUS SYSTEM IX IXFLAMMATIOX, 123 
 
 in the injured area. The distnrbance of vasomotor innervation, 
 however, is seldom strictly limited to the area directly affected 
 by the injury, since the nerve irritation both directly and re- 
 flexly alters the excitability of the vasomotor centers in the walls 
 of the neighboring arteries, and thus causes the local circulators- 
 reaction. ' ' 
 
 My researches have shown that the nerve supply in the alveo- 
 lar process, as compared with that in the peridental membrane 
 and periosteum is very slight. Inflanunation and infection, 
 therefore, taking place in the peridental membrane at the apical 
 end of the tooth root forming alveolar abscess or at the side 
 nearest to the apical end where peridental abscess forms, where 
 the alveolar wall is quite thick, pain is much more severe than 
 when the abscess forms in or near the gingival margin of the 
 process. On account of local and constitutional irritations, 
 nerve end degeneration in alveolar absorption is the rule. Pain, 
 however, in this instance is not as severe in abscess formation in 
 the alveolar process as in other bones. 
 
 These local and constitutional irritations produce paralysis 
 and finally death of the nerve fiber. When degeneration or death 
 of the nerve fiber takes place, the action upon the coats of the 
 arteries is such that inflammation and absorption of the alveolar 
 process ensues. 
 
 The local irritations and infections produce the same effect 
 upon tissue in inflammation as the internal (constitutional) irri- 
 tations and infections. Adami •' says, ''Anything which causes 
 local injury to the tissue is a cause of inflammation, be it a me- 
 chanical trauma, a physical insult, as by heat, cold or electricity, 
 a disturbance brought about by altered metabolism and abnor- 
 mal internal secretions, or bacterial or microbic invasion and 
 growth. This last is the commonest cause of acute reaction and 
 differs from the physical and mechanical causes (although not 
 from metabolic disturbances) in that, as a cause, it is not of 
 momentary duration, but of continued. It is not the mere physi- 
 cal entry of microbes into the tissues that induces inflammation 
 but the liberation of them of their products in growth or disin- 
 tegration. And so long as those products are being liberated. 
 
 ■ Adami. Principles of Pathology, Vol. I, page 420. 
 
124 INTERSTITIAL GINGIVITIS. 
 
 for SO long is the cause of action. It differs from the metabolic 
 causes in that the latter induce tissue irritation of a milder grade 
 and do not induce acute, but rather chronic reaction." 
 
 Kirk'' says, "Viewed as an inflammatory process we have, 
 then, in the study of pyorrhoia (interstitial gingivitis) to regard 
 its clinical or objective phenomena as reactions of the retentive 
 tissues of the teeth toward injuries inflicted by mechanical 
 trauma, physical irritants, altered metabolism, the toxic effects 
 of altered secretions, or by the toxic products of microbic or 
 bacterial invasion. Any of these agencies, severally or collec- 
 tively, ma}^ induce such changes in the retentive structures as 
 will lead to their molecular necrosis and the ultimate exfoliation 
 of the teeth, the process constituting comprehensively what we 
 know as pyorrhoea alveolaris (interstitial gingivitis)." 
 
 The process of inflammation from local irritation and infec- 
 tion proceeds in the same manner as the traumatism upon the 
 web of the frog's foot. 
 
 Patients who have been ill for any length of time, such as 
 those suffering with phthisis, lues, kidney lesions or other linger- 
 ing diseases, and those with low vitality, take on interstitial gin- 
 givitis much more readily than those of strong vitality. 
 
 Summing up this chapter, no matter whether the irritation 
 be local or constitutional or both, the inflammation set up thereby 
 is progressive in its nature and does not cease until the tooth 
 or teeth have been exfoliated by the absorption of the alveolar 
 process, although treatment, changes in environment and sys- 
 temic conditions may check the disease for a limited time. The 
 inflammation is solely the cause of bone absorption and may be 
 slow or rapid in its action. 
 
 * American Text-Book of Operative Dentistry, Fourth Edition, page 470. 
 
CHAPTER XIV. 
 
 RESEARCHES OX AXIMALS IX IXTERSTITIAL GIXGIVITIS. 
 
 All vertebrates possessing two sets of teeth during life 
 the roots of which are situated in bony sockets have interstitial 
 gingivitis to a greater or lesser extent. The mere fact of 
 the eruption and shedding of the teeth, as in human, is an 
 indication that there is an inflammatory process present. Wild 
 animals leading a natural, normal hfe are less liable to have 
 this disease than those having become domesticated. Wild 
 animals domesticated and tamed animals taken out of their 
 natural environment suffer with this disease to as marked a 
 degrees as human. While it is true animals, as a rule, do not 
 suffer with the nervous types of disease like human, yet a wild 
 animal in confinement with artificial feeding must suffer, to 
 a greater or lesser extent, according to the nature of the change 
 and the amount of restlessness produced. Changes in vital 
 resistance are not as frequent or as marked in animals as in 
 human, yet wild as well as domesticated animals do occasion- 
 ally suffer with disease and changes in vital resistance. 
 
 Wild animals roaming at large and obtaining their food 
 are in a much more natural environment than when in captiv- 
 ity. The organs of the body are performing their natural 
 functions, and thus elimination is carried on normally. Old 
 age, even in animals living in their natural wild environment, 
 predisposes weakened eliminating organs, wdiile these, in turn, 
 owing to poisons in the blood, will cause interstitial gingivitis 
 and finally loss of teeth. 
 
 Wild animals under domestication OA\^ng to change of emd- 
 ronment can best be studied in relation to this disease. A visit 
 to the great Zoological Gardens in Dublin, London, Hamburg, 
 Paris, New York City or Chicago, and a careful study of the 
 mouths and jaws of the animals there confined will readily 
 convince the investigator of the truth of these statements. 
 Monkeys are probably more susceptible to disease and death 
 
126 
 
 INTERSTITIAL GINGIVITIS. 
 
 than most animals. Cows fed upon brewers' slop and con- 
 fined indoors have interstitial gingivitis badly; horses which 
 have been biting grass with their front teeth, living in the sun- 
 shine and breathing the fresh air, when returned to the stable in 
 the Fall begin to ''crib," biting the woodwork around the 
 stall. The front teeth feel uncomfortable because of the entire 
 change of environment. The "cribbing" causes the blood to 
 be forced out of the capillaries of the peridental membrane, 
 and for the time being gives relief to the animal. It soon 
 returns and because of the pain the process is repeated. In 
 the course of a week or two, however, the eliminating organs 
 adjust themselves to the new environment and the teeth remain 
 comfortable. House animals are very prone to interstitial 
 gingivitis as well as to other constitutional diseases. In most 
 animals of this kind they are taken out of their natural envi- 
 ronment, and autointoxication and disease is the rule. The 
 carnivora suffer with pyorrhoea alveolaris to a more marked 
 extent than the herbivora owing to the fact that they subsist 
 to a great degree upon pus-ladened nitrogenous food, thus 
 infecting the gums and peridental membrane. Dogs with this 
 disease are the best animals for research. 
 
 As the first step in investigation, two practitioners of 
 comparative medicine, with an extensive hospital practice 
 (Dr. Charles E. Sayre and Dr. Alsop E. Flower), were con- 
 sulted as to the frequency of this disease in animals. All 
 animals under their care suffered from it more or less, but 
 eighty per cent of dogs over eight years of age had the dis- 
 ease. Nearly every dog in the hospital under their care was 
 so affected. These dogs comprised all breeds, from spaniels 
 and terriers to the Newfoundland, St. Bernard and great Dane. 
 On examination, every phase of interstitial gingivitis was found 
 in the mouths of these dogs, from its inception to the loss of 
 the teeth. The number of dogs observed was twenty-seven. 
 The roots of the teeth of some were covered with deposits 
 and so exposed that the teeth could be removed with the fin- 
 gers. Such diseased mouths are rarely, if ever, present in 
 human beings. The outer plate of bone was absorbed, the roots 
 entirely exposed, pus was oozing from around them and the 
 mucous membrane was badly inflamed. 
 
EESEAECHES ON ANIMALS IN INTERSTITIAL GINGIVITIS. 127 
 
 It should be remembered tliat the jaw of the dog, like the 
 jaw of man, is undergoing considerable variation. Like man, 
 the dog, having put liimself under new social conditions (so 
 to speak), is varying greatly both as to brain, skull and jaw 
 from his wolf-like ancestor. As he is under the protection of 
 man, the struggle for existence as to food is less intense than 
 
 F:g. 32. — The Mouth of a Scotch Terrier, Some of the Teeth Have Been Re- 
 moved ON Account of Interstitial Gingivitis. 
 
 in the wild state and consequently there is less occasion, even 
 for fighting purposes, of his jaws and teeth. 
 
 Independently of conditions of this type, many of the dogs 
 suffered from constitutional disorders. Eight had skin dis- 
 eases which in the dog are more likely to produce obvious con- 
 
128 
 
 INTERSTITIAL GINGIVITIS. 
 
 stitutional defects than in man. Some were old and blind. 
 Some had been injured and were under treatment for wounds. 
 Some were suffering from rachitis, nervous diseases, and were 
 overbred. Others were constipated or had germ types of diar- 
 rhoea. One had kidney inflammation and bronchitis with high 
 
 Fig. 33. — The Mouth of a Boston Terrier; Owing to Illness Interstitial Gingi- 
 vitis HAS Caused Absorption of Bone and the Incisors and Molar were 
 Removed by the Fingers. 
 
 fever. In short, these dogs, being house dogs, presented most 
 of the constitutional diseases to which man is liable. 
 
 The mouth of a Scotch terrier is shown in Fig. 32. The 
 molar and premolar had been removed with the fingers. The 
 cuspids and incisors are quite loose. There are large deposits 
 
KESEAECHES ON ANIMALS IN INTERSTITIAL GINGIVITIS. 
 
 129 
 
 of tartar. The gum and alveolar process have been absorbed 
 nearly one-half the length of the roots of the teeth. In Fig. 33 
 is seen the mouth of a Boston terrier with the incisors . and 
 premolars removed. There is extensive pyorrhoea. There are 
 calcic deposits upon the cuspids and molars. There is recession 
 of the gums and alveolar process. In Fig. 34 is shown the mouth 
 
 Fig. 34. — The Mouth or Another Boston Terrier; One Tooth has been Re- 
 moved AND Interstitial Gingivitis is Seen Around the Other Teeth. 
 
 of another Boston terrier. In it one premolar in the upper and 
 one on the lower jaw have been extracted. There is extensive 
 inflammation of the gum about the molar, cuspid and incisor 
 with large calcic ileposits about the teeth. In Fig. 35 are shown 
 teeth covered with calcic deposit the entire length of the root. 
 
130 INTERSTITIAL GINGIVITIS. 
 
 These teeth were removed by the fingers from the mouths of two 
 dogs, one of which was later obtained for scientific study. This 
 was all the material to be obtained from the hospital, since the 
 dogs were pets which had been placed under treatment by their 
 owners. 
 
 Through the courtesy of Poundmaster Hugh Curran, the 
 necessary material was obtained from the Chicago Dog Pound. 
 Here from four hundred to a thousand dogs are killed per week 
 during June, July and August each year. Ninety-five per cent 
 are mongrel curs leading a street life, hence neither luxurious 
 diet nor luxurious care can be charged with any disease in 
 them. They have, at least, i)lenty of outdoor exercise and fresh 
 air. Many, despite this reversion to the life of their wolflike 
 ancestors, have skin diseases and are deaf and blind from old 
 age. The bodies were secured after death, at which time exam- 
 
 Fjg. 35. — Shows Teeth of a Dog Covered -with Cah!K' Deposits which were Quite 
 Loose and were Eemoved by the Fingers. 
 
 inations of the mouths were made. Five per cent of the dogs 
 entering the pound are of good breeds. These, if not called for 
 by the owners, are sold for a moderate price. 
 
 The dogs selected for the death penalty are collected in a 
 large box pen, leading out of which is a door through which they 
 pass into an air-tight box. Communicating with this box is a 
 stove in which sulphur is burned with charcoal. The fumes 
 pass into the box and death is almost instantaneous and painless. 
 After they remain fifteen minutes, a door leading to the air is 
 opened and the bodies are carted away. It was at this time that 
 access was had to them. The mouths were then examined. Such 
 cases as were of interest were placed on one side and the jaws 
 removed from the bodies. Inside of one-half hour the specimens 
 were in a solution to be kept until desired for use. Jaws (with 
 interstitial gingivitis in all stages of progress, from simple in- 
 
EESEARCHES OX ANIMALS IX INTERSTITIAL GIXGIVITIS. 131 
 
 Haiiimation of the g-iims to the most extreme cases of exfoliation 
 of the teeth) were obtained in an abundance for future studies. 
 It is not an easy matter to ascertain the ages of these animals. 
 In a general way, it was found that inflammation of the gums, 
 especially about the canine teeth, was almost always present in 
 dogs over one year. About twenty five per cent of these dogs at 
 four years of age had the disease, eighty per cent at from eight 
 to ten years, ninety-five per cent over twelve years of age. 
 Since I commenced my investigation (twenty years ago), I have 
 examined quite a large number of dogs about homes, but have 
 never found a dog" over four years without this disease to a 
 greater or less extent. Many house dogs at one year had inflam- 
 mation of the gums. Dogs for infection and those used for mer- 
 curialization were picked up in the streets. 
 
 Most of the dogs exhibited at dog shows are young, ranging 
 from one to four years of age. About twenty-five per cent would 
 range four years to eight. A casual examination of their mouths 
 revealed interstitial gingivitis. Occasionally recession of the 
 gums and pyorrlioea alveolaris occurred. On a more careful ex- 
 amination, twenty-five per cent of dogs between the ages of one 
 and four were found to have interstitial gingivitis and seventy- 
 five per cent of dogs from four to eight years were found to 
 have interstitial gingivitis with recession of the gums and pyor- 
 rhoea alveolaris. In the study of this disease, therefore, dogs 
 are excellent substitutes, since for pathologic research they can 
 be obtained at any stage of the disease. 
 
 The technique of the examinations of interstitial gingivitis 
 and pyorrhoea alveolaris in dogs was as follows: After fixing 
 and hardening in two per cent formalin, alcohol, or Muller's 
 fluid, the tissues were decalcified in a five per cent alcoholic solu- 
 tion of nitric acid, imbedded in celluloidin and stained in various 
 Avays, the principal ones being hgematoxylin and eosin. Ten or 
 more slides would be obtained from each tooth. Out of these 
 slides have been selected a series illustrating the progress of the 
 disease from beginning to the loosening of the tooth. 
 
 Fig. 36 is a longitudinal section of a cuspid tooth A\ith the 
 alveolar process in situ. A illustrates the enamel of the tooth, 
 (E) the epithelium passes from the outer margin to the lower 
 
X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 
 
 Fig. 36. — Longitudinal Section of Tooth and Gum Tissue. Slight Gingivitis. Dog. 
 
 A, Enamel. E, Epithelial Tissue. G, Submucous ■Membrane. M, Filirous Tissue. 
 SI, Slight Inflammation. 
 
X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 
 
 Fig. 37. — Longitudinal Section op Tooth and Gum Tissue. Chronic Interstitial 
 
 Gingivitis. Dog. 
 
 A. Enamel. E. Epithelial Tissue. G, Submucous Membrane. H. Periosteum. 
 K, Capillaries. 'V'. ^'folent Inflammation. AA, Point of I''^nion of Epithelial Tissue 
 and Peridental Membrane. ER, Space Pocket from want of Union of Epithelial Fold. 
 
X 75. A. A. obj. Zeiss. Micro-photogTaph, reduced one-third. 
 
 Pig. 38. — Longitudinal Section of Alveolar Process and Peridental Membrane. 
 Slight Interstitial Gingivitis, Extending into Alveolar Process. Dog. 
 
 J, Alveolar Process. U, Inflammation Extending through Enlarged Haversian Canals. 
 I^, Inflamed Peridental Membrane. 
 
X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 
 
 Fig. 39. — Loxgitudinal'Gection of Alveolae Process and Peridental Membrane. 
 Chronic Interstitial Gingivitis, Extending into Alveolar Process. Dog. 
 
 H, Periosteum. J, Alveolar Process. V, Violent Inflammation. AA, Point of 
 Union of Epithelial Tissue and Peridental Membrane. 1\ Inflamed Peridental Mem- 
 brane. L^, Inflammation Extending through Enlarged Haversian Canals. 
 
136 INTERSTITIAL GINGIVITIS. 
 
 border, then folds upon itself and extends down tlie side of the 
 crown of the tooth as far as the neck. Unfortunately, in this 
 specimen, the structure connecting the epithelium and the fibrous 
 tissue of the periosteum has been destroyed. The papillary layer 
 of the sub-epithelial tissue is plainly shown at the outer border. 
 Small round-cell inflammation may be seen extending along the 
 border of this layer. It can also be observed extending do\vn 
 the capillary blood vessels into the submucous tissue (SI and Gr). 
 
 Fig. 37 shows a similar section of another tooth. Here the 
 epithelial structure (E) is pulled away slightly from the edge of 
 enamel (A). In this section the infolding of the epithelium is 
 shown at the neck of the tooth. This structure passes dow^nward, 
 folds outward and upon itself (AA) and returns two-thirds of 
 the distance toward the gingival border, leaving a pocket (RR). 
 The epithelium (E) is very dense and thick. The papillary 
 layer of the submucous tissue (G) is very clearly defined. The 
 capillaries (K) can be distinctly traced from the deeper fibrous 
 tissue through the submucous layer into the papillary layer. 
 The thick and heavy fibrous tissue of the periosteum ("Dental 
 Ligament," Black) may be seen at H, inserted firmly into the 
 cementum and extending outward and downward. Just below 
 (A A) may be seen the interlacing of the coarser fibers of the 
 periosteum with the finer fibers of the submucous tissue. Chronic 
 round-cell inflammation may be seen extending from the papil- 
 lary layer through the capillaries into the interstitial tissue of 
 the subnuicous layer and the periosteum. Marked inflammation 
 has occurred at V. The openings in the folds of the epithelium 
 are fruitful sources for the accumulation of food, epithelial 
 scales and detritus, in which fermentation and decomposition 
 from micro-organisms result, producing inflammation. 
 
 Fig. 38 is a section through the peridental membrane (I) and 
 alveolar process (J) at the lateral incisor. The inflammation 
 has extended down from the papillary layer through the sub- 
 mucous tissue, the fibrous tissue of the periosteum into the peri- 
 dental membrane and into the alveolar process. Round-cell in- 
 flammation may be seen in the blood vessels extending through 
 the Haversian canals (L^). 
 
 Fig. 39 is a similar section from another tooth showing 
 
KESEARCHES ON ANIMALS IN INTERSTITIAL GINGIVITIS. 137 
 
 chronic inflammation extending throughout the peridental mem- 
 brane (I) and alveolar process (J). The Haversian canals (L) 
 are well outlined by the inflammatory progress. Marked inflam- 
 mation has resulted at V and also at the margin of the alveolar 
 process. 
 
 Fig. 40 is a section of the peridental membrane and alveolar 
 process, illustrating the effect of interstitial inflammation upon 
 the blood vessels and alveolar process. Chronic inflammation 
 extends throughout the peridental membrane with very decided 
 inflammatory change (V). The cut ends of the blood vessels 
 which were originally situated in the Haversian canals are seen 
 (BV). They have become involved with the result of a thicken- 
 ing of the walls and endarteritis obliterans. The bone about 
 these vessels has been entirely absorbed. The inflammation 
 has extended beyond, into and througli the Haversian canals, 
 producing the type of absorption of the trabeculae known as 
 halisteresis ossium. Lacunar absorption has also occurred (0). 
 Where decided inflammation (V) has taken place, abscesses are 
 more liable to occur (as will be noticed later) from the large 
 number of blood vessels at this locality. 
 
 Fig. 41 is a section from another location of the alveolar 
 process with a greater amplification, showing the inflammatory 
 process extending through the alveolar process. Endarteritis 
 obliterans may be seen in different locaUties (EO) . Three forms 
 of absorption are evident in this figure : Enlarged areas arising 
 from absorption of the trabeculae (halisteresis ossium) due to the 
 inflammatory process. The vessels of Von Ebner precede per- 
 forating canal absorption (BB), distributed over the entire field, 
 also the result of the inflammatory process and lacunar absorp- 
 tion (0) which may result from inflammation. As long as the 
 fibrous tissue remains in these large areas to retain the osteo- 
 blasts, new bone tissue may be produced under favorable condi- 
 tions. On the other hand, when this tissue and the osteoblasts 
 are destroyed, the alveolar process cannot be restored. 
 
 Fig. 42 shows a section of the alveolar process from another 
 dog. Here lacunar and other absorption (halisteresis ossium) 
 are well shown.' Thirty-seven osteoclasts (0) may be counted in 
 the field while destruction of bone by halisteresis (Q) is rapidly 
 
138 INTERSTITIAL GINGIVITIS. 
 
 going on. Remains of Haversian canals with the blood vessels 
 may be seen (BV, L). In the discussion of the peridental mem- 
 brane extending into the alveolar process (page 37), particular 
 attention was called to the fact that large bundles of fibers ex- 
 tended into the process in such a manner as almost to isolate 
 portions of bone. In the lower left-hand corner (X) may be 
 seen two pieces of the alveolar process entirely separated from 
 each other and the main body of the bone. In interstitial gingi- 
 vitis, it is not uncommon to find pieces of the alveolar process 
 separated by halisteresis and lacunar absorption. When loose 
 teeth are extracted as a result of this disease, pieces of the alveo- 
 lar process come away with the peridental membrane attached to 
 the tooth. Fig. 89 was obtained in this manner. In the upper 
 left-hand corner may be seen eight or ten new osteoclasts (0) 
 in an enlarged Haversian canal, at work isolating one piece of 
 the alveolar process from the other. 
 
 Fig. 43 shows a slide from still another dog. Halisteresis 
 (Q) and perforating canal (P) absorption are here well shown. 
 In the larger space at the lower left-hand corner may be seen 
 two arteries (EO) which w^ere originally the location of Haver- 
 sian canals and which have thickened walls and a tendency to 
 obliteration. The light color shows decalcification, the dark nor- 
 mal bone. At P may be seen perforating canal absorption. At 
 FG fat globules may be seen, while in the larger space at the 
 upper right-hand corner is evident entire destruction of the 
 fibrous tissue. 
 
 Fig. 44 illustrates a cross section of alveolar process and 
 cuspid root, showing absorption of the root. Inflammation 
 extends throughout the peridental membrane (I). The capil- 
 laries (K) are quite numerous. These are cut both crosswise 
 and lengthwise. Absorption (S) of the root may be seen pro- 
 gressing at these localities. 
 
 Fig. 45 shows a longitudinal section of the end of the root. 
 Active destruction has been going on both in the pulp chamber 
 (D) and at the external surface of the cementum (C). The irri- 
 tation and inflammation has caused the odontoblasts to "fill up 
 the pulp chamber with secondary dentine, and obliteration of the 
 chamber has taken placo. Below the constricted pulp may be 
 
X 75. A. A. obj. Zeiss. Micro-photograph, reduce. 1 oue-thint. 
 
 Fig. 40. — LoxGiTUDixAL Section of Tooth, Alveolar Process and Peridental Mem- 
 brane. VlOfcENT EOUND-CeLL INFLAMMATION OF PERIDENTAL MEMBRANE, EX- 
 TENDING THROUGH THE HAVERSIAN CaNALS INTO THE ALVEOLAR PROCESS. 
 
 C, Cementum. J, Alveolar Process. K, Capillaries. L, Haversian Canals. N, Large 
 Spaces arising frohi Absorption of the Trabeculae, starting in the Haversian Caj-als 
 (Halistere«;is). O, Lacunar Absorption. V, Violent Intlamnitttion. BV, Blood 
 Vessels, originally Haversian Canals. I^, Inflamed Peridental Membrane. L^, Inflam- 
 mation Extending through Enlarged Haversian Canals. 
 
X 150. D. U. obj. Zeiss. Micro-photograph, reduced one-third. 
 Fig. 41. — Longitudinal Section of Alveolar Process. Chronic Inflammation Ex> 
 
 TENDING throughout, SHOWING HALISTERESIS, PERFORATING CANAL AND LACUNAR 
 
 Absorption. Dog. 
 
 J, Alveolar Process. N, Large Spaces arising from Absorption of the Trabeculae, 
 starting in the Haversian Canals (Halisteresis). O, Lacunar Absorption. P, Perforat- 
 ing Canal Absorption. BB, Blood Vessels of V. Ebner preceding Perforating Canals. 
 EO, Endarteritis Obliterans. 
 
X 75. A. A. obj. Zeiss. Micro-photograph, rciliiced one-third. 
 
 Fig. 42. — Longitudinal Section of Alveolar Process. Chronic Inflammation Ex- 
 tending THROUGHOrT, SHOWING HaLISTERESIS AND LACUNAR ABSORPTION. DOG. 
 
 J, Alveolar Process. L, Haversian Canals. N, Large Spaces arising from Ab- 
 sorption of the Trabecular, starting in the Haversian Canals. 0, Lacunar Absorption. 
 Q, Halisteresis Ossium or Decalcified Bone. X, Remains of Calcified Bone. BV, Blood 
 Vessels originally Haversian Canals. 
 
X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 
 
 Fig. 43. — Transverse Section, Alveolar Process. Chronic Inflammation Ex- 
 tending THROUGHOUT. DOG. 
 
 J, Alveolar Process. N, Large Spaces arising from Absorption of the Trabeculse, 
 starting in the Haversian Canals. P, Perforating Canal Absorption. Q, Halisteresis 
 Ossium or Decalcified Bone. X, Eemains of Calcified Bones. EO, Endarteritis Obli- 
 terans. FG, Fat Globules. 
 
X 75. A. A. obj. Zeiss. Micro-phot ograpli, reduced one-third. 
 
 Fig. 44. — Cross Section of Tooth, Alveolar Process and Peridental Membrane. 
 Chronic lNFLA*fMATioN of Peridental Membrane and Absorption op the 
 Eoot of Tooth. Dog. 
 
 B, Dentine. C, Cementuni. D, Pulp. I\ Inflamed Peridental Membrane. K, Capil- 
 laries. S, Eoot-absorption. 
 

 i 
 
 
 ^■a: 
 
 ■'.'- i': .A. 
 
 
 /. "^'.^ 
 
 X 75. A. A. obj. Zeiss. Micro-photograph, rediieed one-third. 
 Fjg. 45.— Lokgitudinal Section of the End of the Root of a Tooth Alveolar 
 Process and Peridental Membrane, Showing Chronic InflammaSon op the 
 iB^OR^i Dog'""'- '''''™"'' °' '^"^ '''''' °^ ™^ tooth ANrL^JuN^R 
 
 C, Cementum. D Pulp, with 3 Poramina. J, Alveolar Process. O, Lacunar Absorp- 
 tion. P, Perforating Canal Absorption. CC, Cementosis. 
 
X 75. A, A. obj. Zeiss. Micro-photograph, reduced one-third. 
 
 Fig. 46. — Cross Section of Inflamed Peridental Membrane. Dog. 
 
 II, Inflamed Peridental Membrane. W, Epithelial Debris. 
 
X 15. 75 M. M. obj. Spencer. Micro- j)hotograpb, reduced one-third. 
 
 Fig. 47. — Longitudinal Section of Tooth, Alveolar Process, Peridental Mem- 
 brane, Showing Interstitial Gingivitis and Pyorrhoea Alveolaris, with 
 Tooth About to be Exfoliated. Dog. 
 
 C, Cementnm. E, Epithelial Tissue. H, Periosteum. I, Peridental Membrane. 
 J, Alveolar Process. K, Capillaries. L, Haversian Canals. M, Fibrous Tissue. R, 
 Pus Pockets. U, Nerve Tissue. V, Violent Inflammation. AA, Point of Union of 
 Epithelial Tissue and Peridental Membrane. GO, Cementosis. DD, Calcific Deposits 
 Destroyed by Acids. 
 
X 40. 35 M. M. o])j. Zeiss, ^licro-photograph. reduced one-third. 
 
 Fig. 48. — Longitudinal Section of Tooth, Alveolar Process, Peridental Mem- 
 brane AND Gum Tissue, Enlarged from Fig. 42, Showing Active Inflamma- 
 tion, with Pus Pocket. Dog. 
 
 0, Cementiim. E, Epithelial Tissue. G, Submucous Membrane. I^, Inflamed 
 Peridental ^Membrane. J, Alveolar Process. L^, Inflammation Extending^ through En- 
 larged Haversian Canals. M\ Inflamed Fibrous Tissue. R. Pus Pocket. V, Violent 
 Inflammation. AA, Point of Union of Epithelial Tissue and Peridental Membrane. 
 FF, Food Containing Micro-Organisms. 
 
X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 
 
 Fig. 49. — Longitudinal Section of Tooth, Alveolar Process, Peridental Mem- 
 brane AND Gum Tissue, Enlarged from Fig. 42, Showing Active Inflamma- 
 tion WITH Pus Pocket. Dog. 
 
 C, Cementuni. E, Epithelial Tissue. J, Alveolar Process. M^, Inflamed Fibrous 
 Tissue. E, Pus Pocket. V, Violent Inflammation. 
 
KESEARCHES ON ANIMALS IN INTERSTITIAL GINGIVITIS. 149 
 
 seen three divisions of the pnlp (D) extending through three 
 separate canals in the cementum (C). Cementosis (CC) may 
 be seen at the end of the root. Lacunar absorption is going on 
 (0). Thus results a building up and tearing down of the same 
 tissue from the same cause, interstitial gingivitis. 
 
 Fig. 46 shows inflammation of the peridental membrane {V) 
 with epithelial debris (W) scattered throughout the field. 
 
 Fig. 47 is a section through the jaw and incisor tooth, show- 
 ing the relation of the structures to each other in a severe case of 
 interstitial gingivitis and pyorrhoea alveolaris. The tooth is at- 
 tached at only a very small portion of the apical end of the root. 
 The disease has been of long standing. Absorption of the alveo- 
 lar process on one side has progressed on fully one-half of the 
 root, while upon the other about one-third the distance. Inflam- 
 mation commenced at the gingival border and extended through 
 the periosteum (H). peridental membrane (I) and alveolar proc- 
 ess (J). Marked inflammation (V) has occurred in the mucous 
 membrane fold. An abscess has formed with a fistula extending 
 to the gingival border. The thin border at the left of the fis- 
 tulous tract is the epithelium layer next to the tooth. It is evi- 
 dent that the pus burrowed to the surface through the struc- 
 ture instead of between the epithelium and the tooth. A similar 
 abscess and fistulous tract are evident upon the gingival border 
 on the opposite side of the tooth. The irritation produced by 
 the movement of the tooth has caused the cementoblasts to de- 
 posit large quantities of material upon the sides and the end of 
 the root. The main nerve trunks (U) may be seen at and below 
 the end of the root. 
 
 Fig. 48 illustrates the alveolar border on the right side of 
 Fig. 45, greatly amplified. This shows the progress of intersti- 
 tial gingivitis extending through the alveolar process producing 
 absorption with intense inflammation of the peridental mem- 
 brane and abscess with fistulous tract. 
 
 Fig. 49 shows a similar process amplified from the left side of 
 Fig. 47. It is interesting to note in this illustration that the 
 fibers of the sub-epithelium pass down and become interwoven 
 with the coarser fibers of the periosteum in just the opposite 
 direction from those in the other side of the tooth, and in other 
 
150 
 
 INTERSTITIAL GINGIVITIS. 
 
 illustrations. The fibers from the inncoiis membrane along the 
 side of the tooth extend down and into the peridental membrane 
 without a break in the structure. The arrangement of the fibers 
 of the submucous layer in producing the fold is well illustrated 
 in the figure. This picture illustrates inflammation starting in 
 the gingival border. 
 
 MERCURIAL INTERSTITIAL GINGIVITIS IN DOGS. 
 
 To secure a chain of evidence that interstitial gingivitis (due 
 to the metals, drugs, uric, lactic and other acids) commenced in 
 
 Proj. 1/4 inch, ocular lY^ inch. Spencer. 
 
 Fig. 50. — Longitudinal Section of Gingival Border, Showing Eound-Cell. 
 Inflammation Due to Mercurial Poisoning. 
 
 the papillary layer of the sub-epithelial, mucous membrane, I 
 instituted a series of experiments in mercurialization of dogs. 
 Dogs for the purpose were picked up in the streets. Some 
 of these were operated upon l)y myself, but most of them were 
 under treatment at the Post-Graduate Medical School. Care 
 
MERCURIAL INTERSTITIAL GINGIVITIS IN DOGS. 
 
 151 
 
 was taken to secure those in health and with healthy gums. 
 Mercury was introduced by the mouth, skin and hypodermic 
 injection. It was no easy matter to get them under influence 
 of the drug, since the power of the glands to eliminate the poison 
 was enormous. In no case was salivation produced. The first 
 symptom noticed was exhilaration, which would last from three 
 days to a w^eek. Then paralysis agitans would continue until 
 death. In about a week the appetite would commence to fail 
 and it was difficult to get the dogs to take food of any kind. 
 The kidneys and bowels eliminated the i)oison. There was a 
 
 •# .y 
 
 JBL. 
 
 Pantaclir. oil imin. 1/12 inch ocular. No. 3. Leitz. 
 
 Fjg. 51. — Longitudinal Section of Gingival Border. Higher Magnification, 
 Showing Connective Tissue Infiltration with Plasma Cells and Polynu- 
 clear Leucocytes. Dog. 
 
 rise in temperature. Some of the dogs died before gingivitis 
 was observed. This demonstrated that not only does the nervous 
 system become involved, but the organs of the body may be 
 morbidly affected and death ensue before the gums show symp- 
 toms of disease. Some dogs were killed after the gums became 
 
152 
 
 INTERSTITIAL GINGIVITIS. 
 
 diseased. The time required to obtain results was from three to 
 eight weeks. The age and physical condition of the dog caused 
 this variation in time. After death the gum tissue was dissected 
 from different parts of the jaws and placed in either fifty per 
 cent alcohol, Muller's fluid, or two per cent formaliu. 
 
 Sections of tissue from the gum margin and sides were made 
 on a number of places. Some were imbedded in paraffin, others 
 in celluloidin. The sections were stained according to various 
 
 Pautachr. oil imm. 1/12 inch ocular. No. 3. Lcitz. 
 
 Fig. 52. — Longitudinal Section of Gingival Border. Higher Magnification, 
 Showing Round-Cell Inflammation Extending to the Inner Coat of the 
 Blood Vessel and also Plasma-mast Cells. 
 
 methods: Delafield's haematoxylin, eosin (Unna's), alkalin 
 methylblue, carmin, Gramm's stain, etc. 
 
 Microscopic examination showed that the epithelial lining of 
 the gums did not present pathologic changes, but appeared nor- 
 mal in every respect. Connective tissue below the gum epithe- 
 lium (the tissue analogous to the papillary layer of the derma 
 and the derma proper) presented unmistakable evidences of a 
 
MERCURIAL INTERSTITIAL GINGIVITIS IN DOGS. 
 
 15: 
 
 mild inflammatory process. There occurred in this connective 
 tissue round-cell infiltration, generally moderate but in some 
 places quite dense. This cellular infiltration extended from 
 below (where it was densest) upward into the papillary layer 
 (Figs. 50 and 51). The densest cellular infiltration usually oc- 
 curred around the vessels (Fig. 51). 
 
 Under high magnification, the cellular infiltration was found 
 to consist of polymorphonuclear leucocytes, plasma cells and 
 
 MmdiS^: 
 
 Projection % inch, ocular lY-y inch. Spencer. 
 
 Fig. 53. — Longitudinal Section of Gingival Border, Showing Eound-Cell Infil- 
 tration IN THE Connective Tissue and Extending into the Papillae. Dog. 
 
 plasma-mast cells, the latter with coarse basophihc granulations 
 
 (Figs. 52 and 53). 
 
 In some places were seen between the round cells, short, 
 broad fusiform cells, the protoplasm of which took quite well 
 basic methylblue. These cells resemble very much fibroblasts 
 and appear to be derivations of the plasma cells (Fig. 54). No 
 bacteria were, found either in the areas of cellular infiltration 
 
 (inflammatory areas) or elsewhere. In these cases it is obvious 
 
154 
 
 INTERSTITIAL GINGIVITIS. 
 
 Pantachr. oil inim. ]/12 inch ocular. \o. .!. Lcitz. 
 Fig. 54. — Longitudinal Section of Gingival Border, Showing Round-Cell Inflam- 
 mation Due to Mercurial Poisoning. Higher Magnification. 
 
 Fig. 55. 
 A monkey skull showing absorption of the alieolar process (original). The right 
 central and left lateral have dropped out. The alveolar process is absorbed so 
 that all teeth are loose. 
 
MERCURIAL INTERSTITIAL (ilXCilVITIS IN DOCS. 155 
 
 that there had occurred a mild inflainination of the gums (gingi- 
 vitis). While this could not be seen with the naked eye, micro- 
 scopic examination demonstrated histologic features of an in- 
 flammatory process. The absence of bacteria justified the 
 belief that this inflammation was not of microbic origin, but due 
 to mercury, which by its well-kiiown chemotactic influence pro- 
 duced the histologic changes of an inflammation. 
 
 Fig. 55 is the skull of a monkey who died aged one year of 
 tuberculosis. Absorption of the alveolar process is the result 
 of autointoxication acting upon a depleted organism. The right 
 superior and inferior central and lateral incisors have loosened 
 and dropped out. The roots of all the teeth are exposed to a 
 marked extent. The teeth could be removed with the fino-ers. 
 
CHAPTER XV. 
 
 KESEARCHES ON HUMAN IN INTERSTITIAL GINGIVITIS. 
 
 While hundreds of slides conld be adduced in support of this 
 chain of evidence, sufficient have been given to permit of the 
 introduction of evidence from other phases of the subject. 
 
 The following autopsy was made by L. Hektoen on an old 
 man, in whose case the pathologic diagnosis was as follows: 
 Senile marasmus (senile emphysema, senile sclerosis of the 
 aorta, atrophy of the parenchymatous organs), scurvy (haBmor- 
 rhagic gingivitis); chronic aortic and mitral endocarditis; 
 fibrous myocarditis; chronic nephritis; caseo-calcareous areas 
 in the right apex, spleen and left adrenal ; double hydrothorax ; 
 bronchitis ; fibroma of the stomach ; amputation of the left lower 
 extremity at the lower third of the thigh. The findings unre- 
 lated to the scope of the present investigation are omitted. The 
 gums were found swollen, and here and there infiltrated with 
 blood. There was purulent matter about the roots of the teeth, 
 many of which were loosened and some of which could be 
 removed with the fingers. The roots of the loosened teeth were 
 covered with a granular grayish material. 
 
 Bacteriologic examination of the root of the tooth gave the 
 following results : Tube of bouillon from which agar plates 
 were made, inoculated twenty-four hours before date, July 29, 
 1898. There were two varieties of colonies: Both grayish 
 white. One kind is round, pin-head size, slightly elevated, with 
 thin, wavy, but sharply defined border. Finely granular. Media 
 inoculated from one of these. Agar Slant: White, tallow- 
 like growth along the track of the needle, with thin, more trans- 
 lucent layer covering the rest of the surface. Only moderately 
 elevated. Greenish tinge given to media. Potato: Elevated, 
 *' clumpy" growth, white on top, confined to needle track. 
 Potato much darkened. Blood Serum: Gray, waxy growth, 
 little elevated, sharply defined and thick border. Gelatin Slab: 
 Saucer-shaped liquefaction at upper part, more tubular in deeper 
 
RESEARCHES ON HUMAN IN INTERSTITIAL GINGIVITIS. 157 
 
 portions. Flocculent masses tliroiighoiit. Glucose Agar: Gas 
 produced, white, thick growth on top. Milk: Alkaline, soft 
 coagulation. Bouillon: Cloudy. Characteristics: Rapid growth, 
 a sour, nauseating odor given off from all media. Morphology: 
 Large coccus, single, in pairs and in groups. Stains easily by 
 ordinary methods, also by Grams. The smaller colonies on agar 
 plates (pin-point sized in center) with nearly transparent, illy 
 defined pai'ipheral zone. Border indistinct. Central portion in 
 gray. Finely granular throughout. Agar Slant: Gray film 
 over entire surface, somewhat thicker along the inoculation 
 streak. At bottom there is a nearly white growth. Very light, 
 greenish tinge to media. Blood Serum: Like on agar. Potato: 
 Heavy dirty gray growth, wavy and sharply defined border. 
 Looks like bunch of cauhflower. Gelatin Slab: Liquefied, 
 saucer-shaped at top, tubular in deeper part. Growth mostly 
 in upper stratum. Lit. Milk: Negative. Bouillon: Cloudy. 
 Glucose Agar: Gas produced. Characteristics: Eapid 
 growth, stinking odor from all media. Morphology: Small, 
 slender baciUi; actively mobile, spores. Takes ordinary stains 
 readily and is not decolorized by Gram's method. 
 
 Only the lower frontal teeth and corresponding part of the 
 jaw could be examined. The epithelial covering of the gums 
 appeared to be quite intact. Li some places it was a little thick- 
 ened, and its lower layers infiltrated with new cells. The sub- 
 epithelial tissue was much thickened, presenting the general 
 structure of an inflammatory granulation tissue of some stand- 
 ing. Areas occurred in which there were many new cells and 
 but little stroma. In other foci the tissue was more fibrous, the 
 new cells running in bands. Here and there occurred free and 
 intracellular granular, yellow pigment. Typical hyaline bodies 
 of various sizes, and staining a precise bluish violet with Gram's 
 method, were found in rather small numbers. In some places 
 small sub-epithelial abscesses were met with, which (in the 
 instance of a district including a lower incisor) were really sub- 
 periosteal. TlLe contents consisted of nuclear detritus and bac- 
 teria (mostly cocci) which have accumulated, especially upon 
 and in the walls of the minute cavities extending from such an 
 abscess. There seems to be a complete occlusion of the vessels 
 
X 40. 35 M. M. Zeiss. Micro-photograpli, reduced one-third. 
 
 Fig. 56. — Longitudinal Section of Tooth, Alvj;olar Process and Gingival Border, 
 
 Showing Active Inflammation in Scurvy in Man. 
 
 B, Dentine. C, Cementum. B, Epithelial Tissue. G, Submucous Membrane. 
 H, Periosteum. J, Alveolar Process. L, Haversian Canals. M, Fibrous Tissue. Y, 
 Violent Inflammation. AA, Point of Union of Epithelial Tissue and Peridental Mem- 
 brane. RR, Space Pocket from Want of Union of the Epithelial Fold. 
 
X 40. 35 M. M. Zeiss. Micro-photograph, reduced one-third. 
 
 Fig. 57. — Longitudinal Section of a Tooth, Alveolar Process and Gingival 
 Border, Showing Active Inflammation in Scurvy in Man. 
 
 B, Dentine. C, Cementum. E, Epithelial Tissue. G, Submucous Membrane. 
 V, Violent Inflammation. Z, Sloughing of the Epithelial Tissue Due to Calcic Deposits. 
 AA, Point of Union of Epithelial Tissue and Peridental Membrane. 
 
X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 
 
 Fig. 58. — Longitudinal Section of Tooth, Alveolar Process and Peridental Mem- 
 brane, Showing Blood Pigment in Blood Vessels of Peridental Membrane 
 IN Scurvy in Man. 
 
 C, Cementum. J, Alevolar Process. K, Capillaries. IS Inflamed Peridental Mem- 
 brane. KS Blood Pigment in Capillaries. 
 
X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 
 
 Fig. 59. — Longitudinal Section of Tooth and Gingival Border, Showing Active 
 Inflammation Extending through the Mucous and Peridental Membranes. 
 Scurvy in Man. 
 
 B. Dentine. C, Cementiim. E, Epithelial Tissue. V, Violent Inflammation. AA, 
 Point of Union of Epithelial Tissue and Peridental Membrane. RR, Space Pocket 
 from Want of Union of Epithelial Fold. M\ Inflamed Fibrous Tissue. 
 
162 INTERSTITIAL GINGIVITIS. 
 
 (capillaries) with typical bacteria masses, staining a peculiar 
 bluish violet color with hematoxylin, and blue with Gram's 
 method, so that the vessels presented the appearance of being 
 very successfully filled by an infection mass : the small dilata- 
 tions, the branches and the larger vessels (judging from struc- 
 ture these seemed to be veins) were sometimes brought out very 
 nicely. The intravascular growth of bacteria extended into the 
 bone below as well as, and more especially into, the peridental 
 membrane.^ These abscesses (suppurative periostitis) occur 
 almost exclusively upon the inner surface of the alveolar proc- 
 ess, being confined (as far as there was occasion to observe) to 
 the external aspect of the process. There was always a thin, 
 sound layer of bone separating the abscess from the peridental 
 membrane. Very generally the spaces in the adjacent bone 
 were filled with a cellular fibrous tissue in which occurred islands 
 of osteoid tissue. The bone trabeculne were generally covered 
 by a thin layer of osteoid tissue, which (from the greater num- 
 ber of cells it contains, as compared with the other bones) must 
 be newly formed. Rows of osteoblasts were found often upon 
 the trabeculae. Few Howship's lacunaB were found, and these 
 were filled with small cells. There were no osteoclasts in the 
 areas about the abscesses. The bone outside of the alveolar 
 process was quite unchanged. 
 
 The ''bacterial thrombosis" not unusually extended into the 
 peridental membrane, which then refused to stain as clearly as 
 normal. The upper part of the peridental membrane was 
 usually the seat of cell proliferation, and of the formation of 
 fibrous tissue, due to the direct extension of the similar process 
 in the sub-epithelial connective tissue of the gingivus. There 
 were no indications that the process began below, at the apex of 
 the tooth, for example, and extended upward. In the peridental 
 membrane, and often connected with the cementum of every 
 tooth examined, were very many so-called calcospherites ; cal- 
 cified, concentrically lamellated, round or oval bodies, not unlike 
 the ''corpora amylacea. " In many instances, it seemed as if the 
 
 ^ The abscesses have a definite outline or wall of ordinary cellular fibrous tissue 
 displaying striking evidences of active inflammation. The tissue about the capilla- 
 ries filled with bacteria refuse to stain clearly, but there are no signs of inflammation. 
 
EESEAKCliE8 ON HUMAN IN INTEKtiTITIAL GINGIVITIS. 163 
 
 body liad formed in the cement or at its margin — the cement 
 presenting here a nodular condition. 
 
 Fig. 56 ilhistrates a section through the tissues of the jaw 
 and cuspid tooth. The epitheUum is not so dense and thick as 
 in a similar section from the dog. Inflammation extends along 
 the papillary layer of the submucous membrane (G) and involves 
 the deeper structures. The mucous membrane layer has doubled 
 upon itself, forming a pocket (RR). Violent inflammation is 
 evident at V. This is of unusual interest, since it demonstrates 
 that inflammatory products may be carried by the blood vessels 
 anywhere throughout the alveolar process, and may result in 
 abscesses. The inflammation extends throughout the periosteum 
 (H), the fibers of which extend from the root of the tooth over 
 the border of the alveolar process (J). There the coarse fibers 
 of the periosteum contrast decidedh^ with the finer fibers of the 
 sub-epithelium. Absorption and contraction of the alveolar 
 process (fully one-half the length of the root of the tooth) has 
 taken place, as well as lateral absorption. The inflammatory 
 process extends through the Haversian canals (L). 
 
 Fig. 57 is a section through the jaw at the lateral incisor. 
 The epithelium (E) is seen upon the outer surface of the alveolar 
 process as far as the root of the tooth. The inner fold next to 
 the tooth has disappeared through encroachment of deposits 
 which have been destroyed by nitric acid. Inflammation ex- 
 tends throughout tlie entire submucous membrance (G). The 
 most marked inflammation in this case is entirely upon the 
 outer border (V). 
 
 Fig. 58 shows a section of the peridental membrane (I) 
 and alveolar process (J). Capillaries (K) interlace through 
 the field, the largest number being distributed along the 
 alveolar wall. Blood pigment containing bacteria is notice- 
 able (K'). 
 
 Fig. 59 is an amplification of a section depicted in Fig. 56. 
 This gives a clearer idea of the folding of the epithelium (E) 
 and submucous membrane (G) layer upon itself, forming a 
 pocket (RR), in which may be seen an accumulation of food and 
 bacteria. It also shows extensive inflammation throughout the 
 entire field. Marked inflammation is evident at V. The point 
 
X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 
 
 Fig. 60. — Cross Section Peridental Membrane, Showing Active Eound-Cell In- 
 flammation. Scurvy in Man. 
 
 C, Cementum. V, Violent Inflammation.. W, Epithelial Debris. EO, Endar- 
 teritis Obliterans. 
 
X 75. A. A. obj. Zeiss. Micro-photogvaph, reduced one-third. 
 
 Fig. 61. — Cross Section of Inflamed Peridental Membrane. Scurvy in Man. 
 
 I, Peridental Membrane. J, Alveolar Process. K, Capillaries. L, Haversian 
 Canals. BB, Blood Vessels of Von Ebner Preceding Perforating Canals. EO, Endar- 
 teritis Obliterans. W,. Epithelial Debris. 
 
X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 
 
 Tig. 62.— Cross Section of Tooth, Alevolar Process and Peridental Membrane, 
 ' Showing Active Inflammation and Absorption of Bone. Scurvy in Man. 
 
 C, Cementum. I, Peridental Membrane. J, Alveolar Process. P, Perforating Canal 
 Absorption. V, Violent Inflammation, 
 
X 40. 35 M. M. obj. Zeiss. Micro-photograph, reduced one-third. 
 
 Fjg. 63. — Cross SectioIn of Peridental Membrane and Alveolar Process, Showing 
 Active Inflammation and Abcess. Scurvy in Man. 
 
 J, Alveolar Process. % Bacteria. Y, Abcess. T, Inflamed Peridental Membrane. 
 L, Inflammation Extending through Enlarged Haversian Canals. 
 
■ X 75. A. A. obj. Zeiss. Micro-photograph, reduced oue-third. 
 
 -piQ 64 Cross Section of Peridental Membrane and Alveolar Process, Show- 
 
 " iNG Active Inflammation and Another Larger Abcess. Scurvy in Man. 
 
 J, Alveolar Process. P, Perforating Canal Absorption. V, Violent Inflammation. 
 Y, Abcess. 1\ Inflamed Peridental Membrane. U, Inflammation Extending through 
 Enlarged Haversian Canals. 
 
EESEAECHES ON HUMAN IN INTEESTITIAL GINGIVITIS. 
 
 169 
 
 of union of the siib-epithelial layer and the periosteum is shown 
 (AA). 
 
 Fig. 60 illustrates inflammation of the peridental membrane 
 with epithelial debris (W) scattered over the field. Endarteritis 
 obliterans (EO) is also noticed at various positions. Marked 
 inflammation may be seen at V. 
 
 Fig. 61 illustrates a section of the peridental membrane (I) 
 and alveolar process (J) with inflammation extending through- 
 out. Capillaries (K) are also noticeable in large quantities, 
 
 X 300. No. 2 projection ocular. D. D. obj. Zeiss. 
 
 Fig. 65. — Cross Section of Tooth, Alveolar Process and Peridental Membrane, 
 Showing Active Inflammation with Calcospherite in Membrane. Scurvy 
 IN Man. 
 
 B, Dentine. C, Cementum. I, Peridental Membrane. J, Alveolar Process. 
 HH, Calcospherite. J*, Inflamed Peridental Membrane. L^, Inflammation Extending 
 through Enlarged Haversian Canals. 
 
 nearer the alveolar process than the root of the tooth. Epithe- 
 lial debris is evident at W. Endarteritis obliterans (EO) may 
 be seen in different portions of the field. Inflammation has 
 extended into the Haversian canals (L) but absorption has not 
 
170 INTERSTITIAL GINGIVITIS. 
 
 occurred to any great extent. The blood vessels of Von Ebner 
 (BB) are quite well shown. 
 
 Fig. 62 is a section showing the cementum (C), the i)eri- 
 dental membrane (I) and the alveolar process (J). Marked 
 inflammation extends through the peridental membrane, thence 
 through the Haversian canals (which are entirely obliterated). 
 Absorption of the trabeculae (halisteresis) has resulted to the 
 extent that what remains of the alveolar process (J) are islands 
 of bone held in place by the fibrous tissue. Blood vessels of 
 Von Ebner with perforating canals are seen at P. 
 
 Fig. 63 shows a section of the peridental membrane and 
 alveolar process wdth a large abscess originally within the 
 alveolar wall. Inflammation spreading through the peridental 
 membrane has occurred at Y, while the decalcified alveolar 
 process is also shown (J). Violent inflammation has taken 
 place within the alveolar wall, and an abscess (Y) has formed. 
 The wall of the abscess is distinctly seen, with masses of bac- 
 teria (T) clinging to the inner sides. The process of halisteresis 
 (Q) (bone decalcification) is seen as a result of the violent 
 inflammation. The entire wall next to the peridental membrane 
 and about the abscess has been destroyed, and the different 
 stages in the process by which this has been accomplished are 
 beautifully shown. 
 
 Fig. 64 illustrates a larger abscess (Y) from another loca- 
 tion. This is also situated mthin the alveolar wall, showing 
 that the inflammatory products extend through the blood ves- 
 sels. Marked inflammation is seen upon the side next to the 
 peridental membrane (T), while rapid absorption — halisteresis 
 (Q) and perforating canal (P) — is proceeding at the borders 
 of the abscess and nearest the alveolar process. 
 
 Fig. 65 shows a section of a tooth (B and C), inflamed 
 peridental membrane (I'), with absorption of the alveolar proc- 
 cess (J). In the inflamed peridental membrane may be seen 
 a calcospherite, oblong in form. 
 
 INTERSTITIAL GINGIVITIS IN MAN FROM DRUG ACTION. 
 
 A forty-eight-year-old merchant was dyspeptic, debilitated 
 and asthmatic, and for the treatment of these conditions he had 
 been under calomel and tonics for a little less than two weeks. 
 
RESEARCHES OX HU:MAN IX IXTERSTITIAL GlX(iIVITIS. 171 
 
 When lie came under observation, the mucous membrane and 
 gums were then nuich inflamed. There was marked sialorrhoea. 
 The teeth were loose. The gums were swollen. Pus oozed from 
 the gums. The breath had a decided metallic odor. At my sug- 
 gestion, his medical attendant stopped the calomel. He was 
 then ordered six pints of spring water daily. The gums were, 
 on alternate days, saturated with iodin. In a few days the sore- 
 ness and swelling were so reduced that the de])osits could be 
 removed. The patient was discharged cured in a short time 
 other than as to tlio riglit inferior second molar, which was so 
 loose as to require removal. This tootli was placed immediately 
 
 Fig. 66. — Shows a Small Fragment of Inflamed Peridental Membrane. 
 
 in fifty per cent alcohol for twenty-four hours and then removed 
 to absolute alcohol for twenty-four hours more. The membranes 
 had receded about two-thirds the length of the root. Sections 
 for microscopic purposes were made from the lower third of the 
 root. Of these sections, Fig. 66 shows a small fragment of in- 
 flamed peridental meml)rane. Fig. 67 exhibits violent round-cell 
 inflammation, degeneration and liquefaction of tissue. 
 
 A thirty-five-year-old diabetic painter came under observa- 
 tion for plumbic poisoning. His gums were swollen. There was 
 decided sialorrhcea. The teeth were loose. Pus flowed from the 
 gums. He was placed on ozonate spring water and the gums 
 
172 
 
 INTERSTITIAL GINGIVITIS. 
 
 were saturated with iodin on alternate days. Three loose teeth 
 were removed and placed in alcohol. Sections from the upper 
 third of the left superior second bicusi^id gave results on micro- 
 scopic examination similar to those already described as occur- 
 ring in mercurial poisoning. Fig. 68 shows round cells of in- 
 flammation. Fig. 69 illustrates very marked degeneration of 
 the peridental membrane. In the lower right-hand corner are 
 seen the root of the tooth, dentine and cementum. The whole 
 surface of the peridental membrane is in an advanced phase of 
 
 Fig. 67. — Violent Eouxd Cell Inflammation, Degeneration and 
 liquification of tissue. 
 
 inflammation. Just at the border of the root is evident an area 
 of membrane softening. Just beyond, but joining, is noticeable 
 breaking down of tissue. In the center are seen two areas of 
 softened tissue more advanced in degeneration. 
 
 One occupation disease which has been ignored in the etiology 
 of interstitial gingivitis is ''brass-workers' ague. " In almost all 
 brass-workers, a stain varying from a bright to a brownish green 
 IB detectable on the necks of the teeth between the crowns and 
 
EESEAECHES ON HUMAN IX INTERSTITIAL GINGIVITIS. 173 
 
 the gum insertion. This is most obvious in the upper jaw. 
 After a while, as E. Hogben - has shown, the teeth become 
 loosened and fall out. Before these changes in the gum occur 
 nervous symptoms have developed from the brass poisoning. 
 
 Arsenic should be taken into account in the etiology of inter- 
 stitial gingi\itis. This drug has a very decided tendency in cer- 
 tain subjects to cause, even in small doses, marked stomatitis 
 and irritation of the mucous membranes throughout the body. 
 
 Tartar emetic and the other preparations of antimony, pro- 
 ducing irritation of tlie mucous membranes of the mouth and 
 elsewhere, may act as predisposing and exciting factors of inter- 
 stitial gingivitis." 
 
 
 Fig. 68. — Section of Pericemextai, Membrane Showing Eound Cell Inflammation. 
 
 Among the drugs which should be taken into account in the 
 etiology of interstitial gingivitis is potassium bromide. This 
 produces in certain individuals, or when given to excess, marked 
 increase of the saliva with irritation of the mucous membranes 
 of the mouth, followed later by dryness of the mouth and shrink- 
 ing of the gums. The bromides have, as H. C. B. Alexander * 
 has shown, a teudency to irritate all the mucous membranes of 
 the body as well as the skin. Therefore, in dealing with cases 
 
 ' Birmingham Medical Eeview, 1887. 
 ^Lewin: Untoward EiFects of Drugs. 
 * Alienist and Neurologist, July, 1896. 
 
174 
 
 INTERSTITIAL GINGIVITIS. 
 
 of interstitial gingivitis in wliicli tlic l)roini<les are being taken, 
 this factor should not be neglected. In these cases the symptoms 
 dne to the bromides are ax)t to be charged to the nervous state for 
 which the bromides have been given. The irritation of the 
 
 mncons membrane by the bromides may occur quite early among 
 
 Fig. 69. — Marked Inflammation and Degeneration of the Peridental Membrane 
 Showing Four Peridental Abscesses. 
 
 the untoward effects produced by them. In all probability the 
 bromide rather than the alkali is the source of these untoward 
 effects. 
 
 What is true of the bromides is also true to an even greater 
 degree, as has elsewhere been shown, of the iodides. 
 
CHAPTER XVI. 
 
 RESEARCHES ON HUMAN IN PERICEMENTITIS. 
 
 Referring- to Chapter VI we find that the peridental mem- 
 brane is a tibrons tissue situated between the root of the tooth 
 on the one hand and the alveoUir process on the other. It covers 
 the root of the tooth. This structure, to all intents and pur- 
 poses, is a c«)ntinuation of the trabeculne or fibrous tissue in the 
 alveolar process. In other words, the alveolar process is noth- 
 ing more or less than fibrous tissue filled in with lime salts. 
 
 If a piece of jaw containing teeth be placed in a weak acid 
 solution and the lime salts dissolved, there would be no distinc- 
 tion, under the microscope, in the remaining- structure from the 
 root of the tooth to the outer surface including the periosteum 
 except in quality of fibers. When a low form of inflammation is 
 set up in the alveolar process, the lime salts are absorbed, leav- 
 ing the fibrous tissue in like manner. If on the other hand, the 
 inflammation is more intense, the trabeculcT or fibrous tissue is 
 also destroyed. 
 
 Irritations of a local nature first produce a gingivitis of the 
 gum tissue which extends along the blood vessels into the deeper 
 tissues and assumes an interstitial character. When the irrita- 
 tions are constitutional, due to autointoxication, drug, or other 
 irritation and poisons, the deeper tissues become involved, then 
 assuming an interstitial character, later affect the gums, pro- 
 ducing gingivitis. When the peridental membrane becomes in- 
 volved, whether from local or constitutional causes, it is termed 
 pericementitis. This disease is always recognized by soreness 
 and a slight elongation of the tooth or teeth. 
 
 If the cause be slight or if removed, the membrane will re- 
 turn to its normal condition. On the other hand, if the cause be 
 severe and of long standing- the inflammation will become 
 chronic, resulting in absorption of the alveolar process and per- 
 haps abscess. 
 
176 INTERSTITIAL GINGIVITIS. 
 
 A low form of pericementitis may act upon the surrounding 
 tissues in different ways, depending, to a great extent, upon the 
 nervous system. First, if there are no corresponding teeth for 
 antagonism on the opposite jaw, the inflammation will cause a 
 deposition of lime salts in the alveolar process, causing elonga- 
 tion which continues until the tooth or teeth meet resistance. 
 Second, exostosis of the cementum of the tooth. Third, the 
 inflammation results in peridental or alveolar abscess. Later, 
 especially if the irritation be of a constitutional nature, the 
 inflammation will cause absorption of the alveolar process and 
 exfoliation of the teeth. 
 
 A seamstress bites her thread, pericementitis results. If 
 treatment be resorted to and the habit stopped, the peridental 
 membrane will be restored to health. If, however, this habit 
 be continued, interstitial gingivitis results, with absorption of 
 the bone and loosening of the teeth. The habit of biting threads 
 with the teeth causes an extra amount of work upon the peri- 
 dental membrane. Persons suffering with autointoxication 
 would naturally find such teeth first involved in interstitial 
 gingivitis. The same results follow when a low form of inflam- 
 mation occurs in the three classifications just mentioned above. 
 Persons of low vitality, poorly nourished people suffering with 
 prolonged sickness and pregnant women have periostitis and 
 general interstitial gingivitis. Persons overworked or suffering 
 with neurasthenia are prone to it. 
 
 In syphilis, pericementitis and interstitial gingivitis are set 
 up and not only in the alveolar proces;.;, but all bones of the body 
 may become involved, causing hypertrophy as well as absorp- 
 tion and death of bone. Heat and allied irritation will produce 
 interstitial gingivitis and bone absorption. 
 
 Some more severe forms of pericementitis and interstitial 
 gingivitis deserve attention from the irritation point of view. 
 I have for years moved the teeth of dogs with regulating appli- 
 ances, using a screw with sixty threads to the inch. In some 
 the screw was turned one-fourth round, in otliers one-half, and 
 in still others one full turn once a day. Some of the dogs were 
 killed in three days, others in a week, and still others in two 
 weeks. By this method the simplest and most severe forms of 
 
EESEARCHES ON HUMAN IN PERICEMENTITIS. 
 
 177 
 
 pressure were applied, the length of time being brief as well as 
 extended. These tissues were decalcified, cut, stained and 
 mounted for the microscope. In every case inflannnation of the 
 pericementum was produced. This disproves the theory so long 
 held, that bone absorption in regulating teeth is purely a physio- 
 logic process. Teeth were also extracted from dogs and after 
 a week they were killed. The bone was decalcified, cut, stained 
 and mounted for the microscope. The absorption was inflamma- 
 tory in character. The jaws of dogs and monkeys who were 
 erupting the permanent teeth were treated in like manner. Ab- 
 
 FlGURE 70. 
 
 Inflauimation of the gum margin (original). 
 
 sorption of the alveolar process to allow the teeth to pass into 
 position was of inflammatory type. Simple irritation, as well as 
 severe pressure, hence produces the same pathologic process, 
 pericemental inflannnation and interstitial gingivitis. 
 
 The blood vessels which supply the gums, pericemental mem- 
 brane and alverilar process are, as I have elsewhere demon- 
 strated closely connected. Those in the pericemental membrane 
 form a plexus along the wall of the alveolar process, while only 
 a small number are near the roots of the teeth. So closely con- 
 
178 
 
 INTERSTITIAL GINGIVITIS. 
 
 nected are these that the vessels in one cannot become involved 
 without affecting- those of the otlier tissues. Hence, gingivitis 
 and pericementitis occur wliich in reality become interstitial, 
 or interstitial inflammation appears, which in reality becomes 
 gingivitis. No matter wliat the cause may ])e, or whether the 
 initial lesion be in the gum or interstitial structure, absorption 
 of the alveolar process eventually results. 
 
 I began my experiments upon the peridental membrane in 
 1896. In 1897, I read an article before the Section on Stoma- 
 tology of the American Medical Association, demonstrating the 
 
 Figure 71. 
 
 Section deeper at the alveolar honlev (original). Active inflammation around two 
 arteries which are becoming thickened. 
 
 pathology of the peritlental membrane from simple inflammation 
 to the breaking down of tissue and the formation of abscess. 
 
 A bicuspid tooth with a gold crown attached was taken from 
 the mouth of a fifty-four-year-old man. He was suffering from 
 autointoxication and neurasthenia. The tooth had become quite 
 loose although the gum tissue was still intact. The irritation 
 was both local and constitutional in character, since the gold 
 
EESEAECHES ON HUMAN IN PERICEMENTITIS. 
 
 179 
 
 crown irritated tlie gum margin and a slight attack of Bright 's 
 disease caused self poisoning. 
 
 The following illustrations are taken from microscopic slides 
 and magnified four hundred and eighty diameters. Fig. 70 
 shows the gum tissue. The epithelial layer shows the dipping 
 down of the legs into the true mucous menil)rane below the base- 
 ment membrane, with round cell infiltration due to irritation. 
 Fig. 71 is a cross-section of peridental membrane of the left 
 inferior ceutral incisor of a ladv twentv-nine vears of age who 
 
 inflammat: 
 
 had been under my care for fourteen years. She was in the 
 habit of biting her thread with this tooth. Her occupation, that 
 of dressmaking, gave her little or no exercise and she was also 
 overworked. She drank no water; she was suffering from sleep- 
 lessness and nervousness due to indigestion and autointoxica- 
 tion. Sections of tooth, after decalcification, were made in the 
 usual manner for the microscope. A cross-section shows two 
 blood vessels which are consideraljly thickened (endarteritis 
 obliterans) in its early stages with round cell infiltration in the 
 tissues about them. 
 
180 
 
 liS'TEKSTITlAL GINGIVITIS. 
 
 
 
 
 h 
 
 TlGURE 7lj. 
 Violent inlhiinniation in the jieridental membrane and tiabeeula? (original). 
 
 FlGlTlE 74. 
 
 Shows the root of the tooth, the peridental membrane, active inflammation in the 
 trabecnte and the formation of two abscesses. Xote that both these abscesses are 
 located in what was once the alveolar process. The peridental membrane can be 
 readily observed between the root of the tooth and the nearest abscess (or- 
 iginal). 
 
RESEARCHES ON HUMAN IN PERICEMENTITIS. 181 
 
 The preceding three illustrations show the different stages of 
 inflammation and liquefaction of the peridental membrane of the 
 right superior first molar in a forty-year-old lady, a marked 
 neurasthenic who has had periostitis and interstitial gingivitis 
 with pyorrhoea alveolaris for the last twent}^ years and is now 
 losing her teeth very rapidly. Fig. 72 shows a cross-section of 
 palatal root near the apex, showing active inflammation in the 
 peridental membrane. The round cell inflammation with exudate 
 is rapidly collecting between the bundles of connective tissue 
 fibers. Fig. 73 is a cross-section of the same root nearer the 
 apex showing connective tissue with active inflammation, a stage 
 further advanced than that of the previous illustration. In this 
 area no fibrous tissue can be seen. Fig. 74 shows a still further 
 advance in degeneration and liquefaction, forming an abscess. 
 This is a lower magnification, showing a portion of the two 
 buccal roots of the tooth, peridental membrane and the trabeculae 
 or fibrous tissue which was once alveolar process between them. 
 The peridental membrane may easily be distinguished around 
 each root from the trabeculae between them. Two areas of 
 softening and liquefaction may be seen forming two abscesses. 
 
CHAPTER XVIL 
 
 LOCAL CAUSES OF INTERSTITIAL GINGIVITIS. 
 
 The local irritations producing interstitial gingivitis are the 
 eruption of the teeth, change in function, tartar, uncleanness, 
 lactic acid ferment, irritations' due to modern dentistry, irreg- 
 ular teeth, regulating teeth, implantation of teeth. 
 
 Many years ago' I stated that modern dentistry was one of 
 the most fruitful sources of interstitial gingivitis. Irritations 
 from foreign substances, such as detached bristles of the tooth- 
 brush, too great friction in brushing the gums and alveolar proc- 
 ess, where the latter is prominent, injudicious use of the tooth- 
 pick, the use of ligatures in holding in rubber dam and regulat- 
 ing teeth, regulation of teeth with any applicance, application of 
 the rubber dam, the use of clamps, crown and bridge work, irri- 
 tation and heat due to artificial dentures and regulation plates, 
 overlapping fillings, injuries from instruments, the devitaliza- 
 tion of pulps, root fillings which throw increased work upon the 
 peridental membrane or irritate it, in a word whatever irritates 
 the gum margin, peridental membrane or alveolar process, is 
 likely to produce inflammation which later becomes chronic. I 
 am convinced that the disease is contagious, or progressive, not 
 from one individual to another, but from one tooth to another in 
 the same mouth. 
 
 The greatest and most important local cause of interstitial 
 gingivitis is that of the eruption of the teeth since nearly every 
 person possesses two sets. 
 
 Tooth eruption of both the first and second set ushers in the 
 second and third periods of stress. It is at these periods when 
 great changes take place in the system of the child and mark 
 the early eras of future welfare. The absorption of bone in the 
 eruption of the teeth and the Ijuilding up of bone about the roots 
 
 1 Talbot, The Dental Cosmos, Nov. 1886. 
 
LOCAL CAUSES OF INTERSTITIAL GINGIVITIS. 183 
 
 to hold tliem in place is an inflammatory process. How well this 
 is accomplished depends upon the health of the child. In neu- 
 rotic and degenerate children, when the nervous system is un- 
 stable and the child's vitality is of low order, the process of 
 absorption and deposition of bone cells is not carried on nor- 
 mally. Especially is this true in the building up of the alveolar 
 process about the roots of the teeth. Interstitial gingivitis re- 
 mains in the alveolar process to a greater or lesser extent during 
 the entire period of and until the shedding of the first set of 
 teeth. The extreme illustrations of this disease are those con- 
 nected with rachitis, infantile scurvy, inherited syphilis, marked 
 neurosis, degeneracies and similar diseases. The jaws are often 
 small, the alveolar processes are undeveloped and quite loosely 
 built up. The gums are always inflamed and frequently ulcer- 
 ated. At the second period of stress, when the first teeth are 
 erupting the entire alimentary canal as well as all the internal 
 organs undergoes changes in preparation for the reception of 
 solid starchy food. The effects upon nutrition at this time are 
 severe. In every patient there is more or less inflammation in 
 the alveolar process, gums and peridental membrane until the 
 first teeth are shed. 
 
 When the second set of teeth erupt there is a double inflam- 
 matory process going on in the tearing down of the bone to 
 remove the temporary teeth and bailding up the process for the 
 permanent teeth. So irregular is this action that in many 
 mouths there is a continuous inflammation through the entire 
 process on both jaws. This is noticeable in neurotics and de- 
 generates and in those children whose vitality is low and who 
 are poorly nourished. The bone is porous and loosely put to- 
 gether. The severity of interstitial gingivitis during the erup- 
 tion of both sets of teeth and after all of the second teeth are in 
 the mouth wdll depend upon the nervous system and blood sup- 
 ply. It must not be lost sight of, that, after all of the second set 
 of teeth are in the mouth, there is a restlessness existing among 
 them till all are securely located in their respective localities, 
 although they may not be in their proper relations to each other. 
 As long as this restlessness continues, and it may persist until 
 middle life, interstitial gingivitis is always present. The irri- 
 
184 INTERSTITIAL (!IN(iIVITIS. 
 
 tatioii set up by the Mclvancing teetli causes inflammation iu tlie 
 gums and alveolar process. A visit to schools for defective chil- 
 dren and an examination of their mouths will convince any one 
 of the truth of this statement. 
 
 CHANGES IN FUNCTION. 
 
 Change in function has been discussed in a general way in 
 previous chapters. It is necessary, however, to state here that 
 owing to use and disuse of structures and environment, the func- 
 tion of mastication is gradually being reduced to a minimum. 
 On this account and the gradual reduction of the size of the jaws 
 and straight crowned teeth, the alveolar process, has, in most 
 persons, changed its shape and has become narrow, long and 
 thin. This change in shape and loss in blood and nerve supply 
 makes the process about one or more teeth exceedingly suscep- 
 tible to disease and destruction on account of loss of function. 
 
 TARTAE. 
 
 Tartar is the excess of lime salts in the blood excreted 
 through the salivary glands. It remains soluble in the saliva 
 until it reaches the mouth cavity when it precipitates. Just how 
 precipitation is accomplished has not been proven beyond a 
 doubt. One theory is that the action of ammonia exhaled from 
 the lungs is the greatest factor. 
 
 Kirk says,' "As the saliva contains carbon dioxid in solution 
 it has been assumed with some justification, that the escape of 
 the carbon dioxid wdiich was the solvent of the calcium carbonate 
 and tricalcic phosphate, causes a precipitation of those salts in 
 the presence of the colloid mucin, in comlnnation with which it 
 deposits as tartar upon the teeth." 
 
 H. H. Bouchard' proposed an explanation for the formation 
 of .salivary tartar deserving of consideration, viz., ''that, 
 inasmuch as fermentative processes in the oral cavity give rise 
 to acids, and particularly lactic acid, these acids cause precipi- 
 tation of the mucin of the saliva as a coagulnm which entangles 
 in its structure calcic phosphate and carbonate, and this mass by 
 
 2 Kirk. American Text-Book of Operative Dentistry, page 480. 
 
 3 See Origin of Salivary Calculus by Henry H. Bouchard, Dental Cosmos. 1895, 
 vol. XXVII, page 821. Also Varieties of Dental Calculi, by the same author, Dental 
 Cosmos, 1898, vol. XL, page 1. 
 
LOCAL CArSES OF IXTERSTITL\L GINGIVITIS. 185 
 
 gradual condensation increases in density to the extent of form- 
 ing the coherent deposit known as tartar." 
 
 Tartar accunndations vary in quantity as well as in charac- 
 ter in each individual and even in the same mouth. In some the 
 greatest amount is found upon the molar teeth in opposition to 
 the parotids whose function is apparently to keep the mouth 
 moist. These glands constantly discharge small quantities of 
 saliva without food stimulation. Owing to its special function, 
 the sub-maxillary gland is stimulated by tasteful substances, 
 hence probably does not send out as much lime salts. The sub- 
 lingual glands next to the parotids discharge the greatest amount 
 of calcic salts, which accounts for the quantity of deposit found 
 on the posterior surface of the inferior incisors. The tartar will 
 accumulate so rapidly in some mouths as to completely cover a 
 tooth or teeth in a short time. In some autotoxic states there is 
 always excess of tartar deposit. In a patient in whom mal- 
 nutrition was most pronounced, deposits of tartar would collect 
 so rapidly as to cover all the teeth in from four to six weeks. 
 The teeth were of a degenerate type in that they had no enamel. 
 
 In tartar analysis there is also great variation, that deposited 
 near Steno's duct having the greater per cent of lime carbonate 
 while that from the lower incisors has the greater per cent of 
 lime phosphate. 
 
 Tartar may be black, deep biown, green or yellow. In to- 
 bacco users the deposit is usually black, presumably stained 
 from nicotine. Other agents will stain tartar as well. This is 
 finely exampled in betel-nut chewers where "the rapid accunni- 
 lation of large, dense deposits of tartar which at first are red, 
 then finally become a dark, chestnut brown or black."' Nodules 
 of tartar which cling with such persistency to the roots of the 
 teeth are usually of a greenish or dark brown color and of great 
 density. Tartar is not uncommon in domestic animals and the 
 wild in captivity. I have no means of ascertaining whether wild 
 animals running at large are thus alfected. 
 
 If the deposits of tartar are allowed to remain upon the 
 teeth, they are added to day by day. Sooner or later, they set 
 
 * Kirk. American T'ext-Book of Operative Dentistry. 
 
186 INTERSTITIAL GINGIVITIS. 
 
 np irritation and inflammation in the gnms, in tlie peridental 
 membrane and in tlie alveolar process, with resulting interstitial 
 gingivitis, pyorrluca alveolaris and finally exfoliation of the 
 tooth or teeth. 
 
 IRREGULAR TEETH. 
 
 Every one is familiar with the fact that those persons who 
 possess small jaw^s and irregular teeth are more subject to inter- 
 stitial gingivitis than those persons possessing normal jaws and 
 teeth. This is due first to the fact that those persons possessing 
 irregular teeth have unstable nervous systems. Second, the ir- 
 regularity of the teeth brings the roots closer together, making 
 the alveolar process thin between the roots, thus reducing the 
 blood and nerve supply, and thus reducing resistance. The gums 
 are inflamed from want of cleanliness and proper brushing and 
 the function of proper mastication is lost. The gums thicken 
 because engorged with blood and stasis takes place, resulting in 
 irritation. 
 
 UNCLEANLINESS. 
 
 One of the most fruitful sources of interstitial gingivitis is 
 uncleanliness. Food and tartar collect on the teeth at the gin- 
 gival border setting up irritation and inflammation. A want of 
 proper measures for cleaning the teeth and gum margins after 
 each meal soon allows the accumulation to irritate the gums 
 which become inflamed and the food works its way along the 
 roots of the teeth. The gums become inflamed, swollen and de- 
 tached from the necks of the teeth. This condition allows more 
 food and filth to collect which decomposes and forms lactic acid. 
 This in turn also irritates the gums and further inflammation 
 follows. 
 
 IRRITATIONS DUE TO MODERN DENTISTRY. 
 
 In my researches on interstitial gingivitis many years ago," 
 I called the attention of the profession to the fact that modern 
 dentistry was producing more inflammation of the gums, peri- 
 dental membrane and alveolar process than any one cause. 
 These irritations were most noticeable at that early period about 
 
 5 Talbot. The Dental Cosmos, Nov. 1886. 
 
LOCAL CAUSES OF INTERSTITIAL OUSTGIVITIS. 187 
 
 those teeth which had been "immediately separated for filling," 
 so commonly practiced by the older members of our profession 
 before the rubber dam. A piece of orangewood made V-shaped, 
 with the base resting upon the gum margin, was forcibly driven 
 between the teeth for the purpose of obtaining plenty of room 
 for immediate filling and also to press forcibly against the gums 
 and alveolar process to jjrevent the gums from weeping, thus 
 keeping the cavity dry. In the majority of cases so treated, 
 interstitial gingivitis was set up which in time became chronic. 
 
 The inflammation continued and followed the root upon one 
 side oftentimes to the apex. The alveolar process became de- 
 stroyed on the side of the inflammation and not infrequently 
 pus infection would follow. The tooth would sometimes rotate 
 upon itself or move in one direction or the other out of its posi- 
 tion. The most excruciating pain accompanied the malleting 
 of these wedges into place. 
 
 The modern method of rapid wedging with separators is only 
 a modification of this barbarous method of procedure and is fre- 
 quently the source of interstitial gingivitis and later pyorrhoea 
 alveolaris. 
 
 Wedging teeth by any method sets up inflammation which 
 may or may not be restored to normal. In any event, if poisons 
 circulate in the blood later in life, such irritated or inflammatory 
 localities, owing to the transitory nature of the structures, are 
 the first to be affected by chronic interstitial gingivitis, since 
 these structures have already been previously involved in struc- 
 tural changes. 
 
 CONDENSING GOLD WITH THE MALLET. 
 
 The excessive use of the mallet which was necessary to build 
 out teeth in those early days assisted greatly in producing in- 
 flammation of the peridental membrane and alveolar process in 
 connection with the rapid wedging. I recall a number of in- 
 stances in my early practice where interstitial gingivitis and 
 absorption of the alveolar process occured in neurotic children, 
 the result of malleting in large gold fillings. These cavities w^ere 
 usually located in first permanent molars and sometimes in the 
 
188 INTERSTITIAL (iIN(iIVITIS. 
 
 bicuspid. Absorption of the alveolar process took place, the 
 teeth became loose and (lrop})ed out or were extracted. 
 
 At the present time malleting in lar^^e gold fillings in chil- 
 dren's teeth, especially in neurotic, sypliilitic, rachitic and sim- 
 ilar children should be avoided on this account. The nerve 
 strain, under such barbarous treatment, is very great and the 
 boy or girl suffering from such constitutional conditions should 
 be exempt from such procedure. 
 
 GOLD CROWNS. 
 
 When gold crowns were first introduced about 1880, the 
 method of attachment was to drive the cutting edge of the gold 
 to the alveolar process and disastrous results immediately fol- 
 lowed. Infiammation set in and destruction of the alveolar 
 process, with exfoliation of the tooth, soon followed. Since that 
 time we have learned that gold crowns extending under the free 
 margin of the gums will set up acute inflammation which after- 
 wards becomes chronic and destruction of the alveolar process is 
 sure to follow. 
 
 BRIDGEWORK. 
 
 When a bridge is placed upon two or more roots the function 
 of those teeth has been destroyed. The teeth, owing to the elas- 
 ticity of the peridental membrane, are allowed to yield slightly 
 when pressure is applied in mastication. When they are bridged, 
 they become rigid and the force of the impact in mastication 
 irritates the membrane which together with autointoxication sets 
 up further irritation and inflammation and absorption of the 
 bone takes place. The collection of filth under bridgework is also 
 a fruitful source of inflammation. Particles of food find lodge- 
 ment under bridges and can not be dislodged by either tooth 
 brush or toothpick. 
 
 DEVITALIZING THE PULPS OF THE TEETH. 
 
 Destroying the pulps of the teeth and filling the roots throw 
 extra work upon the peridental membrane. This extra work 
 changes the normal function of the tissues. Poisons circulating 
 in the blood cause an inflammatory process to first attack such 
 teeth and rapid inflammation and absorption occur. 
 
LOCAL CAUSES OF INTEESTITIAL GJINGIVITIS. 189 
 
 CAVITIES IN TEETH AND OVEELAPPING FILLINGS. 
 
 Cavities at the margin of the gums and fillings with rough 
 edges irritate the soft tissues and cause inflammation followed 
 by absorption. 
 
 1,IGATURES AND CLAMPS. 
 
 Ligatures and clamps for holding the rubber dam not infre- 
 quently irritate the gums and set up inflammation. 
 
 ARTIFICIAL DENTURES. 
 
 Partial plates of any description for artificial dentures or 
 regulating plates act as foreign bodies against the mucous mem- 
 brane and gums, producing irritation by heat, by the accumula- 
 tion of foreign substances beneath them and the edge of the plate 
 will irritate the gums about the teeth, thus setting up inflamma- 
 tion. 
 
 INSTRUMENTS. 
 
 Not infrequently instruments used in excavating cavities, fin- 
 ishing fillings, etc., will irritate the gum tissue which will later 
 set up inflamnuition, absorption and finally destruction of the 
 process. 
 
 EXCESSIVE BRUSHING. 
 
 It is not uncommon to find teeth located on the external sur- 
 face of the alveolar process. This occurs in those patients in 
 whom the jaws are small for the long diameter of the teeth. The 
 teeth in erupting will force their way into place and when in 
 their normal condition the dental arch is located upon the outer 
 border of the alveolar process. 
 
 In such patients the bone over the roots of the teeth on the 
 outside is often as thin as writing paper, while it is very thick 
 upon the palatine and lingual side of the jaw. It is not uncom- 
 mon to find the cuspid tooth located toward the outer side of the 
 alveolar process whih' all the other teeth are in their proper 
 places. The nerve and blood supply is almost nil, resistance or 
 restoration is out of the question. 
 
 Under such conditions too great stimulation by the tooth 
 brush causes inflammation and absorption of the outer plate of 
 bone, which in tinre will expose the roots of the teeth. 
 
190 INTERSTITIAL GINGIVITIS. 
 
 PICKING THE TEETH. 
 
 The constant use of the toothpick, irritating the gum margin, 
 is a fruitful source of interstitial gingivitis. This simple pro- 
 cedure is a spendid illustration of the effect of slight irritation 
 producing inflammation of the gum which later becomes chronic 
 with eventual destruction of the alveolar process. 
 
 REGULATING TEETH. 
 
 One of the most prolific sources of interstitial gingivitis is 
 the regulation of teeth. When we consider the nature of the 
 alveolar process and what it is obliged to undergo by the time the 
 permanent teeth have erupted and the sensitive condition in 
 which it is placed as a transitory structure and end organ, after 
 the permanent teeth are in place, together with the unstable 
 nervous system of the patient, as well as the age at which this 
 operation must be performed, the wonder is that after the oper- 
 ation is complete there is any process left. 
 
 The pressure necessary to move the teeth sets up an inflam- 
 mation to produce the entire destruction of bone in line of pres- 
 sure. A third set of teeth in our present phylogenic development 
 is unnecessary and therefore nature is ill prepared, especially 
 in neurotic children with unstable nervous systems, to again 
 build up the alveolar process about the teeth. The degree to 
 which the alveolar process wall be restored will depend upon the 
 condition of the nervous system, the blood and the age of the 
 patient. If the patient is poorly nourished so that material (lime 
 salts) is insufficient or the nerve supply to the part is unstable 
 or the patient has obtained his growth, the process is liable to be 
 deficient in structure. 
 
 This deficiency in structure is easily demonstrable, in persons 
 of middle age or of later life who have had teeth extracted, and 
 a part of the alveolar process has come away. By frequent ob- 
 servation it will be seen that the process is not restored although 
 the periosteum is still present. Again after the extraction of a 
 tooth, although the alveolar process remains normal about the 
 adjoining teeth, a slight absorption of the edges of the alveolus 
 about the cavity will take place. The gums heal over the wound. 
 By the use of a broken excavator, sharpened in a direct line with 
 
LOCAL CAUSES OF INTEESTITIAL GINGIVITIS. 191 
 
 the shaft at the point, this may be readily passed through the 
 soft fibrous tissue of tlie once root cavity. Years after the ex- 
 traction, fibrous tissue without lime salts, is present. The same 
 is true when abscesses have formed. The fibrous tissue is re- 
 stored but not the bone substance. Regulating teeth should be 
 performed before the patient has obtained his growth and with 
 as little movement of the teeth as possible to obtain fairly good 
 results. The indiscriminate spreading of the dental arch with- 
 out extraction should be discouraged. The excessive inflamma- 
 tion set up throughout the entire alveolar process for the pur- 
 pose of enlarging the dental arch and thus bringing all teeth into 
 line is liable to endanger the restorative process. 
 
 I have a record of forty-two patients in whom the teeth re- 
 mained loose from a want of deposition of bone cells to hold them 
 in position and in whom the roots of the teeth were exposed to 
 a greater or lesser extent.' Interstitial gingivitis is always pres- 
 ent and occasionally pyorrhoea alveolaris. The esthetic effect 
 of the large dental arches associated with a small face is not in 
 harmony with good judgment. 
 
 The nerve strain, the inartistic appearance and excessive in- 
 flammation should be reduced to a minimum by adopting such 
 measures as are necessary to perform the operation as quickly as 
 possible with as little nerve strain and with the least amount of 
 work, to avoid interstitial gingivitis. 
 
 The removal of bone in front of the advancing tooth or teeth 
 with a burr (as I have recommended) will save time, prevent 
 undue inflammation, pain, nerve strain, and absorption. 
 
 PLANTATION OF TEETH. 
 
 Plantation of teeth consists of two methods. One the re- 
 placing of a tooth into the ca\T.ty from which it has been acci- 
 dentally removed or a similar tooth has been taken from the 
 mouth of another person, while the other is the insertion of a 
 foreign tooth either into an enlarged natural socket or into an 
 
 G A young woman tineteen years of age called at my office for advice in regard 
 to the restoration of the alveolar process about the six anterior inferior teeth. 
 The bone had been destroyed in regulating. Retaining bands had been in place 
 about two years. The oiierator was afraid to remove the bands for fear that 
 the teeth would drop out. It was impossible to restore the process. 
 
192 INTERSTITIAL GINGlIVITIS. 
 
 artificial alveolus wliicli has been made for its reception. The- 
 replaiitation of a tooth which has been forcibly removed in a 
 healtliy growing child in most cases, if skillfully performed 
 under aseptic conditions, will return to a normal condition with- 
 out chronic infianunation. 
 
 On the other hand, from what we have learned from the un- 
 stable nature of the alveolar process and the many difficulties 
 associated therewith, we hardly expect many favorable results 
 by the enlargement of natural sockets or the formation of new 
 sockets. By these operations the peridental membrane is de- 
 stroyed in the one case and not present in the other. Interstitial 
 gingivitis, with lacunar absorption of the root (which is a foreign 
 body) takes place or absorption of the alveolar process by 
 halisteresis ensues or both with the eventual loss of the tooth. 
 
 If the patient has obtained his growth, the chances of success 
 are hardly to be expected. Especially is this true if the patient 
 has autointoxication or other poisons in the blood or is subject 
 to disease of any of the eliminating organs. 
 
 There are many other irritants, both constitutional and local, 
 not mentioned by the author. Enough have been cited, however, 
 to give the reader a fair idea of the influence of these irritants 
 upjon the alveolar process. 
 
 When inflammation is once established in the gums or alve- 
 olar process by local or constitutional conditions, it is usually 
 progressive as far as the exfoliation of the tooth. If, however, 
 the inflammation is circumscribed and does not extend entirely 
 around a tooth which has one root, or, if only one root of a molar 
 is involved, the inflannnatory process, with absorption will have 
 a limited area and extend only on one side of a single root or 
 may involve only the one root of a molar tooth. This inflamma- 
 tion and absorption will progress to the end of the root. In other 
 words, the disease is progressive after it has become established 
 although treatment both local and constitutional may to a certain 
 limit retard its progress. Illustrations of this may be recalled 
 in those teeth which have been violently wedged apart to obtain 
 room for filling and the inflammation extends along one side of 
 a tooth, or, when gold crowns have been carried under the gums 
 
LOCAL CAUSES OF INTERSTITIAL GINGIVITIS. 193 
 
 and irritation has set up uniformly around the tooth, or, in teeth 
 which have too much pressure in mastication, or, in those teeth 
 for which there are no opposing teeth. The progressive nature 
 of inflammation and absorption is due to the endo-t.ransitory 
 nature of the process. 
 
CHAPTER XVIII. 
 
 CONSTITUTIONAL CAUSES OF INTERSTITIAL GINGIVITIS. 
 
 Pathological changes in the structure and function of the 
 human body, in a more or less severe form, are due to constitu- 
 tional affections. Sometimes they are the result of local diseases 
 of certain organs, or the disease may have general character- 
 istics from the first and still may affect certain individual organs, 
 hence in this way secondary diseases are developed. This has 
 been particularly borne out in trauma, intoxications, contagious 
 infections and some tumor-like forms. 
 
 Diseases are designated as acute and chronic. Acute dis- 
 eases are those of short duration. The acute stage may be ter- 
 minated promptly in recovery or death or it may be prolonged in 
 the chronic period. Disease may occur with or without reducing 
 the tonicity of the body as a whole or a part. 
 
 Fever is a general metabolic disturbance, characteristic of 
 many acute infections and autointoxications. The most impor- 
 tant indication is a rise in the temperature of the body. The su- 
 perficial temperature of a man normally varies considerably but 
 the internal degree of heat is nearly constant. According to the 
 researches of Jurgensen, Ziemssen and Krabler' the minimum 
 internal degree of heat is during the early morning hours and 
 the maximum is reached at about five o 'clock in the afternoon. 
 
 In pyrexia, along with an increased production of heat, there 
 is also an increase of nitrogenous metabolic products excreted 
 in the urine. In regard to heat the amount thrown off varies ; 
 thus in the early stages of fever when the internal temperature 
 is increasing, the surface temperature is below normal with con- 
 tracted vessels and the amount of heat dissipation is lessened. 
 Since the skin produces but a small amount of heat, its warmth 
 is dependent upon the heat brought from the interior of the body. 
 
 1 Thoma, Text-Book of General Pathology. 
 
CONSTITUTIONAL CAUSES OF INTERSTITIAL GINGWITIS. 195 
 
 SO if the skin vessels contract, the amount of blood that flows to 
 the surface is lessened and the temperature of the skin falls. 
 
 The lessened amount of heat thrown off together vntli the 
 greater production causes a rise \\T.thin the body, although aside 
 from a slight feeling of cold, there may be no apparent change 
 in temperature. But if there is marked contraction of the skin 
 vessels, the chilliness is more pronounced, so much that there 
 may be violent shivering of the trunk, limbs and chattering of 
 the teeth. The violent contraction of the skin muscles produces 
 heat. When the fever is at its highest, the contracted cutaneous 
 vessels yield, the skin becomes abnormally dry and hot, while 
 the internal temperature remains high also. When the fever sub- 
 sides, the temperature falls and the skin becomes moist, or there 
 may be an excessive amount of sweat. 
 
 Other symptoms of pyrexia aside from temperature rise are 
 malaise, headache, thirst, rapid pulse and respiration, digestive 
 disturbance and decrease in the amount of urine secreted and 
 passed with abnormal urinary acidity and oftentimes indican. 
 In digestive disturbance, primarily, there is loss of appetite, ex- 
 cessive thirst, the salivary secretions are restricted and the 
 entire alimentary tract becomes so atfected as to prevent normal 
 absorption from the stomach and intestine. The digestive and 
 metabolic disturbance may be less than is usually assumed. Ex- 
 periments show that in typhoid the digestion, absorption and 
 utilization of food may be complete. 
 
 In a search for the connecting etiology of these fever symp- 
 toms we must first take into consideration the infections and in- 
 toxications from which they are derived. Disease producing 
 germs, by their poisons when they enter the blood, cause fever. 
 It may be that many substances produced l)y the metabolism of 
 the human body have similar action. There are also poisonous 
 agents not derived from microbes which cause temperature rise. 
 
 Fever appears to consist of two sets of symptoms, toxemia 
 and pyrexia. The first are due to the direct action on the nervous 
 system while the second constitute a reaction on the part of the 
 system which tends at least to neutralize the effects of the tox- 
 emia. According to the researches of Vaughn, the poisonous 
 substance is a derivative of the albumin molecule resulting from 
 
196 INTERSTITIAL GINGIVITIS. 
 
 a splitting siicli as occurs in digestion or in the destruction of 
 bacteria by the blood serum (bacteriolysis). Thus certain veg- 
 etable proteins, like recin, jjeptones, and the results of the split- 
 ting of bacterial proteins excite fever. Metallic and alkaloidal 
 poisons do not, as a rule, cause fever except by provoking in- 
 flammation which results in secondary bacterial infection. When 
 these poisons are taken into the blood stream, a general faulty 
 metabolism results which gives rise to the symptoms just men- 
 tioned. In regard to the pyrexial rise of temperature, partic- 
 ularly, it must be conceded that the poisons circulating in the 
 blood have a disturbing influence on the structures of the cen- 
 tral nervous system as well as on the vasomotor system of the 
 peripheral nerves. The loss of heat, through the breath, is also 
 controlled by the central nervous system which acts on the fre- 
 quency and depth of respiration. 
 
 The normal heat of the body is produced by every organ in 
 its metabolism. The principal heat producing sources, however, 
 are the heart, muscles and principal abdominal organs. The 
 energy of the heart muscle, when it contracts is exhibited partly 
 as heat and partly as mechanical work. The heat produced by 
 the contraction of the heart is partly radiated into the surround- 
 ing tissues and partly carried away by the blood. In addition, 
 the mechanical work of the heart is completely transformed into 
 heat by friction against the vessel walls and internal friction 
 within the blood stream. The muscles all generate heat by their 
 action. The disturbance of assimilation, digestion and absorp- 
 tion of food occurs at the same time, during fever, with temper- 
 ature rise. This in turn causes metabolic disturbances not only 
 of abnormal products but also a breaking down of organic cells. 
 This may occur in various organs and there may appear any of 
 the cerebral disturbances, such as headache, confusions, dizzi- 
 ness; also rapid decay of the teeth, interstitial gingivitis; ab- 
 sorption of the alveolar process ; diseases and spontaneous death 
 of the pulps of the teeth ; erosion ; abrasion and discoloration. 
 After fevers, loss of the hair and abnormalities in the nails usu- 
 ally make their appearance. 
 
 Degeneration of tissues which form the substance of the 
 heart, liver, kidneys and other structures, are partly due to dis- 
 
CONSTITUTIONAL CAUSES OF INTERSTITIAL GINGIVITIS. 197 
 
 turbances of high pressure and partly due to the direct action 
 of poisons circulating in the blood which have caused the fever. 
 It would not be strange, therefore, that similar degenerations 
 occur as a result of simple action of poisons in non-febrile acute 
 diseases as well as in poisoning by the various inorganic and 
 organic chemical substances. 
 
 Chronic diseases are those of long standing and are usually 
 the result of a prolonged acute condition. Generally there is no 
 rise of temperature though there are instances of pyrexial and 
 apyrexial periods alternating. 
 
 In a general way, I have explained the cause of some chronic 
 diseases, contagions, infections and intoxications, but there are 
 some constitutional disorders, for example, chlorosis, leukaemia, 
 rachitis, obesity, gout, diabetes, osteomalacia whose etiology is 
 still vague, yet are manifested by disturbed metabolism. Path- 
 ologic conditions to which these diseases give rise are many but 
 the two most common are atrophy and malnutrition. One of 
 the best examples of atrophy in the human body is the alveolar 
 process. Atrophy as applied to the tissues and organs of the 
 body is somewhat different in its action on the alveolar process. 
 In all the other tissues and organs, atrophy means a gradual 
 wasting away of structure. While the same condition takes place 
 in the alveolar process, in addition to the wasting away, there is 
 total destruction, owing to the fact that the process is a doubly 
 transitory structure and an end organ. In the mouths of the con- 
 genital deaf, dumb, blind, feeble-minded and delinquent chil- 
 dren, osteomalacia attacks the alveolar process before the 
 osseous system has reached its growth. Here, as a consequence 
 of trophic change, metabolic action and premature senility, 
 osteomalacia may occur in connection with the first set of teeth 
 at two years or any period thereafter. When this condition 
 takes place early in life, I have called it '' juvenile osteomalacia," 
 late in life ' ' senile. ' ' - 
 
 It is those organs of special function which become diseased 
 and atrophy to the greatest extent ; thus in the liver, the cell ; in 
 the kidney, the se'creting epithelial cells ; in the heart, the muscle 
 fibers; in the spleen, the pulp cells; in the subcutaneous tissue, 
 
 ' Pathogeny of Osteomalacia or Senile Atrophy. The Dental Digest, August, 1903. 
 
198 INTERSTITIAL GINGIVITIS. 
 
 the fat cells ; in the lungs, the stroma of connective tissue and 
 elastic fibers, the blood vessels and epithelial lining; in the bones, 
 including the alveolar process, the lamellae; the skin becomes 
 thin and loses its tonicity; the epidermis dry, cracked and scaly; 
 the brain diminishes and the space is filled cither by atrophy of 
 the skull or fluid in the pia-arachnoid. 
 
 Cachexia is characteristic of organ degeneration of a chronic 
 type. In this condition, amyloid degeneration is sometimes as- 
 sociated with albuminous and fatty degeneration of the liver, 
 kidney, heart muscle, etc. The fatty tissue is lost. The epi- 
 dermis, unlike the marasmic states, is smooth and moist. The 
 blood composition becomes changed, in many instances producing 
 capillary hemorrhage or edema. Then, too, the weight of the 
 body and organs is reduced, showing that cachetic conditions 
 are a general disturbance of metabolism. Aside from its chronic 
 character and absence of temperature variability, there are 
 many similar features to those of the pyrexial disturbances of 
 metabolism. 
 
 ACID STATES. 
 
 Having considered the more severe constitutional disturb- 
 ances in which fever is always present, we must now briefly con- 
 sider those constitutional disturbances so fatal to the alveolar 
 process and in which fever does not manifest itself. 
 
 One of the most common causes of irritation producing in- 
 flammation and absorption of the alveolar process is the acid 
 condition of the system. In the human body certain changes are 
 continually taking place. These changes take place in the fluids 
 of the body and are both physiologic and chemic. These changes 
 add to and take away tissues of the body and are alkaline or acid. 
 They are called anabolic when the fluids are alkaline and the tis- 
 sues are built up and katabolic when the fluids are acid and the 
 tissues are broken down. The alkaline and acid states of the 
 body may be ascertained by the examination of the excretions 
 of the body. When the fluids of the body (except the gastric 
 juice) have an excess of acids the saliva, mucus, perspiration 
 and urine will be excessively acid. When the secretions of the 
 
CONSTITUTIONAL CAUSES OF INTERSTITIAL GINGIVITIS. 199 
 
 body are acid it indicates that there is a diminished alkalinity 
 of the blood. This in turn leads to improper functioning and 
 prevents proper nutrition and produces lowered vitality. 
 
 It is known that an acid excess in the system will hinder and 
 often destroy the transmission of nerve impulses. Thus in acid 
 states large areas of skin will be without sensation; the knee 
 jerk is diminished or lost altogether. A continued acid condi- 
 tion of the system mil cause nerve end degeneration in the pulps 
 and fibrillae of the teeth. The teeth will discolor, become brittle 
 and the enamel and dentine will break off. In no part of the 
 body does the excessive acidity manifest itself as in the alveolar 
 process. Its endo-transitory nature makes it very susceptible to 
 irritation through its nerve filaments and its end arteries, set- 
 ting up irritation and inflammation. When the fluids of the 
 body are acid the alveolar process and mucus excreted are, 
 therefore, acid to a greater or less extent, nutrition is thus cut 
 off and absorption of the process takes place. Thus in acid 
 states, as well as in dental states, the alveolar process gradually 
 absorbs away. 
 
 In dealing with the influence of buccal states on the constitu- 
 tion it must be remembered that when the elirainatory system is 
 overstrained, especially when the poison-destroying function of 
 the liver is deficient or impotent, the alveolar process and gums 
 play a great part in elimination, whence come, for example, the 
 "blue" gums of lead poisoning and the "green" gums of brass, 
 as well as those from mercury, arsenic, potassium iodid, bromid, 
 etc. Matter thus eliminated is reabsorbed, enters into the chyle 
 Avith digested products, and readily becomes toxic to the blood 
 cells. That cachetic states, approximating pernicious anaemia, 
 can thus be produced, is clearly evident. Were fecal anaemia 
 existent before the gum and alveolar process changes were set up 
 it would thus be greatly intensified. The toxemia producing this 
 gum and alveolar process state would be greatly increased 
 through the overstrain of oxidizing processes produced by re- 
 absorption of eliminated products. 
 
 The toxins generated in the mouth readily pass into the gen- 
 eral system. As. a result, chronic indigestion with coexistent 
 pigment spots, urticaria, etc., may occur. Pus toxins may thus 
 
200 INTERSTITIAL GINGIVITIS. 
 
 produce a sapremia mimicing typlioid, as pigment spots readily 
 simulate the typhoid eruption. In buccal manifestations of con- 
 stitutional disease the vicious circle of pathology peculiarly 
 occurs. 
 
 The alveolar process may be affected at any period of life 
 after the eruption of the first set of teeth but osteomalacia does 
 not usually occur until the period between twenty-five and thir- 
 ty-five. Before this the osseous system is in its constructive 
 state and lime salts are being deposited rapidly. Later in life 
 the constructive stage is complete and material sufficient only 
 to repair waste is deposited. At the periods of stress metabolic 
 changes are most active — during puberty and adolescence (four- 
 teen to twenty-five), during the climacteric (forty to sixty), 
 when uterine involution in women and prostatic involution in 
 men occur and finally during senility (from sixty upwards), 
 when the disease is always present to a greater or lesser degree. 
 While in allied conditions men are most influenced, in this dis- 
 order the sexes seem to be affected about equally. Here the in- 
 fluence of pregnancy comes into play. Pregnancy disturbs the 
 physiologic balance hitherto existing, especially along the line of 
 assimilation and elimination. The well known dental effects of 
 pregnancy (whose underlying cause affects the alveolar proc- 
 ess) are due to this factor. This is purely a constitutional 
 affection. 
 
 Among the causes are non-elimination of toxic substances, 
 whether due to autointoxication, to bacterial action, or to me- 
 tallic and vegetable drugs. Disorder or disease of any excretory 
 organ (kidneys, bowels, skin or lungs) will produce the most 
 marked effect, first upon the constitution of the blood, and second 
 upon the alveolar process, with resultant osteomalacia. 
 
 The urine, as has been shown, contains each day in a normal 
 individual sufficient toxins to cause death if not excreted. This 
 condition is markedly increased after prolonged nervous ex- 
 plosions like those of epilepsy or hysteria. This was pointed 
 out thirty years ago by Meynert, who demonstrated that the 
 status epilepticus (condition of rapidly-recurring convulsions) 
 was due to the accumulations of a proteid body in the system. 
 The status epilepticus is preceded by a decrease of toxins in the 
 
COXSTITUTIOXAL CAUSES OF INTERSTITIAL GIXGIVITIS. 201 
 
 urine and succeeded l)y an increase. This is likewise true as to 
 the influence of non-elimination by the other excretory organs 
 (bowels, lungs and oral cavity), as well as to the non-exercise 
 of its poison-destroying power by the liver. Xon-elimination 
 moreover interferes with ordinary digestive functions and 
 hence increases its own extent. Another factor in autointoxica- 
 tion is production of toxic products in such quantity as to pre- 
 vent destruction by organs like the liver and consequent elim- 
 ination, since a product to be properly eliminated must be 
 changed to a particular chemical type. Among the factors 
 which affect both these elements of elimination is the power 
 over growth and repair exercised by the nervous system. In 
 part this influence is exerted through control of blood supply by 
 the vasomotor nervous system, and in part by that direct con- 
 trol of the nervous system over tissue change which is known 
 as its trophic function. 
 
 Both influences are affected by nerve strain. Sudden emo- 
 tion may, as Bichat demonstrated decades ago, produce marked 
 defects upon bile secretion and may occasion jaundice. Cases 
 are far from infrequent in which emotions like jealousy pro- 
 duce a mimicry of gall-stone colic in neuropaths. Murchison, 
 Christison and Thompson have traced attacks of biliary colic 
 to jealousy. Other liver changes from sudden nervous disturb- 
 ance, whether of mental type or not, are not rare. As mental 
 impressions are communicated to the central nervous system 
 purely through mechanical changes in the nerves, such influence 
 must be purely material in operation. As the brain exercises a 
 checking influence on the operations of the liver, these mental 
 influences produce two effects. The mental shock increases the 
 checking action of the central nervous system on the local 
 ganglia of the liver, and destroys the checking action of the liver 
 ganglia, and in consequence these go too fast, resulting in their 
 exhaustion. Either of these conditions interferes with the 
 poison-destroying action of the liver, and accumulation of waste 
 products is the result. 
 
 AVhat is true of the liver is true of the other organs. This 
 is especially noticeable, as Tuke points out, in regard to the 
 kidneys. The action of mental anxiety or suspense, in causing a 
 
202 INTERSTITIAL GINGIVITIS. 
 
 copious discharge of pale fluid, is familiar enough to all, espe- 
 cially to the medical student about to present himself for exam- 
 ination, the amount being in a pretty direct ratio to his fear of 
 being plucked. The frequency of micturition may, however, 
 arise from nervous irritability of the bladder without increase 
 or even with diminished secretion. Still the action of the skin is 
 usually checked, the extremities are cold, and the kidneys have 
 to pump off the extra amount of fluid retained in the circulation. 
 Elimination of the substance usually separated from the blood 
 is diminished as compared mth the aqueous character of the 
 whole secretion. The odor may be affected by the emotions in 
 man as in animals. Prout is of the opinion that mental anxiety 
 will produce not only non-elimination but also change in the 
 chemical character, as indicated by odor and otherwise. Disturb- 
 ances in the medulla produce, as Claude Bernard long ago 
 showed, a markedly pale, excessive urine. These disturbances 
 often arise from intellectual strain or emotional shock. The in- 
 fluence of emotional states on secreting processes, and thereby 
 indirectly upon autointoxication states, is illustrated in the fact 
 long ago pointed out by Tuke that pleasurable emotions increase 
 the amount of gastric juices secreted, the opposite effect being 
 jjroduced by depressing passions. Beaumont found in a case of 
 gastric fistula that anger or other severe emotions caused the 
 gastric inner or mucous coat to become morbidly red, dry and 
 irritable, occasioning at the same time a temporary fit of 
 indigestion. 
 
 The influence of fear and anxiety on the bowels is as well 
 marked as that upon the bladder and kidneys. Apart from mus- 
 cular action, defecation may become urgent or occur involun- 
 tarily from various causes. The increased secretion from the 
 intestinal canal may occur from fear and in some cases from the 
 altered character of the secretion itself. While in this respect 
 the influence of fear may be inconvenient in man, it naturally 
 assists escape in some animals, as the skunk. 
 
 Emotions powerfully excite, modify or altogether suspend, as 
 Tuke has shown, the organic functions. This influence is trans- 
 mitted not only through the vasomotor nerves but through 
 nerves in close relation to nutrition and secretion. When the 
 
CONSTITUTIONAL, CAUSES OF INTERSTITIAL GINGIVITIS. 203 
 
 excitement is of peripheral origin in sensory or afferent nerves, 
 it excites tlieir function by reflex action, so that as emotion arises 
 it may excite the central nuclei of such afferent nerves, and this 
 stimulus be reflected upon the efferent nerves, or it may act di- 
 rectly through the latter. Pleasurable emotions tend to excite 
 the processes of nutrition, hence the excitement of certain feel- 
 ings may, if definitely directed, restore healthy action to an af- 
 fected part. Violent emotions modify nutrition. A^arious forms 
 of disease originating in perverted or defective nutrition may 
 be caused primarily by emotional disturliance. Emotions, by 
 causing a larger amount of blood to be transmitted to a gland, 
 increase sensibihty and warmth and stimulate its function or 
 directly excite the process by their influence or nerves supplying 
 the glands. Painful emotions may modify the quality (i. e. 
 the relative proportion of the constituents) of the secretions. 
 
 Imperfect elimination of effete matter from the lungs is a 
 fruitful source of autointoxication. The more marked forms are 
 those of tuberculosis, in which there is great debility and in 
 which there is greater waste than repair. Self-poisoning is con- 
 tinually going on and will continue until death. The chest 
 capacity for the inhalation of pure air is almost nil, hence the 
 blood is improperly oxygenated and soon ceases to convey 
 nutriment to the tissues. Eight per cent of criminals wdio die 
 of tuberculosis in prisons have undeveloped chest walls. De- 
 generacy therefore cuts quite a figure in the role of autointoxi- 
 cation. Degenerates with contracted chest walls are, however, 
 more frequently found. Many undeveloped individuals in every 
 w^alk of life for this reason have tuberculosis. Peojjle with un- 
 developed chest walls and chest capacity may not have tuber- 
 culosis and yet may suffer from autointoxication. Those who 
 have had pneumonia with adhesion; and who are thus unable 
 to oxygenate the blood, are subject to this disease. Asthmatics 
 and hay-fever patients suffer from autointoxication and alveolar 
 absorption. When the skin is overstrained as to excretion 
 through kidney .and bowel overstrain, the lungs are forced to 
 take on increased work with imperfect oxygenation as a result. 
 This is noticed in the odor of the breath in Bright 's disease and 
 in the air-hunger of diabetes, etc. In nerve-strain states and 
 
204 INTERSTITIAL GINGIVITIS. 
 
 in the condition described by Albu not only do excretory organs 
 suffer but the secretions of those glands like salivary and buc- 
 cal glands are so altered as to become irritants. These ex- 
 cretory conditions not only result upon autointoxication states 
 but are modified by trophic nerve function alterations. By 
 trophic changes are meant such tissue alterations as occur in 
 morbid conditions from disordered function of the centers of 
 nutrition. Peripheral as well as central may be involved. The 
 well known law of Wallerian degeneration of nerve fibers is an 
 illustration, the posterior ganglion acting as a trophic center 
 for the fibers of the posterior root in the cord itself. Trophic 
 action may therefore be peripheral, though in extensive changes 
 as a rule central (cerebral or spinal) origin should be looked 
 for. 
 
 The constitutional result of acute and chronic infection and 
 contagions is apt to be an autointoxication plus the action of 
 the germ toxin. All the exanthemata have at times been fol- 
 lowed by wasting or necrosis of the alveolus. Here the con- 
 dition is notably symmetric and accompanied by disorders of 
 the osseous system elsewhere. The same is true of grippe and 
 tuberculosis. The well-marked disorder known as Riggs' dis- 
 ease has been charged by Pierce, Kirk, Rhein, Robin and Magi- 
 tot to the direct influence of an arthritic state (gouty and rheu- 
 matic) and regarded as a special type of arthritic manifestation. 
 The alveolus is clearly vulnerable to the toxins of many infec- 
 tions. It is like\\ise quickly affected by some autotoxic influ- 
 ences from disordered metabolism. Its vital resistance to these 
 agencies is less than that of other tissues. It is the earliest 
 sacrifice when these or any toxins disturb the harmony of the 
 organism. 
 
 A cause other than the actions of toxins exists for impli- 
 cation of these parts. Whenever tissue waste, whether local or 
 general, exceeds repair there is trophic change. This latter 
 depends directly upon disordered local or general nervous func- 
 tions. Trophic alterations from the first cause appear in growth 
 disorders of the nails and loss of hair (alopecia) after fevers, 
 the most familiar obvious examples of this pathologic process. 
 Of the other type are localized atrophies where the direct inter- 
 
CONSTITUTIONAL CAUSES OF INTERSTITIAL GINGIVITIS. 
 
 205 
 
 vention of toxins can be excluded. The alveolus is liable to the 
 first form of trophic deterioration. The influence of acute dis- 
 eases upon the alveolus is probably thus exerted in many cases 
 rather than by direct infection. Where no cause has been as- 
 certained examination directed to this factor would probably 
 reveal it. The general failure of the trophic centers after the 
 prime of life (in senile states), which is attended with loss of 
 teeth and wasting of the alveoli, is the most obvious instance 
 of trophic failure atfecting the part. Even simple anaemia may 
 thus give rise to alveolar wasting. 
 
 Another constitutional disorder in which the alveolus is 
 early affected is diabetes. The exact pathology of this is un- 
 
 HH^H 
 
 ■i-"-"- 
 
 r 
 
 
 i 
 
 >-^ 
 
 ** 
 
 ^ 
 
 
 'M^^ 
 
 ■..■■'' .vfcM '4. 
 
 Fig. 75. — Absorption by Halisteresis. Three Small Arteries are Seen. Two 
 IN the Upper Part of the Illustration with Eound Cell Inflammation Just 
 Beginning, while Another Small Artery is Located at the Lower Border 
 of the Large Absorbed Area. 
 
 certain, but in many cases at least it is largely dependent on 
 disordered action of the central nerve system. Renal disease 
 is another common condition which tests the vulnerability of the 
 alveoli. An ideally normal kidney is probably rare, but only 
 when its abnormalities pass beyond a certain point can it be 
 called diseased. . In the less advanced conditions that have 
 passed the line of morbidity, alveolar implication is often very 
 
206 INTERSTITIAL GINGIVITIS. 
 
 marked. This may be one cause of the unusual frequency in 
 the insane, who are especially liable (as Bondurant and others 
 have shown) to suffer from renal disease. They are very liable 
 likewise to autointoxications and trophic disorders as well, 
 since the balance of the nervous system has been upset. Some 
 (the paretic and organic dements) exhibit especial tendencies 
 to trophoneurotic disturbances affecting- the teeth. In states of 
 depression and stupor, circulatory disturbances predispose to 
 these. 
 
 The constitutional results of acute and chronic infections 
 are apt to include autointoxication in addition to the action of 
 the toxins of their germs. The eruptive fevers, especially 
 scarlatina or measles, have been long known to be followed by 
 wasting or necrosis of the alveoli. Here the condition is notably 
 symmetrical and unaccompanied by exfoliation or necrosis of 
 the osseous system elsewhere. Tuberculosis does not spare 
 the alveolar process. 
 
 The more marked forms of constitutional disorders (typhoid 
 fever, pneumonia, tuberculosis, syphilis, inthgestion and preg- 
 nancy, etc.) produce intense results. 
 
 The second form of trophic failure in the alveolus is less 
 prominent, since it generally coexists with overshadowing dis- 
 turbance elsewhere which it creates to a certain extent. Cruvei- 
 lier noticed its occurrence associated with simple paraplegia, 
 regarding it as of nervous causation. In facial hemiatrophy 
 local wasting of the alveolus has appeared before the disorder 
 has involved the jaws generally. This is sometimes due to a 
 local cause, but its occurrence and association with other neuro- 
 trophic symptoms are suggestive. 
 
 We have seen that the action of the heart plays quite a role 
 in the constitutional diseases of the body. Constitutional dis- 
 eases affecting the heart and diseases of the heart itself cause 
 excessive and diminished action of this organ. This excessive 
 and diminished action causes changes in the flow of the blood 
 in the peripheral capillaries. Those organs first involved in 
 this change of heart pressure are the end organs of the body. 
 The alveolar process, therefore, being the most sensitive end 
 
CONSTITUTIONAL CAUSES OF INTERSTITIAL GINGIVITIS, 
 
 207 
 
 organ, because of its transitory nature and its bony substance 
 is one of the first to be involved in autointoxication. 
 
 In intestinal putrefaction, hepatic and renal insufficiency and 
 drug poisoning as well as in other diseases, the heart becomes 
 enlarged and a high blood pressure is developed. Dilation of 
 the arteries occurs, especially in those of end organs, resulting 
 in arterio-sclerosis, which is present in every case. 
 
 Fig. 76. — Shows Bone Absorption p.y Halisteresis, and Volkman 
 Canal Absorption. 
 
 To ascertain the blood pressure in patients suffering with 
 interstitial gingivitis I used Cook's modification of the Riva 
 Rocci sphygmomanometer, this instrument being best adapted 
 for my convenience and exceedingly simple. The armlet used 
 was sold with the instrument and consists of a rubber bag 4I/2 by 
 40 cm. The patients ranged from twenty-seven to sixty-seven 
 years of age. With this instrument the normal adult female 
 arterial blood pressure is 115 to 125 mm. ; adult male, 125 to 
 135 mm. 
 
 In twenty-six females there were three who ranged between 
 115 mm. Hg. and 125 mm. Hg. and therefore normal. Three 
 
208 
 
 interstitljlL gingivitis. 
 
 ranged below 115 iiini. Hg., and twenty from 133 mm. Hg. to 
 180 mm. Hg. 
 
 In twenty-fonr males there were eight who ranged between 
 125 mm. Hg. and 135 mm. Hg. and therefore normal. Three 
 ranged below 125 mm. Hg., and thirteen from 133 nnn. Pig. and 
 160 mm. Hg. 
 
 When we consider that thirteen of these patients were nn- 
 der forty-five years of age, the high blood pressure is remark- 
 able. 
 
 I have been unable to demonstrate Avhether the interstitial 
 gingivitis is accelerated directly because of the poisons circulat- 
 
 /io.7. 
 
 Fig. 
 
 '. — Illustrates Lacunae or Osteoclast Absorption. 
 
 ing in the blood vessels, causing high blood pressure by their 
 action upon the heart, or because of their action upon the vaso- 
 motor nerve governing the heart or blood vessels, or both. The 
 effect of the toxins and extra blood pressure is to set up irrita- 
 tion and inflammation of the outer surfaces of the Haversian 
 canals, producing halisteresis in the vessels of Von Ebner, pro- 
 ducing Volkmanns' perforating canal absorption and setting the 
 osteoclasts at work, all producing absorption of the alveolar 
 process. 
 
CONSTITUTIOXAL CAUSES OF INTERSTITIAL GIX(;IVITIS. 
 
 209 
 
 The question arises, which end organ is the most susceptible 
 and first involved in autointoxication! When a man visits 
 the physician for treatment one of the first questions asked is, 
 "What is your occupation?" If the man replies that he is 
 working in drugs, metals or mines, the physician examines his 
 patient's gums to note if his system be saturated with poisons. 
 If a physician is treating a patient for lues, the drug is adminis- 
 tered until the "gums are touched," which is the only indica- 
 tion his patient is under the influence. One of the most marked 
 symptoms of scurvy is the inflammatory condition of the gums 
 and alveolar process, which are always taken into consideration 
 in diagnosis. 
 
 Fig. 78. — Loaver Portion' Showing Absorption of the Alveolar Process 
 Below the Boots of the Teeth. 
 
 Physicians agree that the arteries in sucli end organs as the 
 kidneys, brain and retina dilate under blood pressure. The 
 arteries ramifpng bone structure, dilate only imperfectly, if 
 at all. Arteries entering transitory bone structures gradually 
 undergo pathologic changes. After the individual has obtained 
 his growth these arteries certainly are more susceptible to toxin, 
 poison and blood pressure than those in the kidney, brain 
 or retina. I have demonstrated these pathologic changes in 
 the alveolar process many times. The toxic products circulat- 
 ing in the blood affect the heart and cause a high blood pressure. 
 
210 INTERSTITIAL GINGIVITIS. 
 
 High blood pressure, together with toxic products circulating 
 in the blood, set up inflammation in the alveolar process and 
 gingival border. In the alveolar process, tirst, because the ar- 
 teries in the soft gum tissues, under high blood pressure, can 
 and do expand and the tissues recover as soon as the cause is 
 removed, but the arteries running tortuously through the bone 
 cannot expand to any appreciable extent, and the blood pressure 
 and toxic products cause inflammation and absorption of bone 
 tissue without restoration. Hence the term ''interstitial gin- 
 givitis" (deep-seated inflammation in the alveolar process). 
 Cardio vascular, nervous, hepatic and renal diseases, as re- 
 lated to interstitial gingi\dtis, are therefore due to the same 
 cause. In relieving or removing the cause of interstitial gin- 
 givitis the other symptoms and diseases are relieved, and vice 
 versa. 
 
 Figure 75 illustrates a large area of absorption with destruc- 
 tion of the fibrous tissue to a larger extent. Around the border 
 is seen a small amount of inflamed fibrous tissue. An artery, 
 once an Haversian canal, is also seen. About the large area 
 are also seen three Haversian canals with the inflammatory pro- 
 cess just beginning. 
 
 Figure 76 shows four centers of absorption at Haversian 
 canals. Through the picture may be seen dark lines running in 
 all directions. These are vessels of Von Ebner, through which 
 Volkmann's canal absorption takes place. A beautiful illus- 
 tration of this is the canal running from one large area of 
 absorption to the other. 
 
 Figure 77 shows the third form of bone absorption — lacunas 
 or osteoclast absorption. Here a large area of bone is destroyed 
 by these large cells. 
 
 Figure 78 is a low power, showing the distribution of the 
 alveolar process between the roots of two teeth. Very little 
 of the bone remains. When the trabeculae or fibrous tissue is 
 destroyed in large areas, and especially in transitory struc- 
 tures, it is rarely restored. 
 
CHAPTER XIX. 
 
 CLIMATIC INFLUENCES IN INTERSTITIAL GINGIVITIS. 
 
 One of tlie simplest forms of constitutional disturbances 
 which produce interstitial gingivitis is that of climatic changes. 
 The effect of climate which includes heat, cold, moisture, dryness 
 is generally recognized by physicians as having much to do with 
 the action of disease upon the system. To such an extent has 
 this subject been impressed on the profession that the late Dr. 
 N. S. Davis of Chicago, many years ago organized a separate 
 section in the American Medical Association on Climatology, 
 while every medical congress has its section on Tropical Medi- 
 cine. If this subject is of so much importance in the cause and 
 treatment of disease, especially in its influences upon the ex- 
 cretory organs, how much more important must it be in relation 
 to interstitial gingivitis, since the alveolar process, being a 
 doubly transitory structure and an end organ, is always the 
 first affected by sudden and prolonged changes. 
 
 Experiments have shown that cold acts as a stimulant and 
 increases the amount of carbonic acid exhaled, while experiments 
 made by Dfluger and Marcet also show that a similar increase 
 from heat would produce the same result. Both cold and heat 
 then to a certain point act as stimulants. 
 
 The judicious change in climate, that is, moving in winter to 
 warmer climates and vice versa, taking into consideration mois- 
 ture, light, rarification or condensation of air and the increase 
 by the variations in the manner of life and hygiene may prove 
 beneficial or disastrous according as the organs respond to the 
 changed environment. 
 
 In low temperature, the body loses more heat and the loss 
 must be supplied. The older the individual the more marked 
 is the effect of excessive cold and heat. The effects upon the 
 individual are the same as in high temperatures, in part through 
 local injury and death of tissue, in part through refrigeration 
 of the entire body. Severe and lasting lowering of tempera- 
 
212 INTERSTITIAL GINGIVITIS. 
 
 ture causes tissue death; after mild chilling has occurred, as 
 the result of tissue degeneration, thrombosis, hyperaemia and 
 exudations which are relatively rich in leucocytes. A very short 
 refrigeration at the freezing point is sufficient to produce de- 
 generative changes which are quickly followed by regenerative 
 proliferation on the part of the cells remaining uninjured. Tips 
 of the extremities, nose, ears, fingers, feet and toes, are the most 
 easily frozen because of their extreme distance from the heart. 
 
 According to Ziegier, '' Besides the more severe forms of 
 local or general lowering of the tissue temperature there may 
 occur, as harmful pathogenic influences, mild, general or local 
 chillings, the so-called colds, as the result of which disease- 
 phenomena may manifest themselves partly at the seat of chill- 
 ing, partly in organs in distant parts of the body. For example, 
 after widespread refrigeration of the skin there may occur 
 diarrhoea, catarrh of the respiratory tract, or disease of the 
 kidneys; after local chilling of the skin, painful affections of 
 the deep-seated muscles. The exact relation between these phe- 
 nomena and the refrigeration is unknown (the oft repeated 
 hypothesis that they are due to hyperaemia of the internal or- 
 gans caused by the chilling of the body surface has not been 
 proven), but there is no reason on this account to deny the exis- 
 tence of diseases caused by cold. Though many diseases for- 
 merly attributed to "catching cold" have been known to be 
 of infectious origin, there yet remain a number of diseased con- 
 ditions for which we know no other etiology than that of 
 refrigeration. Conditions of the body in which the skin is hy- 
 peraemic and the perspiratory function active favor the taking 
 of cold. Many individuals appear to possess a predisposition 
 on the part of certain tissues to the effects of refrigeration ; in 
 one person certain muscles, in another the mucous membranes 
 will be affected. 
 
 According to the view of many writers, refrigeration of the 
 body increases the susceptibility to infection, so that, for ex- 
 ample, the pathogenic bacteria which may be present in those 
 cavities of the body accessible from without, may, after such 
 refrigeration, be able to exert their injurious influences upon 
 the tissues." 
 
CLIMATIC INFLUENCES IN INTERSTITIAL GINGIVITIS. 213 
 
 There is a great difference between radiated or sun heat and 
 shade heat. Sunstroke is rare in the pure and comparatively 
 dry air of high elevation. The same is true on the ocean. Shade 
 heat, on the other hand, can be borne less easily. One can do 
 hard work in the sun heat when one would rapidly become ex- 
 hausted in shade heat at one-third the temperature. People 
 bear heat very differently. The manner of living must neces- 
 sarily be taken into consideration. It has been shown that Eu- 
 ropeans who go to live in hot climates are injured by continuing 
 the same kind and amount of food and stimulants as they are 
 accustomed to use at home. Parkes says, ''great heat in shade 
 exerts a depressing influence lessening the great functions of 
 digestion, respiration, sanguinification and directly or indirectly 
 the formation and destruction of tissue." 
 
 Dr. G. D. Boak states as to Philippine climatic effects upon 
 the teeth: "While the weather is by no means as hot as it is 
 at times during the summer in the States, the average tempera- 
 ture for the islands is about 89° F. It is a continuous heat Avith- 
 out invigorating change of seasons. This gradually saps vital- 
 ity and enervates, producing the lassitude which is characteris- 
 tic of the tropics. Enervation produces anaemia, with corre- 
 sponding lessening of the resisting powers from the lower 
 vitality, especially in those who have lived previously in tem- 
 perate climates. Caries is frequent and progresses rapidly 
 in this climate." This Dr. Boak attributes to the follomng 
 causes: First, lowering of the vitality by a lessening of the 
 resisting powers ; second, acidity of the oral secretions. 
 
 Among important factors to be considered in connection with 
 hygiene in the tropics are the questions of dietetics as well as 
 the effects of moist and dry heat. The two last produce, as 
 elsewhere shown, a neurasthenia with co-existing and complicat- 
 ing autointoxication. These two peculiarly affect the alveolar 
 process. It is, therefore, not remarkable to find in a recent 
 report by General Otis, the case of Walter Fitzgerald, Com- 
 pany C, twenty-ninth infantry, formerly of the Montana volun- 
 teers, cited. This twenty-three-year-old man had been in the 
 Philixjpines for a, year and seven months. He was one of the 
 first volunteers to reach Manila after the naval battle. Nine- 
 
214 
 
 INTERSTITIAL GINGIVITIS. 
 
 teen months' life in the tropics on the usual army rations had 
 resulted in the loss of nearly every tooth. While the climate 
 undermines nutrition of the alveolar process, and tropical fevers 
 have the same effect, improper diet increases the defect. In the 
 case of Fitzgerald, the teeth dropped out one by one, as is com- 
 monly the case with Americans in the Philippines. 
 
 Soldiers going from a temperate climate to Cuba and the 
 Philippines with change of food, had autointoxication and in- 
 terstitial gingivitis. 
 
 In an examination of the soldiers and officers of two com- 
 panies who had just returned from the Philippines, located at 
 Fort Sheridan, Illinois, I obtained the following results: The 
 total number examined was 127. American, 98; 'Irish, 12; 
 German, 9; English, 3; Norwegian, 1; South American, 1; 
 Danish, 1; Russian, 1; Cuban, 1. The ages ranged from 21 to 
 52. By ages the following data was obtained : 
 
 Age 
 
 Disease 
 
 Age 
 
 Disease 
 
 Age 
 
 Disease 
 
 21 
 
 8 
 
 32 
 
 7 
 
 43 
 
 1 
 
 22 
 
 5 
 
 33 
 
 1 
 
 44 
 
 1 
 
 23 
 
 17 
 
 34 
 
 2 
 
 45 
 
 none 
 
 24 
 
 12 
 
 35 
 
 none 
 
 46 
 
 1 
 
 25 
 
 15 
 
 36 
 
 1 
 
 47 
 
 1 
 
 26 
 
 9 
 
 37 
 
 7 
 
 48 
 
 none 
 
 27 
 
 4 
 
 38 
 
 1 
 
 49 
 
 none 
 
 28 
 
 8 
 
 39 
 
 3 
 
 50 
 
 1 
 
 29 
 
 11 
 
 40 
 
 none 
 
 51 
 
 none 
 
 30 
 
 5 
 
 41 
 
 none 
 
 52 
 
 1 
 
 31 
 
 4 
 
 42 
 
 1 
 
 
 
 Total: 18 none; marked 36; medium 27; slight 46. Per- 
 centage : 14.1 none ; 28.3 marked ; 21.2 medium ; 36.2 slight. 
 
 In studying these figures it will be noted the largest number 
 of cases of interstitial gingivitis occurred between the ages of 
 21 and 30, the period of life at the constructive stage when the 
 disease should not be present. Those over forty were nearly all 
 officers who took better care of the mouth. It must be also noted 
 these men lived most of the time in the open air. In the Amer- 
 ican army mostly young men are enlisted. It will be seen that 
 the effect of climate and food is very severe.^ 
 
 Even in moderate temperatures where changes of climate 
 
 The Dental Summary, 1903. 
 
CLIMATIC INFLUENCES IN INTERSTITIAL GINGIVITIS. 215 
 
 have taken place, strong persons, after long exposure to such 
 temperatures, undergo a certain degree of lassitude, diminution 
 of appetite and impairment of functions of digestion, respira- 
 tion, circulation and metabolism. On the other hand, it is also 
 true that weak persons may gain in weight and the functions of 
 the mind and body be much improved. 
 
 The sudden changes in temperature and atmospheric pres- 
 sure, such as mountain climbing, balloon and aeroplane ascen- 
 sion, may cause great exhaustion, palpitation of the heart, ir- 
 regular breathing, unconsciousness, and sometimes vomiting, 
 ^^ith bleeding of the gums. It is claimed by some research 
 workers that the capillaries of the lungs are unable to take up 
 sufficient oxygen from the liighly rarified air. According to 
 the investigations of Schumburg and Zumtz it appears that a 
 given amount of labor calls for a greater amount of oxygen in 
 an increased elevation than in a lower level. It would seem, 
 however, that the sudden changes from moderate to extreme 
 cold or heat act upon the body in such a manner that the elim- 
 inating organs are unable to adjust themselves quickly to the 
 new environment. The result of this is that autointoxication 
 takes place and faulty metabolism is produced. 
 
 During the building of the Gornergrat Eailway in Sv\^tzer- 
 land, it was found that at a height of three thousand meters, 
 the capacity of the laborers was diminished to one-third. Ac- 
 cording to the researches of Egger, Miescher and others, a so- 
 journ in high altitudes leads, after a short time, to an increase 
 in the number of red cells and a greater haemoglobin content in 
 the blood. 
 
 Hafner ' of Zurich has recently shown that ''the engineers 
 and workmen on the Jungfrau railway, obliged to remain a con- 
 siderable time at altitudes of about 2,600 meters above the sea 
 level, are liable to a disagreeable complaint. After eight or ten 
 days they are seized v\dth violent pains in several teeth on one 
 side of the jaw, the gums and cheek on the same side becoming 
 swollen. The teeth are very sensitive to pressure, so that mas- 
 tication is extremely painful. These symptoms increase in 
 
 *Die Natur, 1900. 
 
216 INTERSTITIAL GINGIVITIS. 
 
 severity for three days and tlien gradually and entirely dis- 
 appear. It seems to be purely a phenomenon of acclimatization. 
 All new comers pass through the experience and the disorder 
 never recurs." The influence of heat, of cold and of the baro- 
 metric pressure shown in a lesser degree in "mountain fever" 
 produce systemic disturbance of metabolism which, causing 
 autointoxication, markedly affect the alveolar process, producing 
 interstitial gingivitis. 
 
 The author has examined the mouths of the workmen on the 
 Jungfrau, Gornergrat and Pillatus Railways at various times 
 and can confirm the statements made in regard to the condition 
 of the men as stated above. The quality of food, the unhygienic 
 condition of the mouth and high altitude have acted severely 
 upon the alveolar process, causing the teeth to loosen and drop 
 out. While the pathology is similar to scurvy, the other consti- 
 tutional symptoms, associated with scurvy, are not observable 
 in these patients. 
 
 When the Government authorities made their report on the 
 survey of the State of Minnesota many years ago, they made 
 the claim that it was impossible for human beings to live the 
 entire year in that state owing to the extreme cold in wdnter. 
 It is now known that in the Northwest, owing to the extreme cold 
 in winter, people who live in exceedingly hot rooms suffer from 
 the extremes of cold and heat and are subject to more severe 
 interstitial gingivitis than those in more moderate temperatures 
 in the United States. 
 
 The results of these extremes in temperature produce many 
 affections of the heart from a want of quick adjustment of the 
 eliminating organs to the new environment. In high altitudes 
 and cold climates, the skin contracts and elimination of the body 
 waste is thrown upon the internal organs, and vice versa in 
 warm climates. 
 
 The result is that in these sudden extremes, the functions of 
 the body are slow in adjusting themselves to environment, nutri- 
 tion is interfered with, vitality is lowered and the structures of 
 the body are affected in the order of their sensibility to auto- 
 intoxic states. The peripheral nerves are usually the first in- 
 volved; then the arterial coats and the blood stream are inter- 
 
CLIMATIC INFLUENCES IN INTERSTITIAL GINGIVITIS, 217 
 
 fered with. Transitory structures and end organs thus receive 
 the first impulses of faulty metabolism. 
 
 This sets up an inflammation in the capillaries of the alveolar 
 process. No matter how short a time the cause may exist, if the 
 inflammation is once set up, owing to its peculiar action on the 
 alveolar process (even though the cause be removed), inter- 
 stitial gingivitis becomes chronic and the destruction of tissue 
 continues. 
 
CHAPTER XX. 
 
 SCURVY IN INTERSTITIAL GINGIVITIS. 
 
 Scurvy is due to poor food and improper hygiene. Insuffi- 
 cient alternation of food, impure air, want of bodily exercise, 
 ennui and uncleanliness combine to form the causes of this dis- 
 ease. Previous to the introduction of canned goods, sailors on 
 long voyages, prisoners and others under confinement were 
 subject to scurvy. Lunatics, idiots or persons who have had 
 long illness, and find it difficult to regulate their diet, are now 
 most prone to it. Anaemic convalescents from protracted fevers 
 suffer from it. Bottle-fed babies and occasionally those fed at 
 the breast on non-nourishing milk are prone to the disease. 
 
 In the British Arctic Expedition of 1875-76 over forty-eight 
 per cent of the men suffered from scurvy. When the potato crop 
 failed in Ireland, in 1846, scurvy became prevalent. In the 
 Crimean war 23,000 cases occurred among the French troops 
 alone. Scurvy contributed over fifteen per cent to the death rate 
 in the late civil war. It occurs among the Klondyke miners. 
 
 Thomas Barlow found scurvy associated with rachitis. Sun- 
 derland found that rachitic diathesis was a very strong factor. 
 Jacobi reports forty cases of scurvy and rachitis. Babies in 
 good families brought up solely on the proprietary infant foods 
 are prone to scurvy. They lose their appetites, become pallid, 
 perspire freely, have diarrhoea, the mouth becomes sore, with in- 
 flamed mucous membrane and gums. Purpura and hemorrhages 
 of mucous membrane are common with pain and swelling of the 
 joints. 
 
 Just how far scurvy may be associated with extreme changes 
 in climate in relation to interstitial gingivitis is an open question, 
 but soldiers going from one climate to another, as exampled by 
 American soldiers to Cuba and the Philippines, and British sol- 
 diers to South Africa and India, are more subject to scurvy 
 
 ^Brit. Epidemiological Society, Feb. 19, 1904. 
 
SCURVY IN INTERSTITIAL GINGIVITIS. 219 
 
 from improper food than native soldiers. Mayer Coplans ^ of 
 tlie British Army Medical Service states, in regard to the South 
 African War, that scurvy developed among the local population, 
 in the concentration camps, fed upon Government rations which 
 were of fairly good quality. The concentration of native women 
 and children in camps containing about 5,000 persons, forty- 
 eight per cent of children under twelve years of age contracted 
 the disease. Among adults the women were to the men as three 
 to one. Enclosed by barbed wire, the camps, though open and 
 airy, were securely isolated. The conditions being identical the 
 varying incidence of scurvy was remarkable. Between March, 
 1901, and .Tanuary, 1903, with no cases at Standerton or Volks- 
 rust, there were one hundred Europeans and one native attacked. 
 Among the soldiers at Standerton and the 22,000 European 
 patients admitted to the hospital there was but one; among the 
 natives in the service of the troops there were attacked 32 per 
 cent of 400 muleteers, 22 per cent of those attached to the Hus- 
 sars and the Eoyal Artillery, 87 per cent of the scavengers en- 
 gaged in removing carcasses of animals, 17 per cent of the 
 porters and about 50 per cent of the muleteers in the employ of 
 the repatriation department. 
 
 The heaviest incidence of scurvy was after the close of the 
 war and when all restriction on food had been removed. In fact, 
 it had no relation whatever to the food but was almost every- 
 where directly in proportion to the neglect of cleanliness, of 
 which the natives had not the most rudimentary notions, espe- 
 cially as regards the hygiene of the mouth. Even the outbreak 
 among the burghers at Middleburg followed overcrowding and 
 neglect of sanitation. 
 
 A. E. Wright, in discussing the subject, said filthy habits 
 were not peculiar to the Kaffirs, and were not always accom- 
 panied by scurvy, which occurred in the nurseries of the rich and 
 in nursing homes. Scurvy was essentially an acid intoxication, 
 a reduction in the alkalinity of the blood which can be observed 
 long before the grosser manifestations, alike in the adult and 
 infantile forms. A large proportion of the troops returning from 
 South Africa were scorbutic in the latent stage. 
 
220 INTEESTITIAL GINGIVITIS. 
 
 K. B. Goadby also, in a discussion of the subject, said he had 
 not seen any scurvy at the Dreadnaught Hospital, but had met 
 much pyorrhoea alveolaris, a disease endemic and occasionally 
 epidemic in West and Central Africa, the Transkei, the Philip- 
 pines and other places. This condition of the gums and the rapid 
 recovery of the patients under antiseptic measures resembled 
 that found in scurvy. 
 
 Coplans pointed out in reply that it required months for 
 its development, for the members of the corps that suffered 
 most were recruited in their homes in October and the corps was 
 dissolved in December, the disease breaking out soon after their 
 arrival in the camp. Recovery followed rapidly on purely local 
 treatment in the way of buccal antiseptics without any attempt 
 to influence the blood. 
 
 The term ''scurvy" frequently employed in this discussion is 
 applied to the disease of the mouth, especially in relation to the 
 gums. Nothing is said in regard to other symptoms of the body, 
 which would be necessary in order to make a clear diagnosis of 
 scurvy. The logical inference is that such were not present. 
 
 Polar expeditions led to the conclusion that a diet of fresh 
 or even raw meat, without any food or vegetables whatever, 
 and associated with hardship, dirt and misery, or one consisting 
 entirely of tinned, preserved and sterilized foods of the highest 
 quality but with no fresh food, animal or vegetable, did not pro- 
 duce symptoms of scurvy, while scurvy appeared when, along 
 with potatoes, etc., and daily doses of lime juice, the bulk of the 
 food consisted of ordinary salt beef or pork. Until the recent 
 Antarctic expedition, from that of Xordenskjold in the Vega, 
 none had been attacked by scurvy except that of Jackson, whose 
 men remained on board the ship where they had lime juice, po- 
 tatoes, etc., but refused the coarse, even "gamey" bear's flesh, 
 on which alone the exploring party subsisted. All were attacked 
 with scurvy, two, indeed, dying. The Laplanders of Finland 
 bartered for farinacea, etc., but ate their fish putrid by prefer- 
 ence, and suffered much from scurvy. 
 
 In scurvy there is inflammation and bleeding gums; the 
 gums puff up, thicken and bleed easily; the teeth become loose 
 and sore upon mastication ; a disagreeable odor comes from the 
 
SCURVY IN INTERSTITIAL GINGIVITIS. 221 
 
 mouth; salivation or ptyalism results from irritation of the 
 teeth, as well as scorbutic anaemia; the patient is languid or 
 tires, perspires freely upon exertion, has shortness of breath and 
 palpitation of the heart; the face is ashy gray, becoming paler 
 each day ; hemorrhage takes place in dilTerent parts of the body, 
 especially beneath the skin, in the muscles and beneath the peri- 
 osteum, as well as in the joints. This often gives considerable 
 pain and sometimes causes inflammation, with resultant pus in- 
 fection. Occasionally hemorrhage takes place in the internal 
 structures. The temperature varies and botli febrile apyretic 
 states occur. 
 
 On the other hand, the symptoms observed in interstitial gin- 
 givitis are confined to the gums and alveolar process. There 
 are no constitutional symptoms. This disease was formerly 
 known as pyorrhoea alveolaris because the disease was not recog- 
 nized until pus was observed about the teeth. It frequently ex- 
 ists for years before pus is noticed. All the teeth may be lost 
 without pus. 
 
 From what has been said, it would seem rather difficult to 
 assume that these mouth conditions herein described were en- 
 tirely due to scurvy. Changes in climate and environment must 
 be considered in relation to the interstitial gingivitis as well as 
 unhygienic conditions. 
 
 It is common to find scurvy in private and state institu- 
 tions w^here many people are confined, due to a monotony of food. 
 The following scorbutic case was referred to me by Dr. George 
 W. Johnson : A twenty -five-year-old American was admitted to 
 Cook County Hospital for the Insane December 2, 1892, suffer- 
 ing wdth melancholia, attended by delusions of persecution and 
 suicidal tendencies marked by refusal of food. June 1, 1896, he 
 again began to refuse food, but took liquid diet on persuasion. 
 June 29, the patient was transferred to the hospital because of 
 his emaciation and scorbutic symptoms were discovered. July 
 18, the constitutional and local symptoms of scurvy were well 
 marked. The teeth were covered with sordes and loosened. 
 Under antiscorbutic treatment these symptoms had fully dis- 
 appeared by August 13. Through the kindness of Dr. Johnson 
 I was allowed to see this patient. I found none of the teeth very 
 
222 INTERSTITIAL GINGIVITIS. 
 
 loose, showing the disease was superficial. I removed two teeth 
 that were decayed and the most loose. These were prepared 
 for the microscope in the usual way. The gums and peridental 
 membrane were in an active state of inflammation. Small blood 
 vessels were observed in different localities with round cell 
 infiltration extending into the tissue. The root of the right 
 superior second bicuspid, with peridental membrane attached, 
 showed active inflammation about an artery which had thick- 
 ened, and an area of tissue degeneration, forming an abscess. 
 The interstitial gingivitis due to scurvy, drug or self-poisoning 
 lias tlie same pathology. 
 
CHAPTER XXT. 
 
 TOXIXS PRODVCIXG TROPHIC CHANGES. 
 
 The retrograde disturbances of nutrition lead to degeneration 
 of the affected tissue. Tissue infiltrations are due to deposits in 
 the tissues of pathologic substances which have either been 
 formed "within the body or introduced into it from without. 
 These disturbances of nutrition may affect the alveolar process 
 during its period of development and growtli, l)ut more partic- 
 ularly in a fully developed state. 
 
 Poisons may be di\dded according to their action into three 
 groups: First, those producing local tissue changes; second, 
 those acting injuriously upon the blood; third, those affecting 
 chiefly the nervous system and the heart without producing 
 recognizable anatomic lesions. The poisons of all these groups, 
 acting on the alveolar process, either by producing irritation of 
 the blood vessels or by disturbing nutrition because they are 
 stored in the tissue by producing trophic and vasomotor changes 
 through their action on the nerves, work toward the ultimate end 
 of its destruction. 
 
 All causes which bring about stasis of blood in the capillaries, 
 such as inflammation, pressure, hemorrhage or blocking the 
 venous outflow from the part, will cause arrest of nutrition. 
 Again, if the arterial supply be cut off from any cause, destruc- 
 tion of the process will take place. Arrest of circulation need 
 not be permanent. It suffices for its evil effect if it persists for a 
 certain time. The more highly specialized a tissue, the briefer 
 its vitality when deprived of blood; thus, when the blood supply 
 is cut off, absorption of the alveolar process takes place before 
 the circulation can be re-established. This is more than likely 
 to take place in the alveolar process since it is a doubly transi- 
 tory structure and an end organ. 
 
 Under the influence of poisons of all kinds, the alveolar proc- 
 ess is liable to be absorbed. The result depends on the condi- 
 tion of the patient and the severity of the poison. The lowering 
 
224 INTERSTITIAL GINGIVITIS. 
 
 of vital resistance is proportional to the depth of the poisoning, 
 and the weakened condition of the tissue invites microbic infec- 
 tion and multiplication, affording a suitable soil for invading 
 micro-organisms which lead to the development of pyorrhoea 
 alveolaris. This is true of the poisons entering the arteries of 
 the process which cause an increased pressure of blood. 
 
 The toxins which leave an indelible stamp upon the alveolar 
 process are divisible into those belonging to the condiments, 
 foods, beverages, drugs, and those arising from occupation. 
 Tobacco, alcohol, tea, coffee, opium, cocoa, cocaine, as well as 
 mercury, lead, brass, potassium iodid, phosphorus, sodium 
 chloride and other metals. 
 
 With tobacco, as with alcohol and opium, the statistic method 
 generally proves fallacious when applied to degenerative effects. 
 The most careful researches show that the typical effects occur 
 as a rule after long continued use of tobacco, sometimes not 
 until twenty years or more. While many smokers reach old age, 
 many fail to live to old age because they are smokers. The skin 
 is subject to itching and reddening; the nerves of taste are 
 blunted and patches develop in the throat; loss of appetite, 
 epigastric fulness, pain, vomiting and disturbance of bowel func- 
 tion are common. Menstrual disturbance occurs in women, and 
 in female cigar-makers abortion and pluriparity are frequent. 
 The sexual appetite is impaired, and sometimes sterility and 
 impotence occur. Disturbed heart action, palpitation, rapid and 
 intermittent pulse, precordial anxiety, weakness, faintness and 
 collapse, with sclerosis of the coronary arteries of the heart and 
 left ventricular hypertrophy occur often. Cigars and cigarettes 
 produce irritation of the nose and mucous membrane, diminished 
 smell, chronic hyperemia of the epiglottis and larynx, and some- 
 times of the trachea and bronchi, predisposing to tuberculous 
 infection. Nicotine amblyopia is common, with central disturb- 
 ances of the field of vision and slight color blindness. Often 
 there is disorder of the ear tubes and congestion of the drum, 
 with loss of auditory power and consequent noises in the ear. 
 The central nervous system is affected. In high schools non- 
 smokers progress faster than smokers. Child smokers, from 
 nine to fifteen years of age, exhibit less intelligence and more 
 
TOXINS PRODUCING TROPHIC CHANGES. 225 
 
 laziness or other degenerative tendencies. Adults have head 
 pressure, sleepiness or drowsy stupor, depression, apathy and 
 dizziness. There may also be ataxic symptoms, paretic weak- 
 ness of bowels and bladder, trembling and spasms. Tobacco 
 insanities, though comparatively rare in smokers, are common 
 in snuffers and still more in chewers.^ In the precursory stage, 
 which lasts about three months, there are general uneasiness, 
 restlessness, anxiety, sleeplessness, and mental depression, often 
 of a religious type. After this occurs precordial anxiety, and 
 finally the psychosis proper, consisting of three stages : 1. Hal- 
 lucinations of all the senses, suicidal tendencies, depression, at- 
 tacks of fright, with tendency to \iolence and insomnia. 2. Ex- 
 hilaration, slight emotional exaltation, with agreeable hallucina- 
 tions after from two to four weeks' relaxation, again followed 
 by excitement. 3. The intervals between exaltation and depres- 
 sion diminish, and the patient becomes irritable, but otherwise 
 not alive to his surroundings. Perception and attention are les- 
 sened. The patient may be cured in five or six months if he stops 
 tobacco during the first stage. In a year or so he may recover 
 during the second stage. After the third stage he is frequently 
 incurable. As the patient becomes (especially by the use of the 
 cigarette) an habitue before puberty, the proper development 
 and balance of the sexual and intellectual system is checked. 
 These patients break down mentally and physically between 
 fourteen and twenty-five. The moral delinquencies, other than 
 sexual, are often an especial tendency to forgery and deceit of 
 parents. Frequently the insanity of puberty (hebephrenia) is 
 precipitated by tobacco. The cigarette, if used moderately, may 
 be a sedative, but, as used, is a stimulant, and is often made of 
 spoiled tobacco, resembling in reaction morphine, and acting on 
 animals in a somewhat similar manner. As tobacco turns the 
 salivary glands into excretory glands, it leads to imperfect di- 
 gestion of starch and to consequent irregular fermentation in 
 the bowels, thus at once furnishing a culture medium for mi- 
 crobes, from which to form violent toxins, and likewise creating 
 leucomaines, to damage a nervous system overstimulated by 
 
 ^ Annual of the Universal Medical Sciences, 1895. 
 
226 INTERSTITL\L GINGIVITIS. 
 
 nicotine. This is one o:reat reason wliy those who use snuff and 
 chew tobacco become insane more frequently than smokers, 
 albeit these last are not exempt. 
 
 Statistics from the female employes of the Spanish, French, 
 Cuban and American tobacco factories, while defective and 
 somewhat vitiated by the coexistence of other conditions pro- 
 ducing degeneracy, support the opinion that the maternal to- 
 bacco habit (whether intentional or the result of an atmosphere 
 consequent on occupation) is the cause of frequent miscarriage, 
 of high infantile mortality, of defective children, and of infantile 
 convulsions. Tobacco, therefore, in its influence on the paternal 
 and maternal organism, exhausts the nervous system so as to 
 produce an acquired transmissible neurosis. 
 
 Alcohol has been repeatedly charged ^ith being the greatest 
 factor in degeneracy. The influence of alcohol on the indi\idual 
 must first be studied to determine its potency and method of 
 action as a cause of race deterioration. Careful medical re- 
 searches have shown that alcohol produces a nervous state 
 closely resembling that induced by the contagions and infections, 
 and often accompani('(l hy mental disturl:)ance. The acute nerv- 
 ous state to which the term "alcohohsm" was apphed by Mag- 
 nus Huss has all the essential characteristics of the nervous 
 state due to the contagions and infections or mental exhaustion. 
 The action of alcohol may be limited to the central nervous sys- 
 tem and thus produce hereditary loss of power. It may cause 
 changes or degeneracies in the peripheral nerves which in the 
 offspring find expression in spinal cord and brain disorder 
 through extension of the morbid process. But for its deterio- 
 rating effects on the ovaries and testicles alcohol would be a 
 most serious social danger. Through these, however, it tends 
 to prevent the survival of the unfit rather than to develop 
 degeneracy. 
 
 Professional tea-tasters have long been known to suffer from 
 nervous symptoms. Very early in the practice of their occupa- 
 tion the head-pressure sjmaptoms of neurasthenia appear. 
 Tremor also occurs early. While changes in the optic nerve 
 have not been demonstrated beyond a doubt, still eye disorders 
 have been observed in the pauper tea-drinkers of the United 
 
TOXINS PRODUCIXG TROPHIC CHAXGES 
 
 90- 
 
 States and tlie tea-ta?tei's of Eussia. iuclicating similar changes 
 to tliose produced by tobacco and alcohol. The tea-cigarette 
 habit has these effects. Bullard - finds that tea has a ciimulative 
 effect. In his experience, toxic eft'ects are not produced by less 
 than five cups daily. The symptoms manifested are those of 
 nervous excitement resembling hysteria, at times almost amount- 
 ing to fury ; nervous dyspepsia ; rapid irregular heart action ; 
 heart neuralgia : helmet-like sensation and tenderness along the 
 spine. James TVood "^ of Brooklyn found that ten per cent of 
 those under treatment at the city hospitals exhibited similar 
 s^miptoms. Of these sixty-nine per cent were females, and every 
 symptom ascribed by Bullard to tea was seen by TTood in his 
 cases, who also found that the women manifested irregularities 
 in menstruation of a neurasthenic or hysterical t^1^e. He found 
 that these symptoms v\-t-re produced by one-half of the quantity 
 of tea charged with these effects by Bullard. The Lancet, sev- 
 eral years ago, from an editorial analysis of the effects of tea- 
 tipphng, took the position that in no small degree nervous symp- 
 toms occurring in children during infancy were due to the prac- 
 tice of the mothers, both of the working and society class, in- 
 dulging in the excessive use of tea, the excess being judged by its 
 effects on the individual and not by the amount taken. Convul- 
 sions and resultant infantile paralysis were frequently noticed 
 among the children of these tea-tipplers. Obsen'ations among 
 the factory population and the workers in the clothing sweat- 
 shops show that tea neurasthenia, presenting all the ordinary 
 symptoms of nervous exhaustion, is especially common. It is 
 eWdent that tea produces a grave form of neurasthenia readily 
 transmissible to descendants. In addition to its eff'ects directly 
 upon the nervous system, tea tends to check both stomach and 
 bowel digestion, and this increases the self -poisoning which is so 
 prominent a cause, consequence and aggravation of these nerv- 
 ous conditions. 
 
 Coffee exerts an action very similar to that of tea. although 
 the nervous s\Taptoms produced by it are usually secondary to 
 the disturbances of the stomach and bowel diirestiou. Coffee 
 
 •Annual of the Uni'tersal Medical Sciences. 1889. 
 ^ Ibid. 
 
228 INTERSTITIAL GINGIVITIS. 
 
 produces tremor, especially of tlie hands, insomnia, nervous dys- 
 pepsia and helmet sensations. With the exception of certain dis- 
 tricts of the United States coffee abuse is not carried to such an 
 extent as tea, albeit in these, as in some portions of Germany, the 
 habit is an excessive one. The conditions described result in 
 Germany as frequently as they do in the United States. Mendel ^ 
 finds that in Germany coffee inebriety is increasing and sup- 
 planting alcohol. Profound depression, with sleeplessness and 
 frequent cortex headache, are early symptoms. Strong coffee 
 will remove these temporarily, but it soon loses its effect and 
 they recur. The heart 's action is rapid and irregular, and nerv- 
 ous dyspepsia is frequent. L. Bremer of St. Louis has observed 
 similar conditions among both Germans and Americans there. 
 Opium seems to be the Charybdis on which the human bark 
 strikes when escaped from the Scylla of alcohol. Its abuse as a 
 narcotic is much older than is generally suspected even among 
 the English-speaking races. Murrell over ten years ago demon- 
 strated that the inhabitants of the Lincolnshire fens had long 
 employed opium as a prophylactic against malaria. The ratio 
 of insanity in these regions proved to be very great. The same 
 conditions obtained in central malarial regions of New Jersey 
 and Pennsylvania, where the use of strong infusions of the 
 poppy was common. The statistics of Rush ^ as to opium-caused 
 insanity in Pennsylvania indicate that the percentage of Amer- 
 ican opium abuses at the beginning of the nineteenth century 
 was very great. The drug differs in two important aspects from 
 alcohol — it is nearer in chemical composition to nerve tissue, 
 and the tendency to its use may be transmitted by the mother 
 directly to the fetus, since it passes through the placenta very 
 often unaltered. Opium is a more dangerous factor of degen- 
 eracy than alcohol, since the opium habitue must be in a contin- 
 uous state of intoxication to carry on his usual avocation, while 
 abstinence from alcohol is perfectly compatible with proper 
 work on the part of the alcoholist. The opium habit is increased 
 by the propaganda carried on by the habitues, who justify their 
 position by urging the use of opium for an}^ ailment, however 
 
 ♦ Neurologisches Centralblatt, 1887. 
 
 ^ Observations on the Brain and Mind. Page 10, 1798. 
 
TOXINS PRODUCING TROPHIC CHANGES. 229 
 
 trifling. Opium, like alcohol, causes nervous exhaustion similar 
 to but greater than that of the contagions and infections. From 
 the affinity of opium to nerve tissue ; from its tendency to stim- 
 ulate the heart, thus causing increased blood supply to the brain ; 
 from its action on the bowels and the increased resultant work 
 of the liver, this nervous state is much intensified. Opium does 
 not interfere with the structure and fecundation of the ovary 
 and testicles like alcohol, hence the danger of the opium habitue's 
 children surviving. Opium, when smoked, stimulates the re- 
 productive apparatus and thus greatly increases the number of 
 degenerates due to this habit, although the defects due to the 
 inheritance of the habit and their consequences lessen survival. 
 
 While coca took its place but recently among the toxic causes 
 of degeneracy, it was a factor of Peruvian degeneration long 
 ere the discovery of America. Forty- three years ago ^ Euro- 
 peans or people of European origin in different parts of 
 Peru had fallen into the coca abuse. A confirmed chewer 
 of coca, called a cocpiero, becomes more thoroughly a slave to 
 the leaf than the inveterate drunkard is to alcohol. Some- 
 times the coquero is overtaken by an irresistible craving 
 and betakes himself for days together to the woods and 
 there indulges unrestrainedly in coca. Young men of the 
 best families of Peru are considered incurable when addicted 
 to this extreme degree, and they abandon white society 
 and live in the woods or in Indian ^dllages. In Peru the term 
 ''white coquero" is used in the same sense as irreclaimable 
 drunkard. The inveterate coquero has an unsteady gait, yellow 
 skin, quivering lips, hesitant speech and general apathy. The 
 drug has assumed an unusual prominence in the field of degen- 
 eracy since the discovery of its alkaloid, cocain. 
 
 In both Europe and the English-speaking countries the world 
 over a habit has resulted which, while much overestimated, is 
 undoubtedly growing and aggravating as well as producing de- 
 generacy. Many of the cases reported as due to cocain are, how- 
 ever, chargeable to the craving of the hysteric or neurasthenic to 
 secure a new sensation, or the desire on the part of the opium or 
 
 " Johnson, Chemistry of Common Life, Vol. II. 
 
230 INTERSTITIAL GINGIVITIS. 
 
 whisky fiend to try a dodge of forgiveness by friends. The habit 
 is very frequently induced by patent medicines taken to cure 
 catarrh by the neurasthenic or to cure nervousness by the hys- 
 teric as well. As deformities of the nose passages predispose to 
 "catarrh," patent medicines for local application containing 
 cocain are frequently employed in the treatment of this supposed 
 constitutional disease, with the result of aggravating the original 
 degeneracy. The youth under stress of puberty frequently 
 ascribes all his ills to catarrh, and for it often employs snuffs 
 containing cocain, and his nervous condition is much aggravated 
 thereby. Among the nostrums urged in the newspapers and 
 magazines for this condition so often resultant from nerve stress 
 alone is a snuff containing three per cent of cocain. From the 
 description given by Johnson of the coquero there can be no 
 doubt that tramps, wandering lunatics and paupers result from 
 this habit to give birth to degenerates in the next generation. 
 
 It is a widespread opinion among dentists that in toxic cases 
 the gums are the first tissues involved. The fact is, however, 
 that when the salts of mercury are taken into the system, as 
 noted elsewhere, they act directly upon the central nervous sys- 
 tem; later occur nausea and vomiting, tremor in the arms and 
 hands. Besides local nerve inflammation (neuritis), mercurial 
 and brass poisoning produce paralysis agitans, and lead poison- 
 ing, drop wrist, etc. 
 
 Excessive secretions of the glands of the body, especially the 
 salivary glands, later occur with rise in temperature, gingivitis 
 with periosteal and peridental membrane swelling, thickening 
 of the gums and loss of teeth. The central nerve system disturb- 
 ance atfects all other structures. Inflammation of the mucous 
 membrane of the mouth, as well as of the gums, and of the ali- 
 mentary canal, frequently occurs with sloughing of tissue. The 
 kidneys become involved, and are unable to carry off the effete 
 matter. 
 
 The cachexia, which resembles that of scurvy, is characterized 
 by great debility, anemia, emaciation, alopecia, atrophy and 
 coarseness of the nails, with pain in the muscles and joints. 
 
 Mercury is eliminated by all excretory organs for which it has 
 a great affinity. The soluble salts pass out by the bowels. So 
 
TOXINS PRODUCING TROPHIC CHANGES. 231 
 
 long as the excretory organs of the body eliminate mercury, the 
 tissues are not affected. Small doses are eliminated, but con- 
 tinuation of dosage soon involves the nervous system, and after- 
 wards the tissues of the body, especially the jaws. The first 
 effect of mercury upon dogs is to produce vivacity and anima- 
 tion. This lasts for two or three days, when the limbs begin to 
 tremble. The kidneys and bowels act at first freely. At the end 
 of seven or eight days paralysis agitans occurs. There is con- 
 stant trembling, whether awake or asleep ; loss of appetite, with 
 slight rise of temperature. At the end of two weeks the gums 
 become inflamed at the margins. If the drug be continued, death 
 occurs in about three weeks. The loss of flesh is remarkable. 
 Miners working in mercury mines, and looking-glass makers, are 
 all affected to a greater or less extent. The nervous system is 
 always involved. The kidneys become diseased. The hair drops 
 out. The miners think it a happy issue from their trouble when 
 they have lost all their teeth, or even the molars. They are 
 henceforth exempt from suffering so far as the teeth are con- 
 cerned. Many are toothless at thirty-five. 
 
 Mercury taken by the mouth is found in the urine in two 
 hours, and in the saliva in four hours. It appears in the urine 
 fourteen hours after it has been applied to the skin.^ Although 
 it is believed to have passed entirely out of the system, it has 
 been found in the brain, liver, kidneys and muscles. It is claimed 
 that, like lead, it forms combinations ^dth albuminoids in the 
 tissues, for a time remaining inert, to be subsequently oxidized 
 and returned to the circulation as an active poison. While a 
 single dose of mercury may be rapidly eliminated from the sys- 
 tem, repeated small doses distributed over a long period are not 
 so eliminated on account of the thickness and occlusion of the 
 walls of the capillaries, producing endarteritis obliterans, hence 
 more or less of it is deposited in the tissue. 
 
 Lead enters the system through the alimentary canal, skin 
 and respiratory tract. A longer time is required to produce 
 plumbism (lead poisoning) than mercurial poisoning. Lead is 
 stored up in the system in minutest quantities for an indefinite 
 
 ' Twentieth Century Practice of Medicine, Vol. Ill, page 935. 
 
232 INTERSTITIAL GINGIVITIS. 
 
 length of time. Its effects are not manifest until the central and 
 peripheral nervons systems have become involved, as evinced 
 by the effect of plumbism upon the wrists. Occasionally, the 
 chief seat of deposit is the liver or muscles. It is chiefly elim- 
 inated through the kidneys, and very sUghtly through the liver 
 and salivary glands. Not until a considerable length of time has 
 elapsed is lead traceable upon the gums. This usually occurs 
 about the lower incisors and cuspids. This deposit (lead sul- 
 phid) is always in the tissue outside of the blood vessels. Plumb- 
 ism causes trembling, nausea and vomiting. The patient loses 
 flesh, becomes anaemic, and has great resultant debility. 
 
 The lead circulating in the capillaries accumulates, owing to 
 impeded circulation resultant on the thickening of the coats of 
 the vessel, producing occlusion. A bluish hue upon the gums 
 indicates that the system is completely saturated. Like mercury, 
 lead collects in the mucous membrane upon the inside of the 
 mouth, producing blue patches from a line to one-half an inch 
 in length. Lead not only produces local irritation, but affects the 
 peripheral nerves as well, producing atrophic changes ; upon the 
 capillaries a thickening of the inner coat results in endarteritis 
 obliterans. 
 
 Lead produces in those exposed to the fumes a systemic nerv- 
 ous exhaustion, characterized by local paralysis about the wrist, 
 as well as the general symptoms of profound systemic nerve 
 tire. This may result, as was pointed out nearly half a century 
 ago,® in acute insanity of the confusional type followed very often 
 by mental disorder of a chronic type resembling paretic de- 
 mentia. In some cases the patient recovers from the acute 
 insanity to suffer thereafter from epilepsy. In other cases "" an 
 irritable suspicional condition also results, in which the patient 
 may live for years, marry and leave offspring. This last condi- 
 tion and the epileptic are the most dangerous as to the produc- 
 tion of degeneracy. The women employed in the pottery fac- 
 tories in Germany suffer, according to Reimert," from a form 
 of lead-poisoning which produces decidedly degenerative effects 
 
 * Tanquerel ties Planches, Lead Diseases, American Edition, 1848. 
 
 • Kiernan, Journal of Nervous and Mental Diseases, 1881. 
 ^° American Journal of Obstetrics, Oct., 1882. 
 
TOXINS PRODUCING TEOPHIC CHANGES. 233 
 
 upon the offspring. These women have frequent abortions, often 
 produce deaf-mutes and very frequently macrocephalic children. 
 
 Brass-workers suffer from a nervous condition very similar 
 to that produced by lead. Hogden " of Birmingham and Moyer ^- 
 have called attention to the grave forms of nervous exhaustion 
 produced among brass-workers. The period during which the 
 patient is able to pursue the occupation without breaking down 
 is longer than that of the lead-workers. Women, like men, are 
 exposed to this condition. The chief effects produced, so far as 
 the offspring have been observed, are frequent abortions and 
 infantile paralysis. The green gum is an early symptom. 
 
 Potassium iodide exerts a like toxic influence to lead and 
 mercury, as its pathology is similar thereto, but it is of infre- 
 quent occurrence. 
 
 The employment of women in match factories and tenement- 
 house sweat-shops is growing. The chief toxic eifect of phos- 
 phorus is not the localized jaw necrosis. This is but an e\ddence 
 of the progressive system saturation with phosphorus, and bears 
 the same relation to the more dangerous effects of phosphorus 
 that the "blue gum" does to the systemic effect of lead. 
 
 In adults, excess of sodium chloride in the blood from con- 
 sumption of salt meats and fish has been noted with scurvy^ 
 For this reason Eawls, of Cincinnati, Ohio, believed that an 
 excess of salt in the system produced gingivitis. Languor, de- 
 pression, anaemia, with a rise of temperature, and enlarged 
 joints with soreness are the first symptoms. 
 
 The effects of this disease upon the system are almost identical 
 with those of mercury and lead. Bruise-like (purpuric) erup- 
 tions occur upon the skin and mucous membrane, on the serous 
 membrane (notably the pleura, pericardium, meninges and 
 synovial linings of the joints), mucous membrane of the mouth, 
 stomach, intestines and bronchi. 
 
 Owing to the anaemia, vascular weakness and altered compo- 
 sition of the blood, edema is common both in the lungs and in the 
 submucous and subcutaneous tissue, especially the feet and legs. 
 The o-ums begin to swell with redness and fibrous thickening of 
 
 Birmingham Medical Eoview, Jan., 1887. 
 Medicine, May, 1904. 
 
234 INTERSTITIAL GINGIVITIS. 
 
 the deep layer, which cause protrusion, especially in the cases of 
 degenerates. The blood vessels, especially the capillaries, be- 
 come thickened, in some cases they are occluded, or erosion and 
 ulceration occur. The patient becomes decidedly pale and 
 markedly debilitated. The skin is dry and blanched. General 
 emaciation is evident. 
 
 The mucous membrane and gums become swollen and bleed, 
 stomatitis ulcerans results in greater or lesser degree. The 
 tongue is at first swollen, then it becomes dry and hard. The 
 gums are at first red and swollen. They bleed easily upon the 
 slightest touch. Later they become pale and are irregularly 
 larger, somewhat fungoid and friable, protruding between the 
 teeth. They are quite tender to the touch. Ulcers appear on 
 the buccal surfaces. The stomach becomes irritable, nausea and 
 vomiting are common. Constipation occurs early and diarrhoea 
 later appears. 
 
CHAPTER XXII. 
 
 AUTOINTOXICATION IN INTERSTITIAL GINGIVITIS. 
 
 Every day we hear or read of individuals, in the prime of 
 life and to all intents in good health, dying suddenly. Post- 
 mortem reveals nothing whereby we may satisfy our minds as to 
 the actual cause of death and the case passes into medical his- 
 tory as an obscure condition. If we were familiar mtli auto- 
 toxic states, I am sure many of these seemingly obscure condi- 
 tions could be accounted for. Autointoxication is the rock upon 
 which the human bark is wrecked and of which phj^sicians know 
 so little. 
 
 The human organism even in its normal state is prone to its 
 own destruction by poisons. These poisons are formed within 
 the organism itself or are taken into it in foods, liquids and 
 drugs. 
 
 Selmi, the Italian toxicologist, gave the name of ptomaines 
 to basic substances formed in putrefying animal matter. From 
 their similarity to vegetable alkaloids, the ptomaines are often 
 spoken of as putrefactive or animal alkaloids. Leucomaines are 
 animal alkaloids formed by the metabolic processes of the 
 organism. 
 
 The processes of intestinal putrefaction and the formation of 
 physiologic and pathologic alkaloids afford an explanation of the 
 pathogenesis of many diseases, the origin of which was obscure 
 until recent investigations gave us the key by which their true 
 nature may be understood. 
 
 We must admit the great impetus given to disintegrating 
 processes in organic matter by bacteria. In no part of the body 
 is this more true than in the alimentary canal. During the proc- 
 ess of digestion, changes of a chemic, putrefactive and ferment- 
 ing nature take place in the small intestine, which give the op- 
 portunity for the formation of poisonous substances, and these, 
 when absorbed have an injurious effect on the system. There 
 is some protection against this, however, if the liver, kidneys, 
 
236 INTERSTITIAL GINGIVITIS. 
 
 lungs and skin (the great sewers of the body) be not too deeply 
 involved. When these poisons are not eliminated, or when any 
 one of the eliminating organs becomes diseased and other organs 
 are obliged to perform that function, these poisons are carried 
 in the blood stream to the remote parts of the body. The organs 
 most frequently involved as recognized by physicians, are the 
 liver, kidney, heart, brain and eye, but the bony alveolar proc- 
 ess, a doubly transitory structure and end organ and the dental 
 pulp, which is the most perfect end organ in tli(^ l)ody, are the 
 first to record symptoms of disease. 
 
 If the disease involves the entire system and all the elim- 
 inating organs, the skin, kidneys, bowels and lungs are perform- 
 ing, or can be made to perform, their natural functions, many 
 of the poisons are soon removed. On the other hand, if any one 
 of these organs be involved, the process of elimination is slower, 
 as the eliminating organs, which are not involved, must do all 
 the work. At best this is imperfectly performed. A great part 
 of these poisons is eliminated by the stools. Owing to the slow 
 movements of the intestinal contents, much of the poison is ab- 
 sorbed by the mucous membrane. In faulty metabolism or tissue 
 changes, toxins are produced which are absorbed and pass into 
 the lymph and blood vessels. All poisons, producing intoxica- 
 tion, whether due to disease, tissue change, fermentation or in- 
 fection, are of interest in their relation to interstitial gingivitis. 
 Many of these auto-infections are of short duration and their 
 intensity is not lasting. On the other hand, the toxic action of 
 mercury, lead, brass, and of the products of syphilis, tubercu- 
 losis, scurvy, etc., is familiar to all. These poisons are of vital 
 importance to the patient and physician, since they act quickly, 
 but, from the viewpoint of the stomatologist, autointoxications 
 of slow progress are the ones of vital importance. These sub- 
 stances are taken directly into the blood vessels and carried 
 throughout the system. This has been repeatedly proven by 
 Bouchard.^ 
 
 That man is born free from microbes, was first demonstrated 
 bv Metchnikoff. Soon after birth the skin and mucous membrane 
 
 Autointoxication in Disease. 
 
AUTOINTOXICATION IN INTERSTITIAL GINGIVITIS. 237 
 
 become infected, either from the air or water used in bathing or 
 both. On an examination of the intestinal contents an hour after 
 birth, during warm weather, bacteria were found. Usually bac- 
 teria are not described until from twelve to twenty hours after 
 birth. Micrococci and bacilli flourish independently of food, for 
 they are found in the alimentary canal before nourishment has 
 been taken. These microbes change in character when mother's 
 milk or other foods are given the child. The bacillus bifidus 
 appears with mother's milk. The colon bacillus, streptococci, 
 staphylococci, lactic acid bacillus, etc., with cow's milk. Later, 
 with the changes in diet, whether purely vegetable or animal, 
 microbic flora grow rapidly in the intestinal tract. Vignas and 
 Suckdorf have shown that an adult man passes from 30,000,- 
 000,000 to 50,000,000,000 of bacteria daily in the faeces. Many, 
 perhaps most of these bacteria, are harmless in healthy indi- 
 viduals and the majority are dead. They become exceedingly 
 virulent after accidents or injuries, such as gun shot, knife or 
 other wounds, strangulated hernia and catarrhal conditions of 
 the mucous membrane. Man therefore, is in constant danger of 
 being infected. The injury resulting from these micro-organ- 
 isms, is not from the bacteria themselves but from their toxins, 
 the products which are absorbed. 
 
 Autointoxication, without other pathologic states, is due to 
 the absorption from the gastro-intestinal tract, of toxic material. 
 Absorption is favored by constipation and the toxic action is 
 enhanced by hepatic insufficiency. 
 
 Before considering further the putrefactive changes within 
 the intestinal canal, I wish to speak here of a subject about which 
 I find little of note by previous writers, namely, changes in the 
 digestive tract, due to evolution. Evolution is based upon the 
 law of economy of growth, laid down by Aristotle, or use and 
 disuse of structures. It is applicable here as in other parts of 
 the body. Man, as a whole, has undergone rapid changes and 
 is still undergoing greater and greater specialization. In no 
 structure of the human body are these changes so great, o^ving 
 to disuse as in the digestive tract. When organs are exercised, 
 like the arms of the blacksmith, the hands of the oarsman, the 
 legs of the maiFcarrier, they become enlarged and strong. On 
 
238 INTERSTITIAL GINGIVITIS. 
 
 the other hand, when organs are not used, like the little muscles 
 of the ear, the small ribs, the little toes, the blood does not flow 
 to the parts in proportion and arrest of development results. I 
 have repeatedly shown many times the arrest of the face, jaws 
 and teeth in the evolution of man, due to disuse. Civilization, 
 by its custom of preparing food and etiquette in eating, has 
 caused rapid degeneration of the jaws and teeth, resulting in ir- 
 regularities and decay. The mastication of food is a lost art with 
 many jDeople, the salivary glands are not excited, arrest takes 
 place and saliva containing ptyaline is scanty. Foods cooked 
 and swallowed without mastication are taken into the stomach 
 with the preparation of first digestion. The gastro-intestinal 
 juices are required to perform all the work. Changes in the 
 liver, either as to size, quantity of bile secreted or disease cause 
 hepatic insufficiency. The same is also true of the pancreas and 
 gastro-intestinal juices. The size of the stomach, the length and 
 deformity of the intestine and last, but not least, the condition 
 of the nervous system and the power of the muscular coats of 
 the intestines to expel the contents from the body are to be 
 considered. 
 
 The evolution of the rectum and anus from the placental and 
 oviparous mammals is interesting, but is too broad a subject to 
 be considered at this time. This evolution, however, in its rela- 
 tion to malformations and muscular tonicity, owing to man's 
 upright position in his phylogeny must not be lost sight of in the 
 study of gastro-intestinal irregularity. 
 
 The sedentary life, due to modes of living, has brought about 
 many of these changes. The digestive apparatus has not had 
 time to readjust itself to the new environment. Micro-organisms 
 and pus germs which have accumulated in the mouth are taken 
 into the stomach and intestines with every swallow. These may 
 produce injurious results. While the process of digestion con- 
 verts the protein or albuminoid substances of the food into pep- 
 tones and then into animo acids, the putrefactive bacteria fur- 
 ther forms alkaloidal and other poisons which pass into the 
 blood. 
 
 Direct demonstration of this fact has been shown by many 
 investigators. Planer, after ligating the colon found HgS in the 
 
AUTOINTOXICATION IN INTERSTITIAL GINGIVITIS. 239 
 
 blood of the portal vein. Garter has found indican in animals, 
 the subjects of intestinal derangements. Bouchard, as well as 
 Planer, has observed alkaloids, not only in the tissues, but in 
 the blood. Poisons formed, not only in the intestines, but also 
 those existing in the tissues, are also observed in the urine. 
 
 That an increase in intestinal putrefaction will cause a large 
 quantity of toxic material to pass through the blood into the 
 urine has been demonstrated many times. Stadeler in 1848 
 found phenol in the urine. Bauman in 1877 found phenol in 
 fecal matter. In 1826, Tiedeman and Gmelin discovered a red 
 colored substance in the duodenum which proved to be indol. 
 Braconnot later found in the urine, indican derived from indol. 
 Prof. Metchnikoff of the Pasteur Institute thinks old age is 
 chiefly caused by two poisons, phenol and indol which are gen- 
 erated in the intestines incUiding such diseases as artero- 
 sclerosis, cirrhosis of the liver, and interstitial nephritis. He 
 might also have mentioned heart lesions and interstitial gingi- 
 vitis. In 1872, Jaffe injected indol under the skin and afterward 
 found indican in the urine. Later experiments by Senator 
 failed to find indol in the meconium or indican in the urine of 
 newly born infants. It is an established fact today that the 
 variation of indican in the urine is governed by the quantity of 
 indol in the faeces. In other words, the amount of indican in the 
 urine depends upon the activity of intestinal putrefaction. In 
 cholera, typhoid fever, intestinal obstruction, Hassal, Gubler, 
 Robin, Carter, Jaffe found large quantities of indican in the 
 urine. Senator showed indican in the urine in constipation. 
 
 Nencki gave a dog two grains of indol by the mouth, and in 
 twenty-four hours there appeared diarrhea. Twelve milligrams 
 of a one per cent solution administered subcutaneously to frogs 
 caused death. One and five-tenths to two grams of indol ad- 
 ministered subcutaneously to a rabbit in twenty-four hours 
 proved fatal. By similar experiments Salkowsky found phenol 
 and cresol in the urine. Especially was this the case in diarrhea 
 and in intestinal obstruction. There is no doubt that in future 
 investigations other poisons will be found in the stools and urine 
 that produce marked poisonous effect upon the system. Prod- 
 ucts of putrefacti'on formed in the intestines, found in the urine, 
 
240 INTERSTITIAL GINGIVITIS. 
 
 must of necessity circulate in the blood throughout the system. 
 There is a natural fermentation going on all the time in the 
 intestines. In young and middle aged people, when the excre- 
 tory organs are performing their office in a healthy manner, the 
 kidneys, bowels, skin and lungs remove the poisonous products 
 from the body. When, however, putrefactive products are 
 formed in excess, or the excretory organs have lost their tonicity, 
 has the system other means of preventing the accumulation of 
 poisons in the blood? Certainly, the liver is intended to per- 
 form that office. This has been proven by Schiff. The experi- 
 ments by G. H. Roger with alcoholic extract of rotten meat 
 show that when injected into the portal vein it is one half as 
 toxic as when introduced into the circulation. 
 
 Bouchard has shown that blood drawn from the portal vein of 
 a dog kills a rabbit in a dose from thirteen to sixteen cubic centi- 
 meters per kilogram ; that blood removed from the liver requires 
 twenty-three centimeters. He has also shown that the injection 
 of the extract of 2.5 grams of decomposing meat is sufficient to 
 kill a man. 
 
 Many other experiments have been made by scientists show- 
 ing similar results. In a summary of the research work, it is 
 safe to say that the liver is intended to give protection to the 
 system by destroying poisons especially those derived from the 
 intestines so that the general system does not receive an amount 
 of these poisons above what the excretory organs are able to 
 remove. 
 
 When all conditions work in harmony, that is, when animal 
 and man, after years of normal environment, have adjusted 
 themselves, disease is less likely to result. When a change of 
 environment, such as food, climate and soil, takes place, the 
 animal or man becomes more susceptible to disease. Thus 
 fifty-five monkeys died of tuberculosis in the Lincoln Park Zoo, 
 Chicago, in one year, due to change in food and temperature 
 and to confinement. House dogs are more susceptible to dis- 
 ease than street dogs. The Indian of North America has been, 
 and is, dying rapidly from change in environment and food. 
 This is true of other primitive races throughout the world. 
 
AUTOIXTOXICATION IX INTERSTITIAL GINGIVITIS. 241 
 
 Scandinavians in American cities are very susceptible to disease. 
 Tlie same is true of the Negro. 
 
 Many people are still in the primitive stages as regards 
 their digestive apparatus. They have inherited an atavistic 
 tendency in their large, well-formed jaws, muscles and teeth. 
 They masticate food and enjoy it like the carnivora, tearing 
 and che^^^.ng meat from a bone. The digestive apparatus is 
 perfect, the bowels, kidneys, skin and lungs do their work nor- 
 mally, and they are in perfect health. 
 
 Many in whom the digestive apparatus is weak have pro- 
 gressed along the line of evolution. These people live a seden- 
 tary life one or two generations in advance of the tiller of the 
 soil. They are in the transitory stage, not yet adjusted to the 
 new environment. A third class, born of neurotic parents, have 
 inherited deformed internal organs the secretions and action of 
 which are not in harmony with each other. They do not chew 
 their food and digestion is impaired. Their nervous systems 
 may be impaired from the first, or may become involved as a 
 result of faulty digestion and assimilation. 
 
 Studying the three classes singly, it is found that the mem- 
 bers of the first class are healthy, that they can eat and drink 
 everything and at all times, day and night. They can eat eight 
 or ten meals a day, like the King of Portugal, and enjoy them. 
 They can drink large quanities of alcohol or beer each day with- 
 out difficulty. They are rarely ill. When the senile stage be- 
 gins, while there are no marked symptoms, the excretory organs 
 fail to perform their work properly. Interstitial gingivitis sets 
 in, the teeth loosen, arteriosclerosis, kidney breakdown, uremic 
 poisoning result and at from fifty-five to sixty-five death takes 
 place from Bright 's disease, diabetes, heart failure or apoplexy, 
 the result of excesses. 
 
 The second class easily produce acute gastro-intestinal fer- 
 mentation, autointoxication, and are subject to sick headaches, 
 acid stomachs, gases in both stomach and bowels and constipa- 
 tion. They suffer with headache, migraine and vertigo, and 
 often with nervous symptoms. In these cases special foods will 
 upset the entire system. Fruits, raw as well as cooked, set up 
 fermentation in the small intestines and putrefaction results. 
 
242 INTERSTITIAL GINGIVITIS. 
 
 Coffee, chocolate, cocoa, beer, and the inhalation of tobacco 
 smoke will distnrb the digestion, produce cold extremities, sick 
 headaches in a few honrs and not infrequently skin eruption. 
 
 The third class are not only subject to all the symptoms of 
 the first and second, but frequently surgical operations are nec- 
 essary to establish healthy relations between the digestive 
 organs. 
 
 Deformities of the jaws and teeth are not uncommon. 
 Macaulay portrays a vivid picture of such a state in Charles V 
 of Spain. Among other physical deformities, he says, "At 
 length a complication of maladies completed the ruin of all his 
 faculties. His stomach failed, nor w^as this strange, for in him 
 the malformation of the jaws, characteristic of his family, was 
 so serious that he could not masticate his food, and he was in 
 the habit of swallowing ollas and sweetmeats in the state in 
 which they were set before him. While suffering from indiges- 
 tion, he was attacked by ague. Every third day his convulsive 
 tremblings, his dejection, his fits of wandering, seemed to indi- 
 cate the approach of dissolution." 
 
 Prof. Eussell H. Chittenden - in his experiments in physio- 
 logical economy in nutrition, has shown that excess of proteids 
 means waste, "but of far greater importance is the unnecessary 
 strain placed upon the body by this uncalled-for excess of food 
 material which must be gotten rid of at the expense of energy 
 that might better be conserved for more useful purposes." 
 
 He has conclusively shown that body equilibrium can be 
 maintained on half the daily intake of food. The brain worker 
 and the muscle worker can maintain health, strength and vigor 
 on a smaller amount of nitrogenous material than is usually 
 consumed ; "that an excess of food is in the long run detrimental 
 to health, weakening rather than strengthening the body and 
 defeating the very objects aimed at." This applies to people 
 who have obtained their growth and not to children. 
 
 Some neurotics and degenerates are very susceptible to auto- 
 intoxication on account of unstable nervous systems. They 
 either become easily constipated or toxic material accumulates 
 
 'Physiological Economy in Nutrition. 
 
AUTOINTOXICATION IX INTERSTITIAL GINGIVITIS. 243 
 
 in the intestines and as a result the system becomes slowly 
 poisoned. Convulsions occur in both children and adults. 
 Most, if not all, insane patients are constipated. While it would 
 ]iot be safe to say that the insanity was due to constipation, yet 
 all are greatly benefited, and some slight forms are cured, by 
 keeping the bowels free from microbic infection. 
 
 Some of the best specialists claim the skin eliminates very 
 little of the blood's poison. Under ordinary circumstances the 
 skin excretes water, salts in small quantities, carbonic acid, and 
 in some volatile fatty acids. As age advances and the elim- 
 inating organs lose their activity, the bowels and kidneys fail 
 to eliminate all the decomposed material. When these organs 
 become diseased, the skin and lungs assist in carrying off the 
 poisons or their products. The skin especially is important in 
 keeping the system in a healthy condition, free from poisons. 
 
 AVhat the laity understand as ''spring fever" is but the re- 
 adjustment of the eliminating organs from winter to spring. 
 People in the senile stages feel better in warm climates than in 
 cold, hence the custom of moving to warm climates in winter. 
 
 During pregnancy, poisons are formed in the mother and 
 fetus which circulate in the maternal and fetal blood. Upon the 
 mother is thrown the burden of eliminating by the kidneys, liver, 
 intestines, skin and lungs the bulk of the poison formed within 
 the two organisms. When these poisons are retained auto- 
 intoxication is produced which varies in degree from heighten- 
 ing the arterial tension, headache, gastric disturbance, and lassi- 
 tude to convulsive seizures as in puerperal eclampsia. Intersti- 
 tial gingivitis is always present to a more or less marked degree. 
 The urine under these circumstances usually contains albumin. 
 That errors of diet often induce puerperal eclampsia, there is 
 no doubt. Pregnancy frequently advances normally until some 
 such improper food as lobster, fish, pork, pie, strawberries, etc., 
 is eaten ravenously, when, as the result of the entrance into the 
 blood of imperfectly digested products or intestinal poisons, 
 eclampsia follows. The presence of these toxins in the blood 
 induces structural alterations in the renal epithelia and as a 
 consequence renal dehris, tube casts, are present in the urine 
 along with albumin. If the patient lives the morbid changes are, 
 
244 INTERSTITIAL GINGIVITIS. 
 
 for the most x^ai't, temporary, for tliey disappear on cessation 
 of the pregnancy. We are famihar with the dropsical legs of 
 women seen near the end of pregnancy, but it occasionally hap- 
 pens that there is in addition to the autointoxication from intes- 
 tines and kidneys, a hepatic toxemia, as well. 
 
 An abnormal degree of urinary acidity extending over a 
 period of nine months accounts for many of the neuralgias, 
 toothaches, destruction of teeth by erosion, decay of the teeth 
 and wasting of the alveolar process, skin diseases, and many 
 other lesions so common in pregnancy which cease to trouble 
 after birth of the child. Mental strain due to overwork, grief, 
 shock, etc., check the secretions, causing an abnormal degree of 
 urinary acidity which eventually results in diabetes. Bright 's 
 disease and arterial degeneration. There are many other lesions 
 traceable to or influenced by a high acidity of the system. 
 
 The liver becomes enlarged and tender, the patient slightly 
 icteric, the stools pale, fluid appears in the abdominal cavity, and 
 there are albumin and bile in the urine. It is not until the preg- 
 nancy has been brought to a natural or an artificial termination 
 that the symptoms and physical signs disappear. In such a case 
 the liver has failed to arrest and destroy the intestinal poisons 
 as they pass through it and the result is that owing to their 
 excess in the blood and inability on the part of the kidneys to 
 eliminate them the patient is poisoned by the products within 
 her own body.^ 
 
 One accustomed to the odor of the skin and lungs and to an 
 examination of the mouth in which there is interstitial gingivitis, 
 can readily detect intestinal fermentation and kidney irregular- 
 ity. Many times I have detected a tendency to kidney lesions 
 or the lesion itself, in this manner, as was confirmed by subse- 
 quent urinalysis. 
 
 Autointoxication in disease is familiar to us all. That the 
 l)lood is charged with effete matter or poison, due to autointox- 
 ication, is abundantly proven. Owing to a swollen mucosa or 
 other obstruction, ordinary nose breathing furnishes an insuffi- 
 cient supply of oxygen. More air is necessary, hence the uncon- 
 
 * Autointoxication in Disease. 
 
AUTOINTOXICATION IN INTERSTITIAL GINGWITIS. 245 
 
 scions opening of the month. A larger vohnne of air by nose 
 and mouth is therefore taken into the hmgs. Most people at the 
 senile stage do this, most noticeably, however, at night. 
 
 The poisonous products of the intestinal canal not expelled 
 from the bowels are absorbed and carried by the portal system 
 to the liver. If toxic material is sufficiently modified by the liver, 
 it will be carried back and emptied into the bowel along A\ith the 
 bile. If, owing to some mechanical obstruction, as catarrhal 
 swelling, gall stones or thickening of bile, the normal function 
 of the liver should be interfered with, hepatic insufficiency re- 
 sults. Any derangement of the bile or liver cells which inter- 
 feres with the proper function of rendering harmful substances 
 innocuous would cause abnormal and poisonous products to be 
 carried in the blood. 
 
 The great outlet for poisons which the liver fails to eliminate 
 are the emunctories, chief of which are the kidneys. If there 
 be too much work in this direction, the eliminating function is 
 soon lost. The toxic material accumulates and results in renal 
 inflammation and albuminuria. When this has taken place the 
 blood becomes charged mth poisons, the heart and arteries 
 undergo degenerative changes with cardiac hypertrophy and 
 arteriosclerosis together ^yit]l the consequent cardio-vascular 
 diseases, insufficient blood supply to various vital organs, nerv- 
 ous disorders. Bright 's disease, diabetes, rheumatism, gout, uric 
 acid diathesis, skin eruptions and asthma result. Before these 
 diseases have become of sufficient importance to be observed by 
 the physician, interstitial gingivitis has obtained full sway. In 
 all the above mentioned diseases interstitial gingivitis is most 
 pronounced. 
 
 The effects of autointoxication on the system are to reduce 
 its vitality or to destroy the tonicity of the nervous system, the 
 result of which, end organs of the body, the kidney, the brain, 
 the eye, the dental pulp and the alveolar process first become 
 diseased. This disease is brought about by overstrain upon the 
 peripheral nerves, change in chemical structure of their blood 
 cells, irritations upon the coats of the blood vessels and a gen- 
 eral weakening of the part. The organ first involved depends 
 
246 INTEESTITIAL GINGIVITIS. 
 
 upon its anatomy, its structure, its function, its weakness, local- 
 ity, power of recuperation, etc. 
 
 The poisons circulating- in the ])lood, due to autointoxication, 
 collect in the peripheral blood vessels of the alveolar process, 
 change the character of the red blood cells and prevent nourish- 
 ment from going to the parts. 
 
 A low vitality of the structure is produced. Irritation of the 
 vessel walls is set up and absorjotion of the process results. Peo- 
 ple in advanced years in comparative good health (not ill), who 
 are attending to their various affairs each day but who do not 
 throw off the poisons of the body as readily as they did formerly, 
 have an absorption of the alveolar process beginning at the gin- 
 gival border and slowly extending toward the apical end of the 
 root or roots of the teeth. The severity of this interstitial gin- 
 givitis will depend upon the vitality of the patient and the degree 
 of poisons circulating in the blood. How much more severe, 
 therefore, must be the absorption when disease of one or more 
 organs of the body occurs, especially the eliminating organs. 
 
 It has been shown that poisons originating anywhere in the 
 alimentary canal have been found in the urine, that poisons en- 
 tering the system subcutaneously have been found in the urine. 
 Some of these poisons are modified in form and intensity of 
 action, while others remain in their original state. It has been 
 a mooted question just how these i^oisons are excreted by organs 
 in which they are not formed but a sensible conclusion must be 
 that they enter the blood and are conveyed by it throughout the 
 system and partly eliminated by the kidney. 
 
 In a logical understanding of autointoxication and its treat- 
 ment an examination of the urine should be made in order to 
 ascertain the extent of poisons circulating in the blood. 
 
CHAPTER XXIII. 
 
 URIXARY SIGNS OF AUTOINTOXICATION. 
 
 That changes in the character of the blood composition take 
 place from week to week is known to every physician. These 
 changes may be due to systemic derangement or to the character 
 of the food, and are often so great as to affect the character of 
 the tissues of the body, especially the alveolar process. We 
 have at present no definite method of testing, from time to time, 
 the chemical constituents of the blood. The best and only method 
 of obtaining an approximate knowledge is by an examination of 
 the urine. For many years I have made a special study of the 
 constitutional condition. 
 
 The examination of the urine is the only means at hand of 
 ascertaining the general condition of the system underlying 
 Interstitial gingivitis. Two factors are of considerable moment, 
 namely, an excess or diminished urinary acidity and indican. I 
 ^dsh to report three hundred and ninety-four examinations. 
 The patients are from twenty-seven to sixty-seven years of age. 
 All had interstitial gingivitis in its most aggravated form with 
 loose teeth in varying numbers. Thirty-two had lost teeth as a 
 result of the disease. Fourteen had pyorrhoea alveolaris that 
 could be observed by the naked eye. Twenty-four hours ' urine 
 was obtained. A part or all was sent to the Columbus Medical 
 Laboratory for examination. In tabulating the reports, the fol- 
 lowing results were obtained : Specific gravity taken in the first 
 fifty only, showed two had 1,005; two, 1,006; two, 1,008; two, 
 1,009; one, 1,010; one, 1,011; one, 1,012; two, 1,013; six, 1,014; 
 one, 1,015; five, 1,016; two, 1,017; one, 1,018; five, 1,020; three, 
 1,023; one, 1,024; three, 1,025; one, 1,026; two, 1,027; one, 1,028; 
 two, 1,029 ; one, 1,031. There were granular casts in six reports ; 
 hyaline casts in twelve ; cylindroid in twenty-two. 
 
 The degree of acidity was obtained by taking 10 c.c. of urine 
 specimen, measured in the graduate glass, then placed in the 
 small glass ; four drops of phenolphtalein were added; then drop 
 by drop NaOH (1-10 normal sodium hydrate) until a slight pink- 
 
248 INTERSTITIAL GINGIVITIS. 
 
 ish color was produced. Having: noted on paper the niimljer of 
 c.c. of the NaOH in the burette before and after the pink color 
 was obtained, the number of c.c. displaced multiplied by 10 (in 
 order to find the number of c.c. NaOH necessary to neutralize 
 100 c.c. urine) equaled the degree of acidity. Each step in this 
 operation must be carefully performed, each instrument must 
 be kept perfectly clean in order to get good results. 
 
 The results showed two had 4 degrees ; two, 6 ; one, 7 ; two, 8 ; 
 nine, 10; three, 11; seven, 12; one, 13; eighteen, 14; five, 15; 
 twenty, 16 ; five, 17 ; two, 17.5 ; fifteen, 18 ; twenty-seven, 20 ; four, 
 21 ; thirteen, 22 ; six, 23 ; fourteen, 24 ; seven, 25 ; fifteen, 26 ; one, 
 27; seventeen, 28; one, 29; thirty, 30; two, 31; nineteen, 32; six- 
 teen, 34 ; six, 35 ; twenty-seven, 36 ; five, 37 ; eleven, 38 ; two, 39 ; 
 twenty-two, 40; two, 41; eight, 42; nine, 44; two, 45; ten, 46; 
 two, 47 ; seven, 48 ; one, 49 ; eight, 50 ; one, 51 ; six, 52 ; two, 53 ; 
 one, 54 ; one, 55 ; fifteen, 56 ; one, 57 ; five, 58 ; two, 59 ; seven, 60 ; 
 six, 62 ; three, 63 ; four, 64 ; three, 66 ; two, 68 ; four, 70 ; three, 72 ; 
 two, 74; five, 75; one, 76; one, 78; one, 79; one, 80; one, 83; one, 
 84; two, 100; three, 104; one, 105; one, 108; one, 110; one, 113; 
 one, 120 ; three, alkaline ; two, neutral. The urea showed two had 
 .3 per cent; one, .5; two, .6; two, .7; two, .9; two, 1; one, 1.1; 
 two, 1.3; one, 1.4; four, 1.5; six, 1.6; one, 1.7; three, 1.8; one, 1.9; 
 one, 2; three, 2.1; three, 2.2; two, 2.4; six, 2.5; two, 2.6; one, 3; 
 one, 3.1 ; one, 7.1. Albumin was found in four cases ; blood in 
 six ; leucocytes in forty-five ; epithelial cells in forty-six ; uric acid 
 crystals in two ; urates in five ; oxalates in fifteen. Of the three 
 hundred and ninety-four examinations, three hundred and 
 twenty showed indican to a greater or lesser extent. Seventy- 
 four were normal in this respect. 
 
 To make a more complete study of each individual case, the 
 following table has been prepared : 
 
 Specific Casts. Acid- Urea- 
 Gravity. Granular. Hyaline. Cyhndroid. Degree. Percent. 
 23 60 2.5 
 20 1 1 1 56 2.5 
 8 1 20 1. 
 6 11 12 .6 
 12 36 1.5 
 31 44 2.6 
 29 1 11 46 2.2 
 
UEINARY SIGNS OF AUTOINTOXICATION. 
 
 249 
 
 Specific 
 
 
 Casts. 
 
 
 
 Acid- 
 
 Urea- 
 
 Gravity. 
 
 Granul 
 
 ar. Hyaline. 
 
 Cylindroid 
 
 [. D. 
 
 egree. 
 
 Per cent, 
 
 16 
 
 1 
 
 1 
 
 1 
 
 
 52 
 
 2.2 
 
 11 
 
 
 
 
 
 1 
 
 
 17.5 
 
 1.4 
 
 17 
 
 
 
 
 
 
 
 
 17.5 
 
 1.6 
 
 27 
 
 
 
 1 
 
 1 
 
 
 62 
 
 2.1 
 
 20 
 
 
 
 
 
 1 
 
 
 24 
 
 2.2 
 
 25 
 
 
 
 1 
 
 
 
 
 44 
 
 2.4 
 
 9 
 
 
 
 
 
 1 
 
 
 16 
 
 1.5 
 
 25 
 
 1 
 
 1 
 
 1 
 
 
 40 
 
 3.1 
 
 29 
 
 1 
 
 1 
 
 
 
 
 58 
 
 2.6 
 
 1-1 
 
 
 
 
 
 
 
 
 36 
 
 2. 
 
 16 
 
 
 
 
 
 
 
 
 30 
 
 1.8 
 
 14 
 
 
 
 
 
 
 
 
 30 
 
 1.5 
 
 13 
 
 
 
 
 
 
 
 
 36 
 
 1.6 
 
 13 
 
 
 
 
 
 
 
 
 36 
 
 1.6 
 
 15 
 
 
 
 
 
 
 
 
 36 
 
 1.7 
 
 15 
 
 
 
 
 
 1 
 
 
 15 
 
 1.6 
 
 14 
 
 
 
 
 
 
 
 
 36 
 
 .9 
 
 28 
 
 
 
 
 
 
 
 
 36 
 
 3. 
 
 5 
 
 
 
 
 
 
 
 degree 
 
 not taken 
 
 .3 
 
 16 
 
 
 
 
 
 
 
 
 ( ( 
 
 1.6 
 
 20 
 
 
 
 
 
 
 
 
 < i 
 
 1.5 
 
 10 
 
 
 
 
 
 
 
 
 i I 
 
 1.1 
 
 25 
 
 
 
 
 
 1 
 
 
 i i 
 
 2.5 
 
 27 
 
 
 
 1 
 
 1 
 
 
 62 
 
 2.1 
 
 25 
 
 
 
 
 
 
 
 degree 
 
 not taken 
 
 2.5 
 
 14 
 
 
 
 
 
 1 
 
 
 30 
 
 1.3 
 
 20 
 
 
 
 
 
 
 
 degree 
 
 not talven 
 
 1.9 
 
 24 
 
 
 
 
 
 1 
 
 
 '< 
 
 2.4 
 
 26 
 
 
 
 
 
 
 
 
 < i 
 
 2.1 
 
 18 
 
 
 
 1 
 
 1 
 
 
 ii 
 
 1.6 
 
 14 
 
 
 
 
 
 1 
 
 
 30 
 
 1.8 
 
 5 
 
 
 
 
 
 
 
 
 15 
 
 .7 
 
 23 
 
 
 
 
 
 1 
 
 
 40 
 
 1.8 
 
 7 
 
 
 
 
 
 
 
 
 14 
 
 1.3 
 
 16 
 
 
 
 
 
 
 
 
 30 
 
 1.8 
 
 9 
 
 
 
 
 
 1 
 
 
 11 
 
 .9 
 
 14 
 
 
 
 
 
 1 
 
 
 22 
 
 1.5 
 
 7 
 
 
 
 
 
 
 
 
 20 
 
 .7 
 
 7 
 
 
 
 
 
 
 
 
 20 
 
 7.1 
 
 23 
 
 
 
 
 
 
 
 
 60 
 
 2.5 
 
 20 
 
 1 
 
 1 
 
 1 
 
 
 56 
 
 2.5 
 
 8 
 
 
 
 
 
 
 
 
 20 
 
 1.0 
 
 6 
 
 
 
 1 
 
 ] 
 
 
 12 
 
 .6 
 
 TOTAL EXAMINATION OF URINE. 
 
 Qualitative Examination. 
 
 Physical condition : 
 Clear 
 
 17 
 
 Present 30 
 
 Absent 29 
 
 Cloudy .' 33 Albumin : 
 
250 INTERSTITIAL GINGIVITIS. 
 
 Reaction : Present, trace 4 
 
 Acid 46 Absent 46 
 
 Alkaline 4 Peptones None 
 
 Color : Sugar None 
 
 Yellow 46 Bile None 
 
 Amber 4 Blood : 
 
 Odor : Present 6 
 
 Negative 46 Absent 44 
 
 Present 4 Indicaii 50 
 
 ^lucin : 
 
 Microscopical Examination. 
 
 Casts : Pns 11 
 
 Hyaline 14 Epitbelial cells 40 
 
 Granular 7 Crystals : 
 
 Epithelial 1 Uric acid 2 
 
 Cylindroids 21 Urates 5 
 
 Cells : Oxalates 15 
 
 Blood 4 Phosphates : 
 
 Leucocytes 45 Calcium 1 
 
 The relation of acid autointoxication and montli acidity is 
 very intimate. The acids taken into the body and those pro- 
 duced by chemical changes within, such as hydrochloric, lactic, 
 acetic, diacetic, oxybutyric, uric, and other acids circulate in the 
 system in the form of salts so that the blood maintains at all 
 times essentially a neutral reaction. If the acid ions in the blood 
 at any time overbalance the metallic ions so that there is a con- 
 siderable number of H ions present, an excretion of acid takes 
 place and passes out through the kidneys, lungs, skin, and 
 mucous membrane, especially of the mouth. If the kidneys do not 
 carry off the surplus acidity, a greater strain is put upon the 
 lungs, skin and mucous membranes of the mouth. The alveolar 
 process and gums, being doubly transitory, as well as end organs, 
 contain excretive and secretive glands. The gums are the first 
 structure of the body which indicate systemic defects partic- 
 ularly noticeable in mercurial, lead, and brass poisoning, scurvy, 
 etc. The mucous glands normally excrete acid fluid, while the 
 salivary glands secrete alkaline fluid. It not rarely happens, 
 however, that the kidneys fail in their function and the system 
 becomes so saturated ^\T.tli acid that the salivary glands continue 
 to cause destruction of the teeth. 
 
 Friction of the lips, teeth, and foreign bodies assist greatly in 
 tooth destruction. Teeth softened by faulty nutrition and acid 
 
UEINARY SIGNS OF AUTOINTOXICATION. 251 
 
 states are easily destroyed by acids and friction. 
 
 In an examination of the urine of diabetics, tabetics and 
 paretic dements, I have the following statistics : 
 
 1. Urinalysis of Diabetic Patients. — Urinalysis by the Co- 
 lumbian Medical Laboratories of three hundred and ninety-four 
 diabetics showed specific gravity, one 1.003, one 1.005, one 1.007, 
 one 1.010, one 1.011, eight 1.012, one 1.013, six 1.014, six 1.015, 
 four 1.016, five 1.017, seven 1.018, six 1.019, seven 1.020, five 
 1.021, thirteen 1.022, fifteen 1.023, ten 1.024, twenty 1.025, thir- 
 teen 1.026, thirteen 1.027, eighteen 1.028, nineteen 1.029, twenty- 
 five 1.030, twelve 1.031, fifteen 1.032, twenty-eight 1.033, sixteen 
 1.034, twenty 1.035, seventeen 1.036, eighteen 1.037, nine 1.038, 
 twelve 1.039, ten 1.040, eight 1.041, eight 1.042, two 1.043, seven 
 1.044, two 1.045, two 1.046. 
 
 Percentage of Sugar. — Twelve had 0.1 per cent, eighteen 0.2, 
 three 0.3, eleven 0.4, seven 0.5, seven 0.6, one 0.7, four 0.8, eight 
 0.9, ten 1, one 1.1, eight 1.2, seventeen 1.3, six 1.4, one 1.5, thir- 
 teen 1.6, seven 1.7, four 1.8, one 1.9, five 2, three 2.1, six 2.2, 
 three 2.3, seven 2.4, three 2.5, five 2.6, one 2.7, three 2.8, three 
 2.9, four 3, one 3.1, five 3.2, six 3.3, one 3.4, two 3.5, ten 3.6, five 
 3.7, five 3.8, fifteen 4, four 4.1, five 4.2, two 4.3, two 4.4, three 4.5, 
 eight 4.6, four 4.7, five 4.8, five 4.9, five 5, two 5.2, ten 5.3, five 5.4, 
 one 5.5, nine 5.6, seven 5.7, five 5.8, one 5.9, nine 6, five 6.1, ten 
 6.2, ten 6.4, one 6.5, five 6.6, one 6.7, three 6.8, five 6.9, three 7, 
 one 7.1, two 7.2, two 7.3, two 7.4, one 7.6, one 7.7, three 7.8, one 
 7.9, one 8, one 8.2, one 8.5, one 8.7, one 9, one 9.1. 
 
 Degree of Acidity. — Two passed 4 degrees, two 6, one 7, two 
 8, six 10, five 12, sixteen 14, one 15, fifteen 16, one 17, thirteen 
 18, twenty 20, one 21, twelve 22, one 23, ten 24, two 25, fourteen 
 26, sixteen 28, one 29, twenty-one 30, seventeen 32, thirteen 34, 
 four 35, twenty 36, two 37, eleven 38, two 39, thirteen 40, one 41, 
 eight 42, seven 44, two 45, eight 46, two 47, five 48, five 50, five 52, 
 one 54, twelve 56, one 57, four 58, five 60, one 62, one 63, three 
 64, two QQ, two 68, two 70, three 72, one 74, one 75, one 100, two 
 104, one 120, one alkaline, two neutral. 
 
 Acetone. — Of this number of cases only nineteen were exam- 
 ined for acetone. In eleven, acetone was present, in eight absent. 
 Thirty-two were examined for diacetic acid ; in six it was pres- 
 
252 INTERSTITIAL GINGIVITIS. 
 
 ent and in twenty-six absent. Twenty-four were examined for 
 oxybutyric ; in all it was negative. 
 
 2. Urinalysis of Tabetic Patients. — Degree of acidity in 
 thirty-five was as follows: One passed 5 degrees, one 6, one 7, 
 three 9, two 10, one 11, one 14, one 17, two 19, two 20, one 22, one 
 46, one 48, one 49, one 50, one 56, one 62, one 73, two 76, one 78, 
 one 81, one 82, one 84, one 97, one 99, one 112, four alkaline. 
 Those patients having the alkaline urine had marked erosion of 
 the teeth showing that at some time there had been a high degree 
 of acidity. Cystitis caused the urine to become alkaline. All 
 showed indican to a greater or less extent. 
 
 3. Urinalysis of Paretic Patients. — Degree of acidity: 
 There were twenty-one males, four females. Three passed 5 
 degrees, one 7, three 8, two 9, one 10, one 11, one 12, one 13, one 
 15, two 16, one 17, one 22, one 28, one 34, one 38, one 39, one 44, 
 one 51, one 52, one 70. These patients were in a quiet state. If 
 the urine could have been examined after excitement or an ex- 
 plosion the degree of acidity would have been greater. 
 
 4. Urinalysis of Private Patients. — Degree of acidity: I 
 examined one hundred and twenty-nine. Three were also sent to 
 me by Dr. J. F. Keefe of Chicago, making in all one hundred and 
 thirty-two. They were from eleven to eighty-four years of age. 
 All showed erosion and abrasion to a greater or less extent. 
 Three passed 2 degrees, three 8, two 10, two 11, seven 12, two 
 14, two 15, five 16, six 18, two 19, eight 20, five 22, five 24, six 26, 
 four 28, two 29, six 30, two 31, four 32, two 33, three 34, nine 36, 
 two 38, two 40, two 44, five 46, one 47, two 48, two 50, five 52 ; five 
 54, four 56, one 58, three 60, two 62, five 70, one 90, one 127, one 
 132, only four or 3.8 per cent had uric acid. I quote here from a 
 previous paper, '' Interstitial Gingivitis Due to Autointoxica- 
 tion," my first fifty patients' degree of acidity, one had 11 de- 
 grees, two 12, one 14, two 15, one 16, two 17.5, four 20, one 22, one 
 24, five 30, seven 36, two 40, two 44, one 46, two 56, one 58, one 59, 
 one 60, two 62 ; 3 per cent had uric acid, all had indican. 
 
 The acidity of a single specimen of urine will vary like the 
 specific gravity within large units, corresponding to the amounts 
 of acid entering the blood from various sources. The normal 
 degree of acidity of the urine is from 30 to 40 degrees. A low 
 
URINAEY SIGNS OF AUTOINTOXICATION. 253 
 
 acidity may arise from several factors : 1. A large excretion of 
 water, as in nervous states, diabetes insipidus, etc. 2. A diet con- 
 taining a large quantity of salts of the vegetable acids. 3. A cor- 
 responding deficiency of meat which yields acid salts. 4. A defi- 
 cient power of the kidney to excrete acid. 5. Excessive elimina- 
 tion of acid by other emunctories. In patients in whom the 
 degree of acidity exceeds 40% there is excessively imperfect oxi- 
 dation which, irrespective of the types of acid, underlies, as is 
 now pretty generally recognized, severe constitutional stress 
 allied to that of diabetic acidosis. 
 
 The quantity of urine passed in twenty-four hours influences 
 the degree of acidity. Thus, if more than 40 ounces (about the 
 normal amount) be passed, the degree of acidity with the same 
 total amount of acid would be low as compared with less than 
 40 ounces. 
 
 On application of the phenolphtalein, if the urine specimen 
 turns pink, it is alkaline, therefore no degree of acidity can be 
 obtained. Litmus paper is applied to the gums and lips to ascer- 
 tain if the mucus be acid. Acid mucus was found in every case 
 tested. The circle of evidence, therefore, is complete. 
 
 Few adult persons have not had an excess of acidity at some 
 period. Complete oxidation is essential to a normal condition. 
 The organs and tissues of the body act as best they can to bring 
 about this condition. In some systems, the liver has all it can do 
 to care for the waste products of the tissues themselves. That 
 the salts of fruit acids may be converted into alkaline substances 
 in the system is true. The liver and tissues become overworked. 
 The fruit habit (especially grape fruit) so generally indulged in 
 to excess in America is producing havoc with the alveolar proc- 
 ess, gums and teeth. 
 
 One case is sufficient illustration of the many requiring treat- 
 ment. A twenty-seven-year-old woman had her teeth and mouth 
 put in good condition in January, 1907. February 16 she re- 
 turned \\dth what she thought a cavity at the cervical margin of 
 the left superior cuspid. Upon examination, I found the gums 
 inflamed and receding, not only at that particular location but 
 about all the teeth. Previous to this, the gums and mucous mem- 
 brane were in fairly good condition. Litmus test showed the 
 
254 INTERSTITIAL GINGIVITIS. 
 
 mucus to be very acid. There was no cavity, only sensitive ex- 
 posed dentine. Much gas was passing from the stomach. Upon 
 interrogation in regard to her food she informed me she had 
 been eating grape fruit every morning for three weeks. Urin- 
 alysis of a twenty-four-hour specimen showed the degree of 
 acidity to be fourteen. Sixteen degrees were retained in the 
 system. The recession of the gums and the sensitive dentine 
 were due to the acid retention. The skin, lungs, and mucous 
 membranes try to dispose of the surplus. If these structures are 
 unable to do so, they are expelled as gas, vomit, or fermentative 
 stools. That the acid excess of the system does pass through the 
 mucous and salivary glands of the mouth to produce destruction 
 of tissue, has already been demonstrated. With these illustra- 
 tions of tissue in the mouth the question arises how far does this 
 acidity affect other tissues and diseases of the body? For want 
 of time, merely a few urinalyses in diseases were made. 
 
 Disease. Degree of Urinary Acidity. 
 
 Arthritis (rheumatoid) One 70. 
 
 Backache (severe) One 10 ; one 25 ; two 30 ; one 35 
 
 one 36 ; .one 40 ; one 50 ; one 79 
 one 82 ; one 87 ; one 90 ; one 95 
 two 100 ; two 110 ; one 120. 
 
 Bronchitis One 56 ; one 58 ; one 60 ; one 61 ; 
 
 one 67 ; one 120. 
 
 Constipation One 25. 
 
 Coryza (acute), children 3 to 13 yrs.0nel2; two 13; one 14; one 15 
 
 one 16 ; one 17 ; one 20 ; one 22 
 one 26 ; one 27 ; one 30 ; one 36 
 one 46; one 47; one 50; one 56 
 three 58 ; one 70 ; one 72 ; one 90 
 
 Cystitis (acute) One 50. 
 
 Diphtheria One 28. 
 
 Dipsomania One 44. 
 
 Eczema (hands) One 50; one 80. 
 
 Enlarged prostate One 100. 
 
 Enterocolitis (chronic) One 35 ; one 80 ; one 110; one 112 
 
 Exoplithalmic goiter (pnl)erty stress) One 54. 
 
 Fibrillae tremor One 21. 
 
 Gastric hyperchloridice One 60. 
 
 Gonorrhea One 120. 
 
 Grippe Two 25 ; one 40 ; one 50 ; one 60 
 
 one 75; one 76; one 80; one 82 
 one 88; one 90; one 94; one 97 
 one 110. 
 
 Hypertrophic rhinitis (acute) One 21 ; one 25; one 113. 
 
URINARY SIGNS OF AUTOINTOXICATION. 255 
 
 Hypertrophic rhinitis (chronic) .... One 32; one 57; one 90. 
 
 Laryngitis (chronic) One 6o ; one 85. 
 
 ]^Iiddle ear, inflammation of One 25 ; one 32 ; one 90. 
 
 Middle ear, chronic snppnrative in- 
 flammation of One 90. 
 
 Meniere's disease One 65. 
 
 oNIigraine One 40. 
 
 ]\Iyocarditis (chronic) One 80; one 100; one 112. 
 
 Neuralgia following grip One 20 ; one 24 ; one 25 ; one 27 ; 
 
 one 40 ; one 46. 
 
 Pneumonia One 18 ; one 26 ; one 27 ; one 33. 
 
 Pregnancy One 10 ; one 12 ; one 14 ; one 16 ; 
 
 one 18 ; one 29 ; one 30 ; one 50 ; 
 
 one 57; one 60; one 62; one 64; 
 
 one 67; one 82; one 84. 
 
 one 82; one 84. 
 Rheumatism and gout One 14 ; one 15 ; one 18 ; one 19 ; 
 
 one 20 ; one 24 ; one 27 ; one 35 ; 
 
 one 52; one 57j one 61; one 67; 
 
 one 70. 
 Rheumatism and heart trouble, 8 
 
 years of age One 40. 
 
 Scarlet Fever One 33 ; one 80. 
 
 Sciatica One 55 ; one 108 ; one 132. 
 
 Sphenoid sinus, inflammation of . . . . One 57. 
 
 Sunstroke One 20. 
 
 Tired feeling One 25 ; one 40. 
 
 Tonsilitis (ulcerating) One 10; one 12; one 14; one 20; 
 
 one 27 ; one 48 ; one 72. 
 Tuberculosis One 16 ; one 20 ; one 21 ; one 36 
 
 one 44 ; one 52 ; one 56 ; one 78 
 
 one 81; one 88; one 102; one 108 
 
 one 115 ; one 142. 
 
 Tuberculous hip disease One 80. 
 
 Typhoid Fever One 76 ; one 88 ; one 90 ; one 109 ; 
 
 one 120. 
 Urticaria One 47. 
 
 On comparing the office patients with those of other special- 
 ists and patients ill at home or in a hospital, it is found that the 
 degree of acidity does not vary to any great extent. A constant 
 abnormal degree of urinary acidity, in an individual attending 
 to his affairs, means that sooner or later an organ or structure 
 is bound to give way. This is particularly true at the senile 
 period of stress (about sixty) when the arteries degenerate. The 
 victim of an abnormal degree of acidity is more subject to dis- 
 ease than one with normal acidity. Study of the effects of a high 
 degree of acidity in an otherwise normal individual whose teeth 
 
256 INTERSTITIAL GINGIVITIS. 
 
 and alveolar xjrocess are being destroyed lias exceedingly inter- 
 esting results. 
 
 Lessened blood alkalinity affects the whole alveolar process 
 by setting up an irritation and inflammation of the coats of its 
 arterioles and in the tooth pulp, producing endarteritis oblit- 
 erans, arteriosclerosis, and nerve-end degeneration. I have dem- 
 onstrated those diseases many times. Disease of the terminal 
 nerves and arteries causes absorption of the bone. The inflam- 
 matory process has been termed interstitial gingivitis ; the bone 
 absorption, osteomalacia, or senile absorption, although it may 
 occur early in life. 
 
 May not osteomalacia in other parts of the body be due to the 
 same cause? 
 
 Cylindruria ^ is not necessarily associated with definite path- 
 ologic alterations of the renal parenchyma. This statement 
 should likewise be accepted as to the occurrence of purely hyaline 
 casts and their presence in small numbers. A few renal epithe- 
 lial cells may be found at the same time occurring either in the 
 urine or adhering to the casts, but never presenting an atrophic 
 or otherwise altered appearance in the absence of definite renal 
 lesions. The presence of compound hyaline and coarsely gran- 
 ular casts, as well as of waxy and amyloid casts, on the other 
 hand, may be regarded as indicating definite changes in struc- 
 ture, so that as far as diagnosis is concerned microscopic exam- 
 ination of the urine furnishes information of more value than the 
 simple demonstration of albumin. 
 
 Hyaline casts are more frequently seen — reference is here 
 made only to the purely hyaline or, at least, but faintly granular 
 form — and are found in all conditions in which albuminuria 
 occurs. When present in only small numbers, and particularly 
 when occurring but temporarily in the urine, it may be assumed, 
 in the absence of other symptoms pointing to renal disease, that 
 there is a mild circulatory disturbance of the kidneys. 
 
 The significance of blood and epithelial cells imbedded on 
 hyaline casts is the same as the significance of blood and epithe- 
 lial casts ; both are pathologic and indicate nephritis. 
 
 Clinical Diagnosis, p. 620. 
 
UEINARY SIGNS OF AUTOINTOXICATION. 257 
 
 Fine granular and hyaline casts often occur from auto-toxic 
 strains on congenitally insufficient kidney in arthritic and allied 
 states. 
 
 The presence of albumin in these cases was exceptional, it 
 being found in but four cases. This would show that in none of 
 these cases had the disease become very marked. When present 
 it does not in itself indicate grave disorder, since albumin may 
 be due to many conditions of the renal tract. It is of interest 
 to us since disturbance of circulation may bring about albu- 
 minuria without inducing structural change in the kidneys. 
 Purdy says: ''Circulatory disturbances, in order to induce 
 albuminuria, must include the renal vessels. In nature they 
 must consist of acceleration of the arterial current or slowing 
 of the venous current, in either case resulting in increased blood 
 pressure. Again, in some derangements of the nervous system 
 which interfere with the vasomotor nerve regulation of the renal 
 vessels, temporary albuminuria is not an uncommon result." 
 Albuminuria is present in auto-toxic neurasthenia, epilepsy, 
 paretic dementia, and the renal crises of locomotor ataxia. 
 
 The specific gravity ranges from 1.005 to 1.031. The normal 
 specific gravity ranges from 1.015 to 1.025. The difference de- 
 pends upon the amount of solids and fluids present, increasing 
 as the solids increase, decreasing as the amount of fluids increase. 
 Specific gravity is hence an index in a general w^ay of metabolic 
 change. The low degree of acidity would indicate that a certain 
 amount of acid was circulating throughout the system. 
 
 Indicanuria denotes the presence in the urine of potassium 
 indoxyl sulphate formed by metabolism of indol absorbed from 
 the intestines. It is supposed to be due to three sources : First, 
 to intestinal putrefaction of nitrogenous substances; second, to 
 suppuration in some part of the body; and third, to the forma- 
 tion of indol in the cells of the body-tissues. The fact that 
 indican is found in the urine is a sufficient indication that this 
 poison has circulated in the blood throughout the entire system 
 and has been returned to the kidneys to be expelled. I have dem- 
 onstrated many times that indicanuria and neurasthenia are in 
 some way related. Reducing the intestinal putrefaction by the 
 use of intestinal antiseptics, the neurasthenic condition of the 
 
258 INTERSTITIAL GINGIVITIS. 
 
 patient is often relieved. The toxic effect of acidosis and indican 
 upon local tissues, especially upon terminal and transitory 
 structure, is very marked. Their injurious effects consist of 
 irritation of the coats of the blood-vessels and changing the 
 chemical quality of the red blood cells. The salivary glands, the 
 mucous glands, the alveolar process, and the dental pulp are the 
 first structures to become involved. 
 
 Indicanuria is one of the great sources of autointoxication. 
 The toxins of indican permeate all the structures of the body, 
 being carried by the blood circulation. While acidosis and in- 
 dicanuria may go hand in hand, the quantity of indican depends 
 to a certain extent upon the acidosis relative to the amount 
 formed in the intestines. Thus, upon reducing a high degree of 
 urinary acidity to normal or below, the indican will be increased, 
 owing to the abnormal bacterial activity in producing putrefac- 
 tion. These germs seem to thrive better in alkaline than in acid 
 media. 
 
 An accumulation of indican in the organism will often cause 
 febrile disturbances, lassitude and gastrointestinal irritation — 
 depending, of course, upon the severity of the attack. The 
 effect of indican is not unlike that of poisonous drugs such as 
 mercury, lead, phosphorus, bromine, quinine, etc., which pro- 
 duce poisonous symptoms in some individuals. In others there 
 are apparently no ill effects. It must, therefore, not be over- 
 looked that in all persons with persistent indicanuria the poison 
 is continuously absorbed from the intestines into the circulation 
 for months and years, and that in many persons it mil not mani- 
 fest itself until the periods of stress at forty-five and again at 
 sixty years of age. Metchnikoff, in considering the phenomena 
 of old age, concludes that autointoxication due to intestinal 
 putrefaction is one of the most important causes of premature 
 senility, in that it causes arteriosclerosis. The accumulation of 
 these toxins in terminal organs, such as the pulp and alveolar 
 process, is as disastrous as the accumulation of any of the poison- 
 ous drugs. Arteriosclerosis is one of the common diseases found 
 in the alveolar process and in the pulp, which is a positive 
 proof of its systemic origin. 
 
 To obtain the amount of indican in a given specimen, take 
 
URINARY SIGNS OF AUTOINTOXICATION. 259 
 
 5 ccm. of urine; pour it into a test-tube; add 5 ccm. of hydro- 
 chloric acid, and shake thoroughly. Let the mixture stand for a 
 few moments. Add 10 drops of hydrogen dioxide, shake thor- 
 oughly, and let it stand for a few moments ; then add 1 ccm. of 
 chloroform, shake thoroughly again, and let it stand. If indican 
 be present, chloroform mil absorb it, turn blue, and settle to the 
 bottom of the tube ; if there be no indican, the chloroform will 
 remain colorless. 
 
 The toxins in the blood which accompany acidosis and indi- 
 canuria are carried to all structures of the body. All structures 
 of the body, however, are not alike. Some, especially those that 
 are active and are needed for the welfare of the body, under the 
 law of economy of growth or use and disuse of structures, can 
 take care of tlie toxins and return the blood to be cleansed of its 
 impurities. Other structures which are of little use, and are 
 called terminal organs and transitory structures, such as the 
 dental pulp and the alveolar process, cannot dispose of the 
 blood so readily. The result of this is an accumulation of tox- 
 ins, and disease follows. Other terminal organs that can stand 
 the strain a little better, but are sure to succumb later if the 
 toxins continue to be present in the blood, are the kidneys, the 
 heart, the liver, the eye and the brain. 
 
 I msh to call the attention of the profession to the fact that 
 early symptoms and systemic disorders may be recognized, and 
 prophylactic means may be adopted to ward off future trouble. 
 Heart-pressure, endarteritis obliterans, arteriosclerosis and 
 dilated arteries are easily demonstrable in the pulp and in the 
 alveolar process by early symptoms of acidosis and indicanuria. 
 It will be seen, then, that acidosis and indicanuria are factors 
 which cannot be overlooked. 
 
 Critical examination of tables must convince a careful ob- 
 server that in every examination two conditions are present; 
 first, autointoxication due to intestinal fermentations and faulty 
 elimination as represented by the indican and an abnormal uri- 
 nary acidity degree ; second, kidney over-strain and renal insuf- 
 ficiency due to hepatic insufficiency. When the liver fails to de- 
 stroy the poisonous "materials and the bowels to eliminate the 
 toxins, over-strain of the kidneys causes the blood to become 
 
260 INTERSTITIAL GINGIVITIS. 
 
 overcharged with toxins and acidity, the heart and arteries 
 undergo degenerative changes, and cardiac hypertrophy and 
 cardio-vascular diseases, with insufficient blood supply, result. 
 
 It may be possible that in the near future other poisons than 
 those already mentioned will be found in the urine, which may 
 produce toxic effects on the alveolar process. Since this chap- 
 ter was wa-itten, the following appears in the Journal of the 
 American Medical Association: "A few unique anomalies of 
 metabolism, notably alkaptonuria and cystinuria, have attracted 
 attention quite as much because of the interpretation w^hich they 
 lend to the normal disintegration of protein in the body as on 
 account of the pathologic features involved. From the fact that 
 certain diamirs, cadaverin and putrescin, characteristic of the 
 putrefaction of jjroteins, frequently are found in conjunction 
 with cystin in the urine of patients, it has at times been assumed 
 that there is an essential connection in cystinuria between ali- 
 m.entary putrefactive changes and the output of characteristic 
 abnormal excretory products. Cystinuria, however, has been re- 
 garded of late rather as an abnormality of protein metabolism 
 in which the amino-acid cystin — a typical degradation product 
 of albuminous substances — is not further broken down and oxi- 
 dized as ordinarily. This view is strengthened by the simul- 
 taneous finding of other amino-acids, leucin and tyrosin, in cer- 
 tain cases. The latest novelty is the discovery of another amino- 
 acid, lysin (diamino-caproic acid), in the urine of a patient with 
 cystinuria. Since this compound is known to be the mother sub- 
 stance of cadaverin, the intimate inter-relation of the various 
 observed constituents is further emphasized. Taken together, 
 the accumulated data strengthen the conception of cystinuria as 
 a condition in which the usual progress of protein catabolism is 
 profoundly inhibited. One by one the unused fragments are 
 cropping out as new cases become available for study." 
 
CHAPTER XXIV. 
 
 AETERIOSCEEROSIS, ENDARTERITIS OBLITERANS AND NERVE END 
 
 DEGENERATION. 
 
 Endarteritis obliterans and hypertropliy of tlie middle and 
 outer coats of the arteries are physiologic processes concerned 
 in the disappearance of blood vessels functional in the fetal 
 state, but losing such function after birth. Like all physiologic 
 processes of the fetal type these become pathologic under ordi- 
 nary conditions of post-natal life. For these reasons they again 
 become physiologic in the involutional periods like the climac- 
 teric and senility. In transitory structures, like the alveolar 
 process, there is continual trembling between the physiologic 
 and pathologic. Undue excitation of the structure brings on an 
 intensity of the process which tends to become pathologic. As 
 I demonstrated a decade ago, endarteritis obliterans and hyper- 
 trophy of the middle and outer coats of the arteries play a large 
 part in interstitial gingi^^tis. 
 
 In consideration of this subject, the changes in the elasticity 
 of the artery and vein walls and the permeability of the capil- 
 lary walls will be discussed. 
 
 The vessel walls are capable of great elasticity and bear the 
 tension of the pressure of the blood A\dthout sho^^ing any condi- 
 tion of being strained. This elastic function of the walls is con- 
 trolled by the muscular coat, which changes the chemic energy 
 of the blood stream into energy of elasticity and in this manner 
 keeps the vessel walls in a normal elastic state. The changes 
 that take place in the arterial walls of the aortic system are of 
 more or less importance, since the normal elasticity of the 
 artery walls, blood pressure regulation, and distribution are 
 dependent upon the depth and intensity of these changes. 
 
 When the vessel walls become diseased there may or may not 
 be serious disturbance in the blood circulation. The acute and 
 chronic contagions and infections, a general nutritional disturb- 
 ance or poisons taken either internally or externally, and a high 
 
262 INTERSTITIAL GINGIVITIS. 
 
 blood pressure tend to weaken the arterial walls so that their 
 elastic tonicity, in some instances, is completely lost. 
 
 This weakened elasticity is easily recognized by a distensile 
 pulse and also registered by the sphygmomanometer. At the 
 same time, arterial murmurs can be heard in the large arteries, 
 especially the femoral, which are apparently a result of the 
 rapid vascular changes characteristic of a high pulse. A pulse 
 sometimes observed in retinal arteries can also be attributed to 
 this source. 
 
 In the conditions just mentioned there are no great circula- 
 tory disturbances, but there is a tendency to change in tlie struc- 
 ture of the arterial walls. As a result of this w^eakened state, the 
 lumen expands and a larger amount of blood flows through the 
 artery, but its rapidity is decreased. So with the alveolar pro- 
 cess, the arteries and veins inclosed within bony walls have little 
 or no expansion, hence the tissues become more susceptible to 
 poisons and toxins circulating in the blood stream. The de- 
 creased flow of the blood stream, in turn, causes new connective 
 tissue to form in the intima of the artery, which thickens this 
 outer coat, making it less elastic and reducing the pulse move- 
 ments. 
 
 Any arteries of the body are liable to become involved, but 
 more particularly those of the extremities and end organs. While 
 puberty changes may produce a severe attack, the condition is 
 more frequently noticed later in life — the later, the more pro- 
 nounced. Men are more subject to the disease than women ow- 
 ing to the fact that women eliminate much more freely than 
 men, and because they are not often subjected to drug poisons. 
 Coldness of the limbs, hard whip-cord arteries with no pulsa- 
 tion, and, in extreme cases, gangrene of the extremities result. 
 The disease begins in the intima and extends to the other coats 
 of the artery. It may be found in all local inflammations of 
 long standing, especially in the extremities, the alveolar process, 
 and may occur in conditions of vasomotor ataxia, such as are 
 present in Raynaud's disease and allied conditions. Syphilis, 
 tuberculosis, typhoid fever, scurvy, and the condition underlying 
 arterio-capillary fibrotic kidney lesions act at times as predis- 
 posing causes. Toxins and autotoxic products of retained waste 
 
ARTEKIOSCLEROSIS, AND NERVE END DEGENERATION. 263 
 
 may disturb physiologic balance, thus giving the pathologic 
 phase of this disorder sway. 
 
 Endarteritis is an inflammation of the internal coat of an 
 artery or capillary, generally of chronic type. Its pathogeny is 
 as follows: In direct contact with the blood streams is the 
 endothelium (a layer of flattened cells) ; next is the tunica 
 intima, composed of elastic fibers arranged longitudinally ; next 
 comes the middle coat, composed of muscular fibers arranged 
 transversely. The outer coat consists of longitudinal connective 
 tissue, which contains the vasa vasorum. In the capillaries, the 
 intima lies in immediate contact with the surrounding tissues, or 
 accompanied by a rudimentary adventitia. In other words, the 
 walls of the capillaries consist of almost nothing but the intima. 
 The capillaries have certain contractility; they contract or 
 dilate without muscular fibers. The veins probably also have a 
 certain amount of contraction and dilatation from irritability of 
 
 Fig. 79. — Endarteritis Obliterans (Kaufmann). 
 A, Adventitia. E, Elastic Tissue between Middle Coat and Intima. M, Muscular. 
 
 J, Thickened Intima. 
 
 the intima. Each coat of the arteries takes on a special type of 
 inflammation. The causes of endarteritis are numerous. 
 
 Inflammation of the intima of the blood vessels may be due 
 to irritation from without or within. When it occurs from with- 
 out, any local irritation will set up an inflammation which may 
 extend to the outer coats of the capillaries. This produces a 
 marked increase of blood. The vasa vasorum become swollen, 
 the white blood corpuscles crowd into the terminal capillaries 
 and migrate into the extra vascular space. Rapid proliferation 
 of the round-cell elements takes place. The walls of the vessels 
 become thickened. Owing to the projecting intervals of the 
 intima, the caliber of the blood vessels diminishes (Fig. 79). 
 
264 INTERSTITIAL GINGIVITIS. 
 
 Irritation occurring from within, results either from trophic 
 changes in the system from direct irritation from toxaemias, or 
 from both interdependently. Under these circumstances toxins 
 may have an affinity for a certain organ, tissue or part, and pro- 
 duce irritation in the capillaries in a distinct part of the body, 
 or the capillaries through the entire body may become involved. 
 Thus, in typhoid fever, the Peyer's gland in the intestine be- 
 comes involved; in scarlet fever, the skin or kidney; in malaria, 
 the liver and spleen; in Bright 's disease, the kidney; while in 
 mercurial and lead poisoning and scurvy, the mucous membrane, 
 and especially the gums, become diseased. In many of these con- 
 ditions, however, before the tissue already irritated becomes 
 involved, the nervous system has become affected. The nervous 
 system may already have become affected from other causes. 
 Thus, locomotor ataxia, traumatic injuries to the spine, paretic 
 dementia, cerebral paralysis, neuroticism and degeneracy, and 
 last, but not least, stomach neurasthenia. The poison in the 
 blood, together with the diseased peripheral nerves, produce irri- 
 tation and inflammation of the inner coat of the capillaries. If 
 this irritation does not disappear soon after its inception, 
 the inflammation tends to affect the other coats of the 
 blood vessels. Under certain conditions, endarteritis may, 
 however, never involve the other coats of the vessels. When 
 irritation of the inner coat of the capillaries takes place, 
 proliferation of the endothelium occurs. This inflammatory 
 growth tends to obstruct the lumen of the vessel. The media 
 may likewise become thickened by an increased connective tissue. 
 The capillaries become obstructed, and finally obliterated. This 
 finally impedes the circulation. Fig. 80 shows such a condition 
 in the scurvy case, elsewhere illustrated. 
 
 Irritation may be of less intensity but greater duration, as in 
 cases of syphilis, tuberculosis, scurvy, mercurialism, plurabism 
 (lead poisoning), etc, and the results are then slowly effected. 
 Proliferation of sub-endothelial connective tissue gradually 
 increases until it reaches its limit (endarteritis obliterans). This 
 influence of the proliferation is exerted in addition to that of the 
 round-cell infiltration about the structure. 
 
ARTERIOSCLEROSIS, AND NERVE END DEGENERATION. 
 
 265 
 
 The recent studies of Hektoen^ on meningeal tuberculosis 
 demonstrate that tubercle bacilli may penetrate the unbroken 
 endothelial layers of the vessel and stimulate marked prolifera- 
 tion of the sub-endothelial connective tissue. An internal irri- 
 tant, such as may be produced in the course of any infectious dis- 
 ease or from sul)oxidation, probal3ly acts upon the endothelium 
 of the walls of the smaller blood vessels in such a way as to per- 
 mit the escape through the walls first of serum, then of leuco- 
 
 X 150. D. D. obj. Zeiss. 
 Fig. 80. — Cross Se(tion of Peridental Membrane, Showing Endarteritis 
 Obliterans. Scurvy in Man. 
 C, Cementum. D, Dentine. I, Peridental Membrane. IT, Nerve Tissue. EO, Endar- 
 teritis Obliterans. 
 
 cytes, the latter infecting and surrounding the vessels. The effect 
 of the chronic endarteritis is to check the blood supply to the gum 
 tissue. Mercury, lead and other poisons circulating through the 
 blood are forced to remain, hence discoloration of tissue along 
 the gum margin. Interstitial gingivitis, resulting in a slow dis- 
 turbance of nutrition, produces overgrowth of connective tissue. 
 In all cases of chronic interstitial gingivitis, as shown in the illus- 
 tration, are the blood vessels thus involved. 
 
 * American System of the Practice of Medicine, page 119. 
 
266 
 
 INTERSTITIAL GINGIVITIS. 
 
 Among the predisposing influences which canse this disease 
 are syphihs, tuberculosis, mercurialism, phimbism, brass poison- 
 ing, lithasmia, nephritis, gout, rheumatism, alcoholism, scurvy, 
 nervous diseases, pregnancy and old age. Under certain con- 
 ditions of the system any and all diseases which tend to lower the 
 vitality, producing anaemia, will assist in producing this disease. 
 The direct cause may be resultant overstrain of the blood vessels. 
 
 Owing to obliteration of the arterioles in the alveolar process 
 stasis of blood must follow. The detritus from the alveolar proc- 
 ess, therefore, must remain in the tissue and collect upon the 
 roots of the teeth. 
 
 Fig. 81. — Longitudinal Section op Gingival Border, Higher Magnification, Show- 
 ing Eound-Cell Inflammation Extending to the Inner Coat of the Blood 
 Vessel, and also Plasma — -Mast Cells. 
 
 Endarteritis obliterans and arteriosclerosis of the blood 
 vessel walls in the alveolar process are always observed in con- 
 nection with both local and constitutional diseases. 
 
 No structure aifords such a favorable opportunity for the 
 study of endarteritis obliterans and arteriosclerosis as the alve- 
 olar process in animals and human, since it can be obtained in 
 quantities at all times and under all conditions. It may be pro- 
 duced in healthy animals by the internal administration of drugs, 
 metals and other poisons. 
 
AETERIOSCLEKOSIS, AND NERVE END DEGENERATION". 267 
 
 My researches on this series of experiments were made upon 
 humans, monkeys, and dogs. Decalcification of the alveohir proc- 
 
 FiG. 82. — Arteriosclerosis in Tuberculous Monkeys. 
 
 ess was made in weak acid solution and prepared for the micro- 
 scope in the usual way. 
 
 Fig. 83.— Transverse Section of Alveolar Process, Chronic Inflammation Ex- 
 tending Throughout. Dog. 
 
 On the administration of drugs, especially mercury or lead, 
 to healthy young dogs, inflammation of the alveolar process with 
 
268 
 
 INTERSTITIAL GINGIVITIS. 
 
 diseased arterial walls is seen at the end of a month or six weeks. 
 Fig. 81 shows the commencement of the thickening of the intima 
 in a dog. The coats of the arteries are well defined and the in- 
 flammatory process has jnst begun. Examination of the alveo- 
 lar process of animals or human beings suffering from disease, 
 in which the eliminating organs are not throwing off effete mat- 
 
 FiG. 84. — Arteriosclerosis and Obliterans in Arteries of a Dog with 
 Interstitial Gingivitis. 
 
 ter, especially in syphilitic, tuberculous and scorbutic patients, 
 easily reveals this morbid state. 
 
 Fig. 82 is a poor illustration of the disease in pregnancy. If 
 such patients are degenerates the process will be exaggerated. 
 
 Fig. 83 illustrates endarteritis obliterans in the artery of a 
 dog with interstitial gingivitis. 
 
 Fig. 84 is from the alveolar process of a tuberculous monkey. 
 
Fig. 85. — Arteriosclerosis from Mercurial Poisoning. 
 
 Fig. 86. — Arteriosclerosis from Lead Poisoning. 
 
270 
 
 INTERSTITIAL GINGIVITIS. 
 
 Fig. 85 illustrates the closing of three arteries from mercurial 
 poisoning. 
 
 Fig. 86 shows endarteritis obliterans with arteriosclerosis in 
 interstitial gingivitis from lead poisoning. 
 
 Fig. 87. — Arterio-sclerosis and Obliterans from Diabetes Mellitus. 
 
 Fig. 87 shows arteriosclerosis and endarteritis obliterans in 
 interstitial gingivitis from diabetes mellitus. 
 
 Pig. 88. — Arteriosclerosis and Obliterans from a Syphilitic. 
 
 Fig. 88 illustrates arteriosclerosis of three arteries in a syph- 
 ilitic. 
 
 It will be seen from the illustrations that these pathologic 
 conditions in the blood vessels of the alveolar process produce 
 stasis of blood which cuts off the nutrition of the tissues. This, 
 in turn, not only lowers the vitality of the parts, but together 
 with local disturbances causes rapid destruction of the gums, 
 peridental membrane and alveolar process. 
 
AETEEIOSCLEROSIS, AND NERVE END DEGENERATION. 271 
 
 NERVE END DEGENERATION. 
 
 Since the brain presides over development of the tissues of 
 the body through its trophic and vasomotor systems, it must be 
 as fully developed and normal in construction as possible so that 
 body tissues may develop normally. Pleasure, happiness and 
 laughter aid digestion, while melancholia and grief may retard 
 growth and function and produce tropho-neuroses. An unstable 
 nervous system produces unstable tissues, i. e., either excessive 
 or arrested. 
 
 While the nervous system has other special functions, the one 
 great object is that of regulating growth and repair. As Mari- 
 nesco has shown, this function resides even in the neuron or 
 nerve unit. Growth and repair are regulated through the trophic 
 and vasomotor systems. In the domain of bone growth, trophic 
 nerve anomalies were first observed. Brown-Sequard demon- 
 strated anomalies in tabetic joints of sufferers from locomotor 
 ataxia and later similar states were observed in the jaws. An- 
 other allied neurosis, paretic dementia, presents similar trophic 
 disturbances, as Kiernan pointed out thirty-five years ago.- 
 
 Among these tropho-neuroses is one characterized by loosen- 
 ing and falling out of the teeth by alveolar resorption, gingival 
 ulceration and perforation, with at times maxillary necrosis. 
 This condition has long been recognized by alienists and neurol- 
 ogists as causing that loss of the teeth which occurs in paretic 
 dementia, locomotor ataxia and diabetes. This function of the 
 trophic nerves, as I have elsewhere shown, has received but little 
 attention from dentists, albeit its influence has been recognized 
 in dental pathology in connection with the great neuroses in 
 which gum disorder occurs, followed by a loosening of the teeth. 
 
 Degeneration of the peripheral nerves due to interruption of 
 the connection with the central nervous system was first shown 
 by Nasse and Valentine in 1839. Not until 1850, however, was a 
 thorough study made of nerve degeneration by Waller, the 
 pathology of which is now known by his name. Wallerian degen- 
 eration implies change in the terminal ends of the peripheral 
 nerves after they have been cut, which consists in coagulation or 
 
 "Journal of Nervous and Mental Diseases, 1878. 
 
272 INTERSTITIAL (MN(;i\^ITIS. 
 
 breaking np of tlie myelin sheatli, destruction of the axis cylin- 
 der, tlie neurilemma with its nuclei remaining for some time pre- 
 served. If a sensory nerve be cut through peripheral to the 
 spinal ganglion complete degeneration ensues. 
 
 Similar experiments showed that if the dorsal root of a spinal 
 nerve be cut through at a point between the ganglion and the 
 spinal cord the portion of the nerve attached to the ganglion did 
 not undergo the typical degeneration, while the portion still con- 
 nected with the cord showed the characteristic degeneration phe- 
 nomena which could be traced throughout the whole course of its 
 constituent fibers in the dorsal funiculi of the cord. The cells of 
 the spinal ganglia have therefore been looked upon as trophic 
 centers for the peripheral sensory nerves and their intramedul- 
 lary continuations. 
 
 Similar degenerations in the domain of the central nervous 
 system likewise occur ; secondary descending degeneration of the 
 pyramidal tract, established by Turck, and ascending secondary 
 degeneration in the spinal cord after transverse lesion being 
 analagous. 
 
 Converting then, as Barker^ remarks, the Wallerian doctrine 
 into terms of the neuron concept, the following general law may 
 be laid down: "Whenever it has suffered a solution of continu- 
 ity, with severing of its connection with the cell body and den- 
 trites of the neuron to which it belongs, the axon, together with 
 the myalin sheath covering it, undergoes in the part distal to the 
 lesion acute and complete degeneration. This degeneration 
 includes not only the main axon, but also its terminals, together 
 witli the collaterals and their terminals connected with it." 
 
 Some investigations have shown that the slightest injuries to 
 nerve cells or neura will give rise to easily demonstrable degen- 
 erative lesions in other parts of the cell. The most significant 
 instance is in lateral sclerosis, where the pyramidal motor cells 
 of the cortex show no marked lesions, though the most distal por- 
 tions of the nerve fibers arising from them have gradually 
 degenerated. 
 
 In some peripheral nerve diseases, according to Strumpell, 
 
 The Nervous System. Barker. 
 
AKTERIOSCLEKOSIS, AND NEEVE END DEGENERATION. 273 
 
 the degeneration of the distal portion of the axones may be due 
 to direct action of toxins exerting a deleterious influence upon 
 the cell body or the whole neuron. In WoUenberg's opinion the 
 primary type of disease of the sensory neura in tabes is of this 
 kind. 
 
 As Sidney Knli* has shown, in some of the toxic forms, as for 
 instance in neuritis due to poisoning ^yiih lead and arsenic, the 
 cells of the spinal cord as well as those of the spinal gangUa and 
 brain may be diseased, and according to the neuron theory the 
 toxic substances attack these cells before the nerve fiber itself is 
 altered. Such an assumption explains why pronounced degen- 
 eration of peripheral nerves may occur without causing any ap- 
 preciable symptoms. Toxins and intoxications will produce the 
 same results, especially in those nerves extending into and 
 through the alveolar process. Pitres and Vaillard first showed 
 that after typhoid fever, many nerve fibers are found degener- 
 ated, in cases in which, during life, symptoms of neuritis were ab- 
 sent. The same observers found like states in the nerves of those 
 who had died from tuberculosis. Later observations have ex- 
 tended these states to such diseases as diphtheria, syphilis, alco- 
 holism, carcinoma, inanition, marasmus, arteriosclerosis ^and 
 leprosy; in the so-called rheumatic neuritis of the facial nerve 
 and to inflammation due to articular rheumatism, gout, puerperal 
 infection, tuberculosis, etc. 
 
 The method of cell poisoning has been observed in other 
 intoxications. Certain groups of neura are more susceptible 
 than others to a given toxication. The same group of nerve 
 cells in two individuals may react very differently to similar 
 doses of the same poison. Syphilitic toxin shows a decided 
 preference for certain parts of the cerebral cortex, other areas 
 being less affected. The nerve enchngs in all parts of the body 
 are markedly involved, especially those in and about the teeth. 
 Peripheral nerve degeneration results where the blood current 
 or the nerves themselves are involved from faulty metabolism, 
 etc. 
 
 Nerve lesions more readily result where nerves are confined 
 within restricted walls of transitory structures where the pulp 
 
 * American Medicine, Vol. Ill, No. 21, pp. 865, 
 
274 INTERSTITIAL GINGIVITIS. 
 
 has degenerated, especially in cases of hypercementosis of the 
 root. When degeneration of the peripheral nerves in the pulp 
 takes place there may at first be pain, continuously perceptible 
 to the patient or absent except under manipulation or replaced 
 by analgesia. In most cases there is analgesia, owing to the 
 peculiar anatomic construction of the tooth and nerve degen- 
 eration. There is loss of function. The same condition exists 
 in the alveolar process when diseases or intoxications occur, the 
 junction of the peripheral nerves is destroyed, resistance is low- 
 ered, disease of the process and peridental membrane results. 
 
CHAPTER XXV. 
 
 ABSORPTION OF THE ALVEOLAE PROCESS AND CALCIC DEPOSITS UPON 
 THE ROOTS OF THE TEETH. 
 
 Absorption of tlie alveolar process is the result of irritation, 
 resultant malnutrition, and subsequent inflammation. The 
 osteoblasts and osteoclasts are ever present to build up and 
 tear down bone structure on the slightest provocation. Hyper- 
 trophy (building up of bone tissue) is the result of intermittent 
 pressure, and atrophy, or absorption of bone, is due to constant 
 irritation and pressure. As has been elsewhere shown, from 
 its transitory nature the alveolar process is unusually sus- 
 ceptible to these influences. The causes of absorption are loss 
 of teeth by extraction, undue pressure upon one or more teeth 
 from improper articulation (Bomvill), wedging and irregular- 
 ity correction, heat under artificial dentures, and interstitial 
 gingivitis of local and constitutional origin. 
 
 According to Kaufmann, lacunar absorption is the most 
 common type. This may be true in morbid anatomy of bone 
 tissue generally, but it is not true of absorption of the alveolar 
 process. On an examination of hundreds of slides prepared 
 from canine and human jaws (of which characteristic types are 
 illustrated), by far the most common form of absorption was 
 found to be halisteresis. Perforating canal absorption, which 
 Kaufmann has ''occasionally met ^^dth," is certainly very com- 
 mon, while lacunar absorption holds third position. This order 
 of absorption is accounted for by the fact that where structures 
 are transitory, halisteresis, as quickest method, follows by the 
 law of the survival of the fittest. For the same reason per- 
 forating canal absorption should stand second. The blood ves- 
 sels of von Ebner being most numerous, although considered 
 smaller, would naturally be the second tissue involved. As in 
 interstitial gingivitis, absorption of the alveolar process is in- 
 variablv due to inflammation, halisteresis apparently starts at 
 
276 INTERSTITIAL GINGIVITIS. 
 
 the larger Haversian canals from which this form of absorption 
 invariably originates. 
 
 Interstitial gingivitis extends to the alveolar process through 
 the periosteum as well as the peridental membrane (not, as den- 
 tists usually believe, by way of the peridental membrane alone). 
 This is demonstrated by the illustrations. The entire alveolar 
 process thus becomes involved. The products of inflammation 
 extend through the Haversian canals (a path obviously evident 
 in pathologic illustrations), setting in action the three forms of 
 absorption as elsewhere illustrated. 
 
 Halisteresis Ossiuni (uoAo? of salt, (rre/yAots^ deprivation) or 
 decalcification, is that process of absorption wherein solution of 
 the lime salts first takes place, while the cartilage or matrix 
 remains for the time undisturbed. 
 
 Solution of the lime salts begins at the periphery of the 
 Haversian canal and advances toward the center of the tra- 
 beculae. This absorption follows, as a rule, the bone layers. 
 Bone centers are, therefore, usually the last to be absorbed. 
 Frequently decalcification becomes complete ; nothing remaining 
 but the organic matrix or cartilage. Finally, this is also en- 
 tirely destroyed. As the osteoblasts occur in the matrix or 
 cartilage, it is not difficult to understand that absorption may 
 extend far, yet restoration of the alveolar process may occur. 
 After destruction of the matrix such a restoration is impossible. 
 New fibrous tissue may be partly restored, but it is doubtful if 
 the alveolar process can be. 
 
 Both Ziegler ^ and Kaufmann - divide osteomalacia into senile 
 and juvenile. The latter occurs most frequently during preg- 
 nancy. In senile absorption, after a certain period, the entire 
 skeleton is affected. The condition begins most frequently in 
 the "vertebra^ and thorax; later extending to the extremities." 
 In pregnancy ''the pelvic bones are first involved, the process 
 then extends to the other bones." It is singular that the alveolar 
 process should have been so much neglected by pathologists, 
 since, in both states, the alveolar process becomes involved long 
 before the bones of the body. 
 
 ^ Special Pathological Anatomy, page 151. 
 " Pathologisehe Anatomie. 
 
ABSORPTION AND CALCIC DEPOSITS. 277 
 
 This is due to three reasons: first, to trophic changes; sec- 
 ond, to the alveolar process being a transitory structure; and 
 third, to improper care of the gums at these periods. 
 
 Osteomalacia occurs in the alveolar process much earlier 
 than at the so-called ' ' senile ' ' period. It is found at twenty, or 
 even earlier, and has been termed juvenile osteomalacia. At 
 any period beyond that year, it occurs probably from the pre- 
 maturely senile states of which precocity is a type. The lost 
 tissue is regained often after confinement in the ''pregnancy" 
 type, but is never regained in the senile. 
 
 The causes which produce morbid decalcification are not thor- 
 oughly determined. Some believe it to be due to lactic acid in 
 the system, others attribute it to an increased amount of carbonic 
 acid in the blood. Eisenhart believes it to be due to a want of 
 alkalinity of the blood, while von Recklinghausen charges it 
 to a local irritation of the vascular mechanism of the bones. It 
 would seem, from examinations already cited, that, so far as the 
 alveolar process is concerned, local irritation from biochemic 
 changes in the blood, as suggested by von Recklinghausen, is 
 the chief cause. Premature absorption of the alveolar process 
 accompanies the movement of the teeth in their correction or in 
 rapid wedging. Frequently the alveolar process is never fully 
 restored, thus producing a predisposing factor for future 
 disease. 
 
 Premature absorption, or osteomalacia of the alveolar proc- 
 ess, is easily recognized. A shrinking of the gums and alveolar 
 process exposing the necks of the teeth is very conspicuous. 
 Frequently the gums and mucous membrane covering the alveo- 
 lar process are quite red (this is very noticeable in dogs), and a 
 thinning of the alveolar process over and between the roots of 
 the teeth. The process of one tooth only may become involved ; 
 again the process over two, or the whole jaw, and again both 
 jaws become affected. 
 
 When osteomalacia occurs, either of pregnancy or senile 
 type, although the tissues be seemingly restored to health, struc- 
 tural change has taken place to such an extent that it ever 
 remains a predisposing factor to interstitial gingivitis. 
 
 In I'ig. 41 may be seen the blood vessels of von Ebner. 
 
278 
 
 INTERSTITIAL GINGIVITIS. 
 
 These blood vessels are also to be observed in Fig. 61. They 
 are very common in the alveolar process and, according to Volk- 
 mann, are the source of the perforating canals which bear his 
 name. 
 
 X 50. i/i;-iiich obj. No. Oc. 
 Fig. 89. — Cross Section of Tooth, Alveolar Process and Peridental Membrane, 
 
 C, Cementum. 
 
 D. 
 
 Showing Lacunar Absorption. Man. 
 Dentine. I, Peridental Membrane. J, Alveolar Process. 
 O, Lacunar Absorption. 
 
 These canals run in all directions. After absorption has gone 
 on to form medullary spaces, these canals penetrate through the 
 trabeculae from one space to the other (Fig. 43). The position of 
 this type of absorption in the order of frequency comes from the 
 fact that, in this disease, absorption is almost entirely due to 
 inflammation; hence the blood vessels are the first to become 
 involved. Those entering the Haversian canals, being the larger, 
 are first affected, and hence halisteresis naturally precedes. 
 
ABSORPTION \y\) CALCIC DEPOSITS. 
 
 279 
 
 When irritation takes place in a nerve or part of bone wliicli 
 is about to be a])sorbed, niultiniiclear cells arise at the border in 
 the periosteum and jjeridental membrane. They attach them- 
 selves to the surface of the bony trabecule^, xlccording to Sud- 
 dutii, ^'the absorber and the absorbed must be in touch with each 
 
 X 300. No. 2, projection ocular. D. I), obj. Zeiss. 
 
 Fir,. 90. — Section of Peridextal Membrane, Showing Lacunar Absorption in Dog. 
 
 J, Alveolar Process. O, Lacunar Absorption. I^, Inflamed Peridental Membrane. 
 
 other." Kolliker has named these cells ''Osteoclasts," which 
 term has come into general use. Very soon after these cells 
 make their appearance, cavities are seen in the bone tissue. 
 These cavities are called Howship's lacunae. Lacunar absorp- 
 tion, as elsewhere shown, takes place as a result of irritation and 
 overstinnilation. Fig. cS9 shows a cross section of the end of one 
 of the buccal roots of Fig. 91. As will be observed, this tooth 
 was held in place by two buccal roots. As much resistance was 
 h'(|iiii-(Ml of tliese. two I'oots as was formerly required of three. 
 
280 INTERSTITIAL (ilNCilVITIS. 
 
 Trritatioii due to excessive force in mastication was causing 
 absorption. Round-cell inflammation is not yjresent in the peri- 
 dental membrane. The irritation may be continued until inflam- 
 mation sets in and until the bone is entirely al)Sorbed, as noticed 
 in Fig. 90. Small round-cell inflammation is (juite noticeable in 
 the surrounding- tissue. 
 
 Sometimes these lacuiur may be seen extending along the 
 entire length of l)one. As many as thirty-seven may be counted 
 in some fields (Fig. 42). Lacunar absorption frequently so 
 extends through the Haversian canals as to cut off pieces of the 
 alveolar process. A casual glance at Fig. 89 demonstrates this. 
 This figure could be multixjlied many times from other slides. 
 These frequently come away with the peridental membrane when 
 the tooth is extracted. This is often noticed in removing loose 
 teeth due to interstitial gingivitis. By passing the finger over 
 the surface of the root, the rough pieces of bone may be easily 
 felt. 
 
 Aside from the forms of absorption already noted, absor])tion 
 of the alveolar process is often seen, the result of neuropathic 
 lesions. Paretic dementia, diseases of the spinal cord, low forms 
 of inflammation, general debility and traumatism, together with 
 unhygienic conditions of the mouth, are fruitful sources of in- 
 terstitial gingivitis and absorption of the alveolar process. Ab- 
 sorption of the alveolar process takes place also in diathetic 
 diseases in which the nervous system has l)een involved (syphilis, 
 scurvy, lithaemia, etc.). 
 
 CALCIC DEPOSITS. 
 
 There are many instances in which interstitial gingivitis 
 takes place, with absorption of the alveolar process and exfolia- 
 tion of the teeth, without calcic deposits. In such cases the blood 
 is charged with only sufficient lime salts for the nourishment of 
 the body. The waste products are carried off with the excreta. 
 In absorption of the alveolar process, inflammation does not 
 seem to extend to the capillaries, the result of which is, tliis 
 waste material is carried into the circulation. In this way, 
 calcic material does not collect in the fluids and upon the teeth. 
 In those cases in which pus is not present (there being a lessened 
 amount of carbonic acid) calcic deposits rarely take ]»lace. The 
 
ABSORPTION AND CALCIC DEPOSITS. 
 
 281 
 
 percentage of teeth so found, however, is not so large as those 
 with deposits. 
 
 Examination, by a magnifying glass, of a recently extracted 
 tooth (with the root covered with sernmal deposits) shows the 
 lime deposited in a manner resembling that of stalactite forma- 
 tion. The deposits often stand out distinctly independent of 
 each other (Fig. 91). This condition is due to deposits from the 
 blood, resultant on biochemic changes in the inflamed tissues. 
 Blood stasis occurs in the gum tissue, fibrous tissue of the perios- 
 
 FiG. 91. — Palatine Eoot of a Molar Tooth Showing Calcic Deposits. 
 
 teum, peridental membrane and alveolar process, through which 
 last much of the blood circulates. This stasis may be consequent 
 upon conditions varying from simple inflammation to disease of 
 the endothelium, producing endarteritis obliterans. 
 
 The blood has become surcharged in all constitutional dis- 
 eases, but more especially in kidney lesions. Deposits occur in 
 the fluids and upon the roots of the teeth. Frequently the de- 
 posit is found only on one side or only at one particular spot 
 on the side of the root; again at the apex, when the pulp is de- 
 stroyed. It may encircle the root. The inflammatory process 
 
282 INTEESTITIAL GINGIVITIS. 
 
 may therefore be circumscribed as to area or the whole tissue 
 may be involved. The deposit is circumscribed in the area of 
 inflammation. The calcareous matter absorbed from the alveolar 
 process in the immediate vicinity of the root is soon deposited 
 upon the root or roots because of the impeded circulation.'' ** Os- 
 sification, as has been well remarked, is an active development 
 in which the tissues are abundantly supplied with blood. There 
 is a rapid cell proliferation, and the calcareous matter forms an 
 intimate and permanent union with the tissues. Calcification, 
 on the other hand, is passive, and indicates an impaired vitality. 
 Calcification begins as a rule in the interstitial tissue. In regard 
 to the origin of the calcareous salts, it is generally believed that 
 they come more or less immediately from the blood, although 
 Rokitansky supposes that they were formed by a metamorphosis 
 of the tissues involved." 
 
 Calcification is due to two varieties of causes: general and 
 local. The former are dependent upon changes in the blood or 
 its circulation, due, for example, to disease or senile change. In 
 composition the blood may be so altered as to contain an ab- 
 normal amount of calcareous matter. This effect is most com- 
 monly produced by absorption of lime salts from osseous tissues 
 which are the seat of extensive caries, osseous cancer, osteo- 
 sarcoma or osteomalacia. The calcareous matter thus taken up 
 is conveyed to other and often remote parts and there deposited, 
 constituting the ''metastatic calcification" of Virchow. Kiitt- 
 ner, of St. Petersburg, has observed a rapid calcification of 
 nearly all of the small arteries as a result of caries involving the 
 dorsal and lumbar vertebrae in a nineteen-year-old boy. Virchow 
 has observed a case in which, as a result of bone cancer (affect- 
 ing nearly all of the larger bones, particularly the borders of the 
 vertebrae and the skull), the calix and pelvis of the kidneys, the 
 lungs, parenchyma, and the stomach mucous membrane were 
 calcified. 
 
 Circulation of the blood may be retarded and thus favor pre- 
 cipitation of calcareous matter normally held in solution. To 
 this is chiefly due the frequency of calcareous degeneration from 
 general loss of vitality. 
 
 'Wood's Handbook of Medical Sciences, Vol. 1, page 743. 
 
ABSORPTION AND CALCIC DEPOSITS. 283 
 
 Calcification rarely, if ever, depends upon general causes 
 alone. There is, as a rule, a local influence. Very often this is 
 due to pre-existing chronic inflammation. Old accumulations of 
 pus and exudates are exceedingly prone to calcification. The 
 deposit frequently occurs also in fibrous walls surrounding the 
 accumulation. A mere loss of function predisposes to calcifica- 
 tion. Such is the case in and about the tissue of the alveolar 
 process. The decalcified material from the alveolar process col- 
 lects in the soft tissues as well as upon the roots. In his paper 
 George T. Carpenter * asks the question : Can a tissue be ab- 
 sorbed and still remain as debris in the pocket"? Such is the con- 
 dition found, and this can be easily proven. Take the contents 
 of a pocket and dissolve it in hydrochloric acid, add three times 
 its bulk of water, to this add ammonia, which will precipitate 
 the phosphate and the calcium. The same results may be ob- 
 tained by rinsing a freshly extracted tooth of a pyorrhoea case 
 in cold water. With a stiff brush remove the accumulation and 
 place it in a test tube, add hydrochloric acid and more water if 
 necessary. To this add a solution of ammonia and the lime salts 
 are precipitated. 
 
 Roots of teeth that have become entirely denuded of peri- 
 dental membrane and bathed in pus accumulate large quantities 
 of calcic deposits direct from the absorption of the alveolar 
 process. 
 
 Difference of opinion exists as to the nature of the process 
 immediately involved in precipitation of lime salts. The sim- 
 plest and seemingly most logical explanation is that the process 
 is similar to that involved in the formation of stalactites. A cer- 
 tain amount of calcareous matter is a normal constituent of the 
 blood. Herein it is held in solution by carbonic acid, always 
 present in sufficient quantity for this purpose. When the cir- 
 culation is impeded the free carbonic acid (because of its great 
 diffusibility) is readily absorbed by the tissues or goes to form 
 new compounds, necessitating a precipitation of the calcareous 
 matter. Calcareous matter may be deposited in either a fibrous 
 or fluid matrix. It shows a preference for newly formed fibrous 
 tissue, particularly when this is associated with old tissue under- 
 
 * Some Points on the Etiology, Pathology and Treatment of Persistent Pyorrhoea 
 Alveolaris. 
 
284 INTEESTITIAL GINGIVITIS. 
 
 going fatty degeneration and absorption. In a fibrous matrix 
 the infiltration usually begins in the intercellular substance, but 
 may involve the cellular elements at a later period. In a fluid 
 matrix (like pus) the granules are frequently deposited pri- 
 marily within the cells. The process may advance slowly or 
 rapidly. When local causes exert the chief influence it is more 
 limited in area of invasion than when there is a general factor 
 in its production, as in the metastatic forms. 
 
 From research it has been shown that calcic deposits (other 
 than tartar) may be due, in a limited degree, to a direct deposit 
 from the blood vessels (serumal deposits of Ingersoll) while the 
 greater collection upon the roots of the teeth and in the fluid 
 contents of alveolar and peridental abscesses, is the deposit of 
 the absorbed alveolar process. Analysis of the deposits and of 
 the alveolar process as observed in Chapter VII, shows a close 
 similarity between the two. 
 
CHAPTER XXVL 
 
 PYORRHCEA ALVEOLAR IS. 
 
 I have shown how inflammation of the alveohir process might 
 be caused by mechanical or local irritation and substances within 
 the organism, without the aid of external infection, namely, irri- 
 tants in the blood stream. In the last named group are to be 
 included the drug and metal poisons, poisonous gases, etc., auto- 
 intoxication and metabolic disturbances affecting the coats of 
 the blood vessels. The alveolar process is more easily affected 
 by these irritants which may set up inflammation (interstitial 
 gingivitis) in a particular localit}^ and remain there, or it may 
 spread and the entire process become involved. The alveolar 
 process may be destroyed by interstitial gingivitis; it is only 
 necessary that there should be a low form of inflammation taking 
 place in and about the arteries and capillaries to produce ab- 
 sorption of bone. This is what occurs in fully ninety per cent of 
 patients. 
 
 When the inflammatory exudate is made up of leucocytes, 
 there is produced within the tissue small round-cell infiltration 
 which becomes so thick as to obscure the tissue. When the 
 leucocytes are in large numbers upon the surface of the mucous 
 membrane about the cervical margin of the alveolar process 
 their appearance on the inflamed surface is that of a white fluid 
 called pus. Owing to the tortuous position of the blood vessels 
 in the alveolar process, the thinnest part being at the gingival 
 border, the inflammatory process usually begins at that point. 
 The pus germs collect at the border, stasis of blood generally 
 being greatest at that locality. This leads to a superficial loss 
 of substance and is known as ulceration or purulent catarrh. 
 When the leucocytes collect in large numbers, within the tissue, 
 and are followed by liquefaction and dissolution, it is called an 
 abscess. These various infections are termed pyorrhoea alveo- 
 laris, alveolar abscess or peridental abscess, according to the na- 
 ture and location- of the infection. 
 
286 INTERSTITIAL GINGIVITIS. 
 
 Pus infection due to interstitial gingivitis, whether it pro- 
 ceeds from the ulcerated surface or deep down in the interstitial 
 tissues from an abscess, whether it discharges between the gum 
 and root of the tooth or upon the surface of the jaw, must be 
 considered pyorrhcea alveolaris^ since the source of the pus is 
 always in connection with the peridental membrane lining the 
 socket of the alveolus. Pyorrhcea alveolaris, therefore, consti- 
 tutes the second part of this study. About ten per cent of the 
 patients visiting the specialist are thus infected. 
 
 Recovery from interstitial gingivitis and return to normal 
 conditions without change in structure is called restoration. 
 Should the damage be extensive, and accumulations of cell and 
 liquid exudate so press upon the tissues as to extinguish their 
 vitality, ordinary restoration is impossible. This is also true 
 when the inflammation is more decided and persistent. This 
 inflammation may extend throughout the tissue. The tissues 
 may be in a favorable condition for infection, yet the mouth and 
 blood vessels be free from pus germs. The tissues are often in- 
 vaded, however, by micro-organisms, resulting in suppuration. 
 Interstitial gingivitis, with pus infection in and about the alveo- 
 lar process, resembles suppuration elsewhere in the body. 
 
 Suppuration (due to pyogenic cocci) is the usual termination 
 of infective inflammation. Healthy gum tissue is intolerant of 
 bacteria, and will resist the invasion of micro-organisms. When 
 inflammation takes place, the diseased part is unable to resist 
 them. Lowered vitality of tissue is a fruitful source of infection 
 and suppuration. Since, as Miller ^ has shown, pus germs are 
 found in almost every mouth, infection is a very probable out- 
 come of gingivitis. 
 
 The organisms most frequently producing pus are the staphy- 
 lococcus pyogenes aureus, and albus. These have a tendency to 
 accumulate in groups. When they collect at a given point in the 
 tissue, suppuration results. The streptococci (occasionally pres- 
 ent in the mouth) do not as a rule produce local suppuration, but 
 spread through the tissue by way of the lymphatics and blood 
 vessels, and eventually give rise to abscess. The delicate reticu- 
 lum of the blood vessels found in the Haversian canals is a 
 
 ^ Micro-Organisms of the Human Mouth. 
 
PYORj^jj(£^ ALVEOLARIS. 287 
 
 convenient lodging place for swarms of bacteria, owing to the 
 slowness of the blood cnrrent and the tortnous course of the 
 blood channels. When - the circulation has been impeded or 
 arrested by an extravasation of blood or congestion of a part, the 
 conditions are favorable for intravascular infection if organisms 
 happen to be circulating in the blood at the time. As w^e have 
 seen, micro-organisms may from time to time be found in the cir- 
 culation, particularly in individuals of feeble constitution. The 
 anatomic nature of the part will therefore determine suppura- 
 tion in certain localities. 
 
 In whatever part or tissue the change may occur, the process 
 is the same. The original structures disintegrate. Their place 
 is taken by a closely packed crowd of migrated leucocytes. 
 Should the cause continue to act, the process culminates in the 
 formation of pus. The migrated cells cut off from proper nutri- 
 tion by pressure are exposed to the injurious action of micro- 
 organisms. The central cells of the group degenerate from want 
 of nutrition or die from direct action of the irritation. The 
 intercellular substance softens, and the liquid exudate from the 
 surrounding parts mingles with the broken-down tissue to form 
 an abscess. 
 
 As I have shown, foci of infection and intense inflammation, 
 to the point of degeneration and liquefaction, occur in almost 
 every locality within the peridental membrane, periosteum and 
 what was originally alveolar process. These abscesses are just 
 as likely to point upon the surface of the gum as on the inner 
 surface next to the root of the tooth. 
 
 Abscesses in and about the alveolar process (other than those 
 due to dead pulps) are very common. This is due first to the 
 unstable condition of the structures, and second to the ready 
 access of pus germs through the inflamed gums and peridental 
 membrane. Those most susceptible to infection are patients who 
 are anaemic and below par in vitality, and whose gums have 
 become inflamed either from local or constitutional causes. 
 Especially is this the case in those who have osteomalacia where 
 the gums have receded quite a distance from the necks of the 
 teeth. Pus germs collect at the necks of the teeth, infect the raw 
 
 * American Text-Book of Surgery. 
 
288 INTEESTITIAL GINGIVITIS. 
 
 inflamed surfaces of the epithelial layer, and entering the cir- 
 culation are carried into the deeper structures. Intense inflam- 
 mation results. Abscesses form, discharging their contents upon 
 the surface. Pus germs also enter the deeper structures through 
 exposed pulps. 
 
 Two cases of interest in this connection occurred recently in 
 practice. An active business man, fifty-five years of age, pre- 
 sented himself with an abscess over the buccal roots of the left 
 superior second molar. There were no dead pulps in any of the 
 teeth upon that side of the jaw. Absorption of the alveolar proc- 
 ess and contraction of the gums had occurred around all the 
 teeth. He had been overworked and was nervously exhausted. 
 Five years ago cataracts were removed from both eyes. He is 
 exceedingly sensitive to pain. Examination of blood revealed 
 slight anaemia. On examination of urine, other than a specific 
 gravity of 1028, it was found normal. The abscess was lanced 
 and cavity cleansed. It healed within a week. Subsequently 
 he returned with another abscess over the root of the right 
 superior central incisor. Live pulps were in all the teeth upon 
 this side as far as the second molar. Infection, therefore, must 
 have occurred through the gum and peridental membrane. 
 
 The teeth of a lady forty-six years of age were being put in 
 order ; after the filling of a cavity she called attention to a space 
 between the second and third superior right molars, and stated 
 food lodged at that point, causing pain and bleeding. The space 
 was cleansed with an excavator and the cavity syringed with 
 warm water and then explored. Absorption of the gums and 
 alveolar process had extended one-half the length of the buccal 
 root. Applications of iodoglycerole were made to reduce the in- 
 flammation. The patient was dismissed with an appointment for 
 further treatment. She returned at the appointed time with an 
 abscess over the palatine root as large as the thumb. The lady 
 had had acute pain from the time she left the office until her 
 return. The parts had become infected with pus germs through 
 the peridental membrane. The pus was collected in a tin tea 
 spoon, from which cultures were obtained and glass slabs 
 smeared for microscopic examination. The pus was examined 
 
PVORRHCEA ALYEOLARIS. 289 
 
 by George T. Carpenter for calcic deposits ; the usual aseptic 
 precautions having been taken. 
 
 Many dentists, ignoring the laws of pathology, insist that 
 intense inflammation in remote parts of the alveolar process is 
 not due to toxins and irritations but is the result of gouty de- 
 posits. The utter lack of foundation for this theory must be 
 apparent on the slightest study of pathology. 
 
 Ulceration is always located upon the surface of a tissue. 
 When ulceration occurs fi'om contact irritation of the gum mar- 
 gin or by mechanical or chemical means, congestion and oedema 
 result, thickening of the epithelial layer and increased growth of 
 cells. The sub-epithelial tissue becomes inflamed. The process 
 is not unlike that of the formation of an abscess, since the 
 infected tissue resembles part of an abscess wall. In slowness of 
 progress only does ulceration differ from acute inflammation. 
 
 Such is the condition of the peridental membrane. When 
 simple gingivitis becomes chronic, the inflammation extends to 
 the surface of the peridental membrane. This is situated at the 
 lower extremity of a cul-de-sac, formed by the gum on the one 
 hand and the tooth on the other. This cavity is filled with for- 
 eign material in which decomposition continually occurs. The 
 tissues are thereby constantly irritated. Necrosis occurs at the 
 surface. In the deeper tissues that have l)ecome inflamed pus 
 cells also are found. These not only arise from the normal blood 
 vessels in the vicinity, but also from the granulation tissue. The 
 causes of peridental membrane ulceration are disturbances of 
 nutrition, endarteritis obliterans (a disease of the blood vessels 
 due to constitutional diseases, such as syphilis, scurvy, tubercu- 
 losis, uric acid and other blood poisons) and starvation of tissue, 
 feeble circulation (as in anaemia) and inflammation. If the 
 ulcerated surface be examined under the microscope, a general 
 thickening of the tissues will be seen. In the papillary layer de- 
 posits of blood pigment occur. The surface is covered with 
 granulation tissue. The tissue may, in part, resemble the type 
 of healthy granulation. It is composed of round cells closely 
 packed together and supplied with rich capillary network. Co- 
 agulation necrosis from breaking down of granulation tissue 
 may be present. ' 
 
290 TXTERSni'l'IAL OINCIVTTIR. 
 
 Pus pockets start with any local iri'itation which sets up in- 
 flammation (interstitia] gingivitis) at tlic gingival hordci- of the 
 gnms. Tiie inflannnation spreads to the blood vessels of the peri- 
 dental membrane and alveolar process. Round cell infiltration 
 I'apidly takes f)lcice and the bone becomes destroyed, beginning 
 at the gum margin or in the peridental membrane and extending 
 toward the apical end of the root or to the mucous membrane 
 of the mouth. The irritation which is confined to narrower areas 
 may ])ecome so intense and the inflammatory exudate increase 
 so rapidly that nothing remains except the fibrous tissue which 
 originally held the bone cells, or the tissue becomes entirely lost. 
 The leucocytes now collect in large numbers within the fibrous 
 tissue and liipiefaction and disintegration of tissue results, form- 
 ing y)us pockets. 
 
 M 
 
 Fig. 92. — TiiicKEXiNG of the Peridental Membkaxe and Trabeculae (OriginaiO. 
 
 Alvcohir abscess is a term applied to an accumulation of pus 
 at the apical end of the root of a tooth due to death of the dental 
 pulp and other irritations. When death of the pulp occurs, de- 
 composition takes place and gases form in the pulp chaml)er, 
 Tlie gases expand and an outlet is acfiuired through the end of 
 the root of the tooth. Tlu^se gases and other irritations set up 
 inflammation in the peridental meml)rane, pi'oducing an nlvcohnr 
 abscess. 
 
PYOERHCEA ALVEOLARIS. 
 
 291 
 
 The other irritations may be foreign substances forced 
 through the end of the root or poisons in the organism passing 
 through the blood stream. These irritants set up interstitial gin- 
 givitis in the arteries running through the peridental membrane 
 and also into the alveolar process and maxillary bone. Inter- 
 
 FiG. 93. — Shows the Eemoval of the Outer Plate or Bone and Exposing the 
 EooT OF the Tooth and the Alveolar Abscess (Original). 
 
 stitial gingivitis becomes quite diffused. Bone absorption 
 (halisteresis and Volkmann's canal absorption) immediately 
 takes place and a considerable area of bone about the end of the 
 
 Fig. 94. — Tooth With Abscess Attached Removed From the Bone (Original). 
 
 root is destroyed, leaving the fibrous tissue (formerly the tra- 
 beculae of the bone) in a thickened condition tightly attached to 
 the end of the root (Fig. 92). 
 
292 
 
 INTERSTITIAL GINGIVITIS. 
 
 As absorption proceeds, the lime salts in the inflamed area 
 are thus destroy ed and the fibrous tissue or trabecule become 
 organized (Fig. 93). If the tooth is extracted before liquefaction 
 occurs, the fibrous mass may be removed in situ (Fig. 94). A 
 
 .M 
 
 Fig. 95. — Microscopic Illustration of the End of the Root of the Tooth. 
 A, Cemeiitum. B, C, Abscess attached. D, Two Points of Liquefaction. (Original). 
 
 low microscopic section of this picture shows the end of the root 
 with fibrous mass attached and degeneration and liquefaction 
 of tissue just commencing at two points near the center of the 
 mass (Fig. 95). A higher magnification showing round-cell 
 
 Tv-.^ 
 
 
 r 
 
 
 ^K%kt^ 
 
 Fig. 96. — Microscopic Alveolar Ap,sce.s.s Sac (Original). 
 
 infiltration and breaking down of tissue, liquefying into pus is 
 seen in Fig. 96. The pyogenic membrane forming the abscess 
 walls is well shown. 
 
PYOERHCEA ALVEOLARIS. 293 
 
 The cause of the irritation producing interstitial gingivitis 
 may be so severe and active that not only is there destruction 
 
 Fig. 97. — Tooth Showing Formation and Destruction of Abscess With Carious 
 Cavity (Original). The Irritation Which Caused the Inflammation and 
 Formed the Abscess Was so Great as to Cause Destruction of the Sac. 
 
 of bone, but also of the trabeculae. Under such conditions the 
 root of the tooth is seen denuded of surrounding tissue (Fig. 97). 
 
 Fig. 98. — Four Abscesses in the Peridental Membrane and Trabeculae in a 
 Diabetic Man (Original). 
 
 In Fig. 9(S four pericemental abscesses are seen along the 
 side of the root of the tooth. These are due to the lowered vital- 
 
294 INTERSTITIAL GINGIVITIS. 
 
 ity of the individual and infection after interstitial gingivitis 
 has become quite extensive. These abscesses are very common. 
 The tissues about the roots of the teeth become inflamed, infec- 
 tion takes place, abscesses form and discharge. The fistula heals 
 without pain or inconvenience to the patient. 
 
 In summing up this chapter on pyorrhoea alveolaris, the 
 reader must not lose sight of the fact that pus infection in no 
 way influences the absorption of the alveolar process and exfolia- 
 tion of the teeth. It is always the primary inflammatory stage 
 that causes the absorption and the pus infection is only 
 incidental. 
 
CHAPTER XXVII. 
 
 CONSTITUTIONAL EFFECTS OF PYORRHOEA ALVEOLARIS. 
 
 Every person with pyorrhoea alveolaris has pus germs in the 
 mouth which are constantly being carried into the fauces, stom- 
 ach and throughout the ahmentary canal. That these pus germs 
 under certain conditions are destroyed in the stomach by the 
 gastric juices, to my knowledge, has never been demonstrated. 
 A factor unfavorable to this theory is the non-presence of the 
 hydrochloric acid in the stomach except when food be present, 
 whereas the saliva, laden with pus germs, is continually passing 
 into the stomach and the germs must, without doubt, find their 
 way into other organs, causing grave constitutional states which, 
 in many instances, finally result in death. 
 
 The degree of organic infection varies in intensity. The 
 germs passing into the stomach with the food are, on account of 
 the presence of the hydrochloric acid, changed in character, while 
 those passing into the stomach other than during digestion, are 
 more virulent and act with greater intensity upon the intestine 
 and organ walls, since they produce a catarrhal condition, first 
 acute which later becomes chronic. It has been shown repeat- 
 edly that many stomach troubles have improved or recovery has 
 been complete when the mouth has been put into an aseptic 
 condition. 
 
 The influence of the stage of interstitial gingivitis known as 
 pyorrhoea alveolaris on the system has been discussed by John 
 Fitzgerald,^ who points out that pyorrhoea alveolaris may act 
 in three different ways in the causation of systemic disease. 
 First, the pus with its multitude of putrefactive organisms and 
 decayed food remnants from the pus pockets is swallowed and 
 either acts locally upon the stomach wall or sets up fermentation 
 of the stomach contents; second, the toxins generated in the 
 mouth may be absorbed by the mucous membrane of the mouth 
 or stomach and thus pass into the general circulation; third, the 
 
 ^ Clinical Journal, March 6, 1899. 
 
296 INTERSTITIAL GINGIVITIS. 
 
 local conditions of the mouth may favor the growth of patho- 
 genic organisms and thus render the patient more liable to cer- 
 tain infectious disorders, noticeably influenza. The power of 
 pyorrhoea alveolaris to produce aggravation of existing gastric 
 trouble reaches its maximum in cases where there is retention 
 of food residue. This happens when the muscular walls of the 
 stomach are in a state of atony and also when there is some 
 pyloric obstruction which prevents the organ emptying itself. 
 In both these conditions stomach dilatation is eventually pro- 
 duced, with the result that the stomach is never completely emp- 
 tied. The first condition is a very frequent concomitant of 
 neurasthenia and allied states. It is easy to see how pyorrhoea 
 can at once be predisposed to by neurasthenic states and at the 
 same time increase the neurasthenia by causing gastric trouble 
 through its interference with gastro-intestinal digestion under 
 the conditions mentioned. 
 
 Fitzgerald points out that the bacillus coli communis is a 
 constant inhabitant of the oral cavity, and, as a rule, seemingly 
 harmless. Under the influences of a culture medium, such as 
 would be furnished by pyorrhoea or an inflammatory state of the 
 gum, this bacteria might, as elsewhere in the mucous membrane, 
 acquire sufficient virulence to produce serious disturbances of 
 the system, such as colitis, dysentery and cholera nostras. 
 
 Herschell - is of the opinion that many of the chronic indi- 
 gestions are due to continual absorption of pus into the system 
 from pyorrhoea alveolaris. In these cases he remarks there 
 should be other evidences of the absorption of toxins, such as 
 X)igment spots, urticaria, etc. 
 
 Within the past few years medical thought has centered 
 around the mouth and its infection as a possible cause of many 
 diseases even far removed from it. The many germs of more or 
 less virulence which have already been isolated in the mouth 
 must of necessity affect mucous surfaces in other parts of the 
 body. Medical researches have shown that diseases like per- 
 nicious anaemia, arthritis deformans, all rheumatic states, bac- 
 terial endocarditis, headaches, many other obscure conditions, 
 
 Indigestion, 1895. 
 
CONSTITUTIONAL EFFECTS OF PYORRHCEA. 297 
 
 etc., yield more readily to treatment when the mouth has been 
 put into an aseptic condition. Every dentist has experienced the 
 fact that when a poorly nourished patient has had loose teeth 
 extracted, artificial ones substituted and the mouth entirely 
 cleaned up, there will be increase in weight and better health. 
 American and foreign journals are full of experiences of like 
 nature. 
 
 Many writers who believe in the theory of the conveyance of 
 j)us germs throughout the body have recorded histories of pa- 
 tients who are believed to have been thus infected. Some of 
 these are interesting and here mentioned to show what serious 
 constitutional conditions take place from an unhygienic condi- 
 tion of the mouth and teeth. 
 
 There are many affections of the tonsils, neck glands, etc., 
 directly traceable to the sei)tic condition of the mouth and teeth. 
 Especially is this true of school children. Stewart ^ reports 231 
 cases of tonsil enlargement in which 135 had a caried condition 
 principally of the lower molars on the enlarged tonsil side; 67 
 had caries and an unhj^gienic mouth ; 16 had no septic condition 
 of the mouth and 15 had caries and a septic state on the opposite 
 side. He also mentions cases of laryngitis which yielded to 
 treatment after putting the mouth in an aseptic state. 
 
 It has long been known that nearly all glandular conditions 
 are dependent upon bacterial infection of more or less virulency. 
 Many cases of gland infection have been shown to be directly 
 due to a sej^tic condition of the mouth. A case coming under the 
 author's notice was that of a twenty- three-year-old man whose 
 original mouth condition of pyorrhoea alveolaris was augmented 
 by a local spirrilla infection. After being under treatment for 
 some weeks with no recovery results, he was referred to me. I 
 found the gums, peridental membrane and alveolar process in a 
 severe inflammatory state with pus oozing from the tooth 
 sockets. The neck glands were enlarged on both sides and tender 
 to touch. After the mouth was put in an aseptic state, the glands 
 became their noimal size and the tenderness disappeared. 
 
 'Stewart, C. J. Oral Sepsis in its Connection With Throat Diseases. The Lancet, 
 June 25, 1902. p. 1882! 
 
 * Hunter. W. The Lancet, 1900, 1904. 
 
298 INTERSTITIAL GINGIVITIS. 
 
 Hunter * reports a case of gastritis which he claims is directly 
 due to infection from the mouth. A sixty-two-year-old woman 
 was suffering- with subacute gastritis. There was severe pain 
 and intermittent sickness, so much so that morphia was often 
 resorted to. The illness had been of eight months' duration 
 coupled with loss of weight and great weakness. Examination 
 for cancer of the stomach, abdomen, rectum or uterus revealed 
 nothing. There was continually a bitter taste in the mouth, 
 nausea and loss of appetite. Examination of the vomit found it 
 filled with streptococci, staphylococci and a few bacilli. There 
 were three roots of teeth remaining in the mouth from whose 
 sockets there was a constant flow of pus. With the extraction 
 of the roots the stomach condition was benefited. 
 
 It has been a much discussed question among physicians as 
 to w^hether gastric ulcers are not directly due to a septic condi- 
 tion of the mouth, but convincing proof has not been evidenced 
 since gastric ulcers are known to occur in persons with healthy 
 mouths. In the chronic ulcer type, however, an unclean mouth 
 with pus coming from the tooth sockets is the rule. 
 
 Dr. Frank Billings, in a paper on "Chronic Focal Infections 
 and Their Etiologic Relation to Arthritis and Nephritis"^ 
 speaking of the site of local infection, mentions "the faucial 
 tonsils, abscesses of the gums and alveolar sockets, pyorrhoea 
 alveolaris and septic types of gingivitis may also cause systemic 
 diseases of various types. The systemic results of focal infec- 
 tion are: 1. Chronic arthritis is one of the most common re- 
 sults. 2. Nephritis, both acute and chronic. 3. Cardiovascular 
 degenerations. 4. Chronic neuritis and myalgia (myositis)." 
 He says further, "The studies and experiments embodied in this 
 paper are limited to the arthritides and to subacute and paren- 
 chymatous nephritis. Of these, chronic deforming arthritis, com- 
 monly known as arthritis deformans, and chronic osteo-arthritis 
 of hypertrophic or atrophic type, comprise the majority of the 
 studies. Next to the arthritides the largest number of cases com- 
 prises subacute parenchymatous nephritis and chronic paren- 
 chymatous nephritis. The work has been done on private and 
 clinic patients in the Presbyterian Hospital. The bacteriologic 
 
 » The Illinois Medical Journal, March, 1912. 
 
CONSTITUTIONAL EFFECTS OF PYOEEHCEA. 299 
 
 and histologic studies and the animal experiments have been car- 
 ried on by Dr. D. J. Davis and by Dr. Homer K. Nicoll." 
 
 Ten cases of arthritis and six cases of subacute and chronic 
 parenchymatous nephritis are described. Among this number 
 case Number III is worthy of special mention here. 
 
 Case 3. — Mrs. E. W., aged 50 years. I-para. Osteoarthritis 
 chronica, mixed type. Admitted to the Presbyterian Hospital 
 Oct. 16, 1909. For two years there had been swelling, tender- 
 ness, pain upon motion and deformity of many of the joints of 
 extremities. Began in feet and hands and extended to larger 
 joints and finally involved cervical spine. The condition was 
 progressive. There was malnutrition, loss of weight from 160 
 to 120 pounds. For years the patient had been subject to attacks 
 of acute tonsilitis. She had also suffered for years from pyor- 
 rhoea alveolaris. 
 
 Examination : Poorly nourished, very nervous and irritable. 
 Mouth badly infected, many stumps of carious teeth, some of 
 them loose in the sockets, gums retracted and infected, tonsils 
 large, rough, adherent to pillars of fauces and crypts infected. 
 Breath offensive. Heart, lungs, abdominal organs and pelvic 
 organs normal. There was swelling with some deformity of 
 both ankles, right metatarsophalangeal, both knees, right middle 
 and left fingers, the wrists, and elbows. Some contraction of 
 hamstring muscles prevented complete extension of legs. Both 
 bleep tendons of the arms contracted which prevented extension 
 of the forearm. Twenty-four hours' collection of urine was nor- 
 mal in amount and specific gravity and contained a few hyalin 
 casts. Blood : Hemoglobin, 90 per cent ; reds, 4,600,000 ; whites, 
 13,400. On Oct. 18, 1909, both f aucial tonsils were enucleated by 
 Dr. George E. Shambaugh and one week later the roots of cari- 
 ous teeth were removed by Dr. Frederick Moorhead. From the 
 cut surface of the tonsillar tissues a pure culture of streptococcus 
 was obtained. A rabbit inoculated A\itli a culture suffered from 
 acute multiple arthritis and died in a few days. The strepto- 
 coccus was regained from the infected joints and from the 
 heart's blood. The patient was permitted to return to her home 
 too soon and did not fully carry out directions as to rest treat- 
 ment. Some time elapsed before the alveolar processes were 
 
300 INTERSTITIAL GINGIVITIS. 
 
 absorbed and the mouth remained sore. On April 3, 1910, she 
 returned to the hospital, where rest treatment was instituted 
 with resulting marked improvement. The patient gained in 
 weight from 129 to 140 pounds. After the return home fre- 
 quent communications by letter with the patient and her physi- 
 cian have shown that the progress of the disease has entirely 
 stopped. Some of the deformities were so great that one could 
 not expect entire anatomical restoration. The last communica- 
 tion is dated December, 1911, in which the patient says that the 
 strength of her ui3per extremities and spine is entirely normal. 
 There is some fatigue in the lower extremities after attempting 
 to walk for any great distance, but there is a continued improve- 
 ment even in this respect. 
 
 All the cases cited in this article are of unusual interest be- 
 cause they are based upon researches and actually demonstrate 
 the source of infection and the results of such infection upon 
 animals. 
 
 Osier says of the twenty cases of pernicious anaemia which 
 he had under observation in 1909, pyorrhoea alveolaris was pres- 
 ent in more than half. Certain types of nephritis are also be- 
 lieved to be due to oral infection.*' 
 
 Zilz ' reports four cases of cysts at the roots of teeth in which 
 bacteriologic investigations revealed the presence of Much's 
 granula, which he defines as the non-acid-fast form of the 
 tuberculosis germ. The findings are profusely illustrated and 
 the questions discussed are "why it is so difficult to detect acid- 
 fast, Gram-staining bacilli in the gangrenous pulpa," and ''why 
 primary tuberculosis starting in carious teeth is not of more 
 common occurrence." He regards Much's granula as merely 
 ordinary acid-fast tubercle bacilli which have lost their acid-fast 
 properties ; hence the organic fluids are able to disintegrate them 
 and the vital centers, the granula, escape into surrounding me- 
 dium. When conditions become more favorable to the bacilli, 
 they may become impregnated again with acid-fast substance 
 and the acid-fast form thus develop again, which in turn may 
 break up anew into granula. His plates show the process dis- 
 
 • Practice of Medicine, p. 440. 
 
 '' Beitrage znr Klinik der Tuberkulose, Wiirzburg, Vol. XXII, No. 2, pp. 97-264. 
 
CONSTITUTIONAL EFFECTS OF PYORRHOEA. 301 
 
 tinctly, the granula causing no tuberculous changes in the dental 
 cyst. The bacilli probably found their way through the blood 
 into the cyst and while there remained latent but regained their 
 virulence when conveyed farther to lymph-nodes or lungs. In- 
 oculation of animals with the granuUi always gave positive 
 results. 
 
 W. Hunter ® has repeatedly called the attention of the pro- 
 fession to the close relationship existing between the mouth 
 infection and the various forms of anaemia, particularly the per- 
 nicious type. He contends that the pus taken into the stomach 
 produces an unhealthy state of that organ and also the intes- 
 tines, thereby favoring the destruction of the red blood cells. 
 
 In all forms of arthritis there is an association in the condi- 
 tion of the mouth. The disease stamps itself indelibly upon the 
 alveolar process. There is gum recession and absorption of the 
 alveolar process of more or less intensity and pus infection. 
 
 A case referred to the author for treatment of the mouth is 
 of more than passing interest. The patient, a twenty-seven- 
 year-old woman, unmarried, had been a sufferer from arthritis 
 deformans for many years. For ten years previous to her com- 
 ing to me she had been unable to leave her home except when 
 carried. The entire osseous system was involved, but more 
 especially the extremities. The hands had become so malformed 
 and stiff that she was unable to pick up or hold anything. The 
 mouth was in frightful shape. There were loose teeth with pyor- 
 rhoea alveolaris, absorption of the gums and alveolar process, a 
 number of large cavities, tartar and calcic deposits. After the 
 loose teeth had been extracted, the tartar and calcic deposits 
 removed, the cavities filled, an artificial denture inserted and 
 the pyorrhoea alveolaris treated, the constitutional condition 
 commenced to improve. At the end of three months she could 
 walk with the aid of crutches, in six months with only the use of 
 a cane, and at the end of a year had no use for either. The stiff- 
 ness in the hands disappeared to such a degree that she could 
 use them. She has now recovered to such an extent that she is 
 able to assist in the housework. 
 
 8 The Lancot. 1900, 1904. 
 
302 INTEESTITIAL GINGIVITIS. 
 
 Dr. Kenneth Goadby,'' of London, England, reports four in- 
 teresting cases of arthritis which are worthy of consideration at 
 this time. They are as follows : 
 
 Case 1. — A girl, aged tw^enty-two, was attacked somewhat 
 suddenly by swelling of the hands and feet and fever lasting 
 tw^o or three weeks. With the subsidence of the fever the joints 
 did not return to their normal size but remained painful and 
 stiff ; walking was almost impossible. The affection was bilateral 
 and the swelling was evidently peri-articular, and to a limited 
 extent affected the synovia of the joints, but no fluid was dis- 
 covered. Treatment at Bath and a long course of salicylates 
 produced little improvement. There was no family history of 
 rheumatism or of gonorrheal infection and no septic focus was 
 thought to exist. On examination of the mouth, the right upper 
 central incisor was missing, the teeth and gums were apparently 
 quite normal. A closer examination revealed a small sinus lead- 
 ing up to the root of the missing central incisor and a film made 
 from the sinus showed a large number of pus cells loaded with 
 organisms. Cultures were made and an organism was isolated 
 in practically pure culture ; the blood tested against this organ- 
 ism gave a very low^ opsonic as well as a low^ phagocytic index. 
 A vaccine was prepared and injections given, commencing with 
 ten million dead bacteria. After four injections the sinus was 
 opened under a general anesthetic and was found to lead into a 
 cavity in the bone about the size of a small hazelnut. This was 
 cleared out ^vith a sharp spoon and the lateral incisor also was 
 removed, the cavity extending under its root and invading the 
 periosteum of the tooth. The improvement of the joints which 
 had commenced with the inoculations received a slight tem- 
 porary setback as the immediate result of the operation, but 
 improvement soon recommenced with continued vaccine therapy 
 and the patient has steadily improved and is almost well. 
 
 The second case is that of a man of thirty-eight years. He 
 was suffering from acute pain and swelling in both knees and 
 both feet, ulnar deflection of both hands and acute pain and 
 swelling on the dorsal aspects, fluid and deformity of the left 
 elbow joint and of the left shoulder joint, anaemia and neuras- 
 
 The Practitioner (London), January, 1912. 
 
CONSTITUTIONAL EFFECTS OF PYOERHCEA. 303 
 
 tlieiiia, partly owing to the constant pain and partly toxic. I 
 may note in passing that secondary septic neurasthenia is com- 
 mon in cases of oral infection, probably due to the long-continued 
 infection with small doses of bacterial toxins. The patient had 
 been under all sorts of treatment, residence at Continental and 
 English Spas, had been to the Canary Islands, had taken vast 
 quantities of iodid of potassium, had had massage, electric baths, 
 ionisation and ''Christian Science" and all with no avail. 
 
 His mouth was a veritable gold mine ; he had two bridges, two 
 in the upper, two in the lower jaw, and four gold crow^ns in addi- 
 tion to the bridges; pus was welling up from his gums in all 
 directions. The builder of the bridges told him he could do noth- 
 ing for him as he had rheumatism in his gums. He was treated 
 by the removal of all the crowns and bridges and by vaccines 
 made from his two organisms. He made a slow but steady recov- 
 ery and is now enabled to resume his ordinary avocation which 
 he had been obliged to give up for three years previous. Unfor- 
 tunately the right knee-joint is partially disabled owing to 
 exostosis. 
 
 The third case, a man aged forty, in March, 1908, had a sud- 
 den attack of pain behind the left ear, progressive stiffness and 
 muscular rheumatism and stiffness of the right shoulder and 
 right hip joints. Ten days later, rigor, temperature 102° F. and 
 evening temperature of 100" F. for two or three weeks which 
 gradually subsided. In the following spring another acute attack 
 with fever, pains in the head and neck, swelling of sterno-mastoid 
 sheath and stiff neck, lasting five weeks. An X-ray photograph 
 of the chest was taken and it was thought the case was one of 
 early tuberculosis ; the patient was sent to a sanatorium where 
 he derived no benefit. He was in constant pain, unable to move 
 his head, and had constant attacks of fever at night, the tem- 
 perature running up to 100° F. and falling to subnormal in the 
 morning. He became wasted, losing more than a stone in weight, 
 was greatly depressed mentally and had to give up his work. 
 On examination in October, 1909, considerable thickening was 
 found in the left shoulder joint and right knee joint. The left 
 sterno-mastoid was thickened in the region of the rectus, capitis 
 posticus and complexus, and thickened tender areas along the 
 
304 INTERSTITIAL GINGIVITIS. 
 
 spine process of the cervical and dorsal vertebrae. Hyperes- 
 thesia over all cranial nerves. The patient could walk only with 
 difficulty. 
 
 The molar teeth had been lost on both sides in both jaws. 
 The patient resented any suggestion that his mouth was at fault, 
 as he had recently seen his dentist who pronounced his gums and 
 teeth quite sound, and the gums appeared normal in color. 
 Careful examination with a fine platinum probe brought to light 
 several deficiencies between the remaining teeth and passing 
 down to bare bone, and microscopically pus was demonstrated. 
 A vaccine was therefore prepared and inoculations were per- 
 formed. The patient made an uninterrupted recovery, the inoc- 
 ulations were discontinued and a slight relapse took place. The 
 vaccine was therefore continued for a further six months. The 
 patient made a complete recovery. 
 
 In the fourth case, a w^oman aged forty-two, there was a 
 severe general infection of the mouth. All the teeth were loose 
 and copious discharges of pus came from all sockets. There had 
 been chronic progressive arthritis for the last four years asso- 
 ciated with occasional acute exacerbations, constant pain in both 
 knee joints which were swollen and thickened, especially the ex- 
 ternal and lower portions of the capsule; creaking was well 
 marked in the knees and shoulders, with ulnar deflection of the 
 right hand. All teeth were removed and considerable improve- 
 ment took place. Six months after removal of teeth pain re- 
 curred in the right knee and in the shoulders but passed off. A 
 year later, eighteen months after removal of teeth, the pain and 
 stiffness of the knees again recurred together with fusiform 
 swellings and local vasomotor disturbances of the fingers. On 
 examination the gums were found quite healed; there was no 
 inflammation, but small patches of thickening were seen along 
 the outer surfaces of the alveolar process. A puncture was made 
 into these and a pure culture of the streptobacillus malae was 
 found. Vaccine therapy was instituted and the rheumatoid symp- 
 toms rapidly disappeared and two years later no recurrence 
 had taken place. 
 ' Every specialist has noted the marked improvement in his 
 patients, some of whom were suffering with obscure ailments, 
 
CONSTITUTIONAL EFFECTS OF PYORRHCEA. 305 
 
 after liaving loose teeth removed, pyorrhoea alveolaris treated 
 and cured, gums and mouth placed in an hygienic condition, 
 artificial teeth inserted to fill vacant spaces, and many expe- 
 riences could be recorded. 
 
 Gilmer ^° reports three interesting cases. He says, ''Some 
 years ago, a man, a little beyond middle life, consulted me rela- 
 tive to a trivial dental lesion. On making a careful examina- 
 tion of the entire oral cavity, I found several small sinuses dis- 
 charging pus above the bicuspid teeth on one side of the upper 
 jaw. On exploring these openings with a sharp steel probe a 
 large cavity was discovered in the bone, the result of alveolar 
 abscess, the presence of wliich was unsuspected by the patient. 
 On inquiring into his physical condition I learned that for the 
 past year he had had a cough, his digestion was impaired, and 
 much of the time his temperature was slightly above normal. 
 He had frequently consulted his family physician who examined 
 his heart, lungs, sputum, urine and blood. These gave no clue 
 to the cause of ill health. His appearance indicated a toxemia. 
 I removed several teeth, curetted the abscess in the jaw and 
 followed it by suitable after-treatment. His fever at once sub- 
 sided, his digestion was soon much improved, his cough was 
 lessened and finally disappeared altogether. Although seem- 
 ingly his physician had made a careful examination he had 
 overlooked one important factor, the mouth. 
 
 ''Mrs. C, aged thirty years, noticed the appearance and dis- 
 appearance at frequent intervals of an erythemic patch about 
 the size of a silver quarter on the skin over the left canine fossa. 
 On examining the mouth for a possible cause for this reddened 
 condition of the skin I found the left lateral incisor pulpless. 
 There was no sinus and the tooth had given no trouble. The 
 only e\^dence of disease found in the mouth was a slight hyper- 
 emia of the gum over the lateral incisor root indicated. The 
 radiograph showed a pus cavity in the bone at the end of the 
 root about the size of a large pea. Disinfection of the root did 
 not effect a cure. I made an opening through the labial wall of 
 the alveolar process, excised the end of the root and curetted 
 
 ^oThe Illinois Medical Journal, March, 1912. 
 
306 INTERSTITIAL GINGIVITIS. 
 
 the cavity. The erythemic patch on the cheek disappeared and 
 did not return. 
 
 *'Mr. S., aged about twenty-five years, was directed to my 
 clinic for the treatment of a chronic abscess in the upper jaw 
 in the vicinity of the incisors and cuspid which had proven in- 
 tractable to ordinary treatment. His physical condition was 
 much impaired, he was emaciated, his skin was sallow, his 
 cheeks hollow, his conjunctivas pale, eyes dull, and his lips lacked 
 the color of health. His temperature was slightly above normal. 
 I could elicit no history of any other illness, recent or other- 
 wise. His appearance gave the picture of a toxemia. In this 
 case, likewise, the sharp steel probe revealed a large cavity in 
 the bone, extending from the central incisor to the first molar. 
 On Oct. 20, 1911, I extracted the cuspid tooth and curetted the 
 bone cavity. On Oct. 27th, he returned to the clinic much im- 
 proved. Nov. 10th, his color was normal, his eyes clear, and he 
 seemed well." 
 
 Dr. T. B. Hartzell, of Minneapolis, reports the following 
 four cases: 
 
 ''Case 1. A typical case of pyorrhoea alveolaris. Patient, 
 male, aged 50 years. Molar and bicuspids in both lower and 
 upper arches freely movable in sockets, having lost the bone 
 to about one-half of the original depth of sockets, pus discharg- 
 ing freely from the sockets about the teeth, temperature nor- 
 mal, specific gravity of urine 1018, no albumen, no sugar. Pa- 
 tient reports a tender area in the stomach wall. Diagnosis, 
 ulcer of the stomach accompanied by chronic dyspepsia. Patient 
 has had treatment for ulcer of the stomach for two years with 
 but temporary benefit. The treatment in this case was first ex- 
 traction of two of the loose teeth followed by accurate planing 
 of the root surfaces of all the teeth which had lost alveolar 
 process. Absolute cessation of pus flow. Gums resume normal 
 tint and after two months no tenderness in the region of the 
 ulcer, digestion about normal. 
 
 ''Case 2. Male, aged 48. Chronic pain and tenderness in the 
 masseter muscles of the left side. Tenderness of the sublingual 
 glands and torticollis. Tenderness of left shoulder joint. Ex- 
 
CONSTITUTIONAL EFFECTS OF PYORRHCEA. 307 
 
 amination of the mouth revealed dead pulp in left lower 8 with 
 free pus discharge from deep pyorrhoea pockets. Left lower 6 
 and 7 vital pyorrhoea pockets one-third the depth of the root. 
 General pyorrhoea of all the molars and bicuspids on both sides 
 of the mouth. Chronic acid indigestion with constant eructa- 
 tion of gas after the ingestion of food. Treatment, extraction 
 of loose left lower 8. Planing of the root surface of all the 
 teeth affected by pyorrhoea. Pockets were pencilled with tinc- 
 ture of iodin. After two weeks, rheumatic pains in shoulder 
 and tenderness of sublingual glands disappeared. Digestion 
 improved. End of fourth week all inflammatory symptoms con- 
 tiguous to the teeth absent. Teeth no longer tender on occlu- 
 sion. Patient has resumed vigorous mastication of food. End 
 of two months all symptoms of dyspepsia absent. This case is 
 typical of a group of five cases in which joint involvements have 
 been present from one to three years which have all disappeared 
 upon the stamping out of oral infections. 
 
 ''Case 3. Mrs. J., aged about 50, with mild inflammation of 
 the gum margins. Abscess in the region of left upper 2 pen- 
 etrating the palatal tissues an inch and a quarter. Patient 
 enjoys moderately good health though a constant sufferer from 
 constipation, rheumatism of the arms, wrists and fingers, and 
 of the feet, ankles and knees. Pains sufficiently sharp on rising 
 to cause marked discomfort. Draining of the abscess and treat- 
 ment of the interstitial gingi^dtis results after two months in 
 complete freedom from rheumatic pain and also freedom from 
 constipation. 
 
 ''Case 4. Miss A., aged 26, suffered chronic dyspepsia and 
 neurasthenia. Has been treated for three years in various 
 sanatoria and has also spent two A^dnters in Southern Califor- 
 nia. Patient presented the winter of 1906. Mentally, much 
 depressed. Physically, very weak. Weight, 86 pounds. No 
 albumen, no sugar. All the teeth exceedingly loose. Deep 
 pockets discharging pus freely. Teeth all extracted except four 
 in the upper and four in the lower jaw. These eight teeth were 
 treated for pyorrh.opa and although they were so placed that they 
 were of no value for mastication the patient showed a marked 
 improvement. At* the end of one week had gained one pound in 
 
308 INTERSTITIAL GINGIVITIS. 
 
 weight altliougli obliged to subsist largely upon liquids. Arti- 
 ficial dentures were placed, and the patient increased in weight 
 steadily at the rate of a pound a week until her normal weight 
 of 106 pounds had been regained, after which time she returned 
 to her home. ' ' 
 
 Dr. David J. Davis,'' Pathologist of St. Luke's Hospital, re- 
 ports the following: ''Pyemia, septicemia, meningitis, neuritis, 
 endocarditis, etc., as acute infections originating from alveolar 
 abscesses and infected food about the teeth, are well known oc- 
 currences. Chronic generalized or systemic infections are rarer 
 and less commonly recognized. As an illustration I may men- 
 tion briefly one rather striking case which came under my 
 observation. 
 
 "A young man had been suffering for several weeks with 
 symptoms of severe multiple neuritis associated with some 
 anaemia, marked emaciation and slight fever. The joints were 
 not involved and physical examination revealed no heart lesion. 
 For a long time the patient had been troubled with severe pyor- 
 rhoea and at the time of examination the gums of the lower jaw 
 were red and swollen, bled easily and on pressure abundant 
 pus exuded from between teeth and gums. Smear and culture 
 examination of this pus revealed, in nearly pure growth, many 
 Gram-positive diplococci resembling pneumococci. The colonies 
 produced a green zone on blood-agar and the organism acidi- 
 fied and coagulated milk and fermented inulin. A blood-culture 
 made by taking several cubic centimeters of blood from the vein 
 at the elbow yielded in each of three inoculated culture-tubes a 
 pure growth of the same diplococcus. In animals this organism 
 was not highly pathogenic. One broth-culture intraperitoneally 
 would kill guinea-pigs in twenty-four to forty-eight hours. Two 
 rabbits were inoculated repeatedly with large amounts of cul- 
 ture mthout manifesting serious or fatal effects. Apparently 
 these diplococci are identical with the cocci often found in endo- 
 carditis and called endocarditic cocci and they are also probably 
 identical with the diplococcus almost constantly found in the 
 mouth and usually called Streptococcus viridans (Schottmliller . 
 I may say, too, that they appear to be the same as the diplococci 
 
 ^Archives of Internal Medicine, April, 1912. Vol. IX, pp. 505-514. 
 
CONSTITUTIONAL EFFECTS OF PYORRHCEA. 309 
 
 wliicli I have found at times in the tonsillar crypts, especially in 
 cases of endocarditis, and which I will discuss later in the paper. 
 In this particular case the tonsils were carefully examined and 
 appeared to be normal and no suspicious foci of infection other 
 than the teeth could be held accountable for the condition. 
 Unfortunately, the patient did not remain long under observa- 
 tion and the termination is not known." 
 
 Dr. Edward E. Rosenow of the Pathological Laboratory, 
 Rush Medical College, says, in a letter to the author, ** Clinical 
 observation convinces me that the low grade infections about the 
 teeth, etc., which are looked upon so often as harmless, are far 
 from being so. The evidence is practically conclusive that endo- 
 carditis may have its origin in some such infection. In the Sep- 
 tember number of the Journal of Infectious Diseases there will 
 appear an article on endocarditis in which these points ^\t.11 be 
 taken up. The mechanism of how the organisms which are so 
 common in these infections about the teeth can produce endo- 
 carditis is shown experimentally in the rabbit." 
 
 At the meeting of the American Medical Association held at 
 Atlantic City in June, 1912, Dr. E. Libman of New York exhib- 
 ited in the pathological exhibit a series of twenty-two hearts 
 showing bacterial endocarditis due to mouth infection. 
 
 Medical literature records many ailments and cures of dis- 
 ease associated with pus infection in the mouth. While every 
 practitioner would logically reason from his every-day experi- 
 ences that there is a relationship existing between cause and 
 effect, yet more absolute data in the way of research is neces- 
 sary to show more clearly that such relationship exists. The 
 work of Billings, Rosenow, Davis and others should be con- 
 firmed by many more experiments upon animals to verify these 
 facts. 
 
 The author is one of those who believes that infections of 
 the mouth are taken into the stomach mth every swallow; and 
 that infection of the glands of the neck as well as absorption of 
 pus directly into the blood and carried to all parts of the body, 
 occurs in a large percentage of our patients, because he has 
 cured many thus infected and improved the health of others by 
 putting the mouth in a healthy condition. 
 
CHAPTER XXVIII. 
 
 TREATMENT. 
 
 The treatment of interstitial gingivitis as a whole is very 
 unsatisfactory both to the operator and the patient. The clin- 
 ical history of each structure is essentially that of any other 
 disease of the mucous membrane, periosteum and bone tissue. 
 From a microscopic viewpoint, however, as illustrated by the 
 author's researches, the pathologic aspect is quite complicated, 
 since the relation of tooth, peridental membrane, alveolar proc- 
 ess and gum tissue has no counterpart in any other part of the 
 body. 
 
 The etiology of most of the disease to the dentist is obscure 
 in nearly every person under treatment, as there are consti- 
 tutional factors involved in connection with the local irritation. 
 The dental specialist not having a medical education and a gen- 
 eral knowledge of disease intoxications, the faulty metabolism 
 and lowered resistance are not understood. 
 
 There is a general law in medicine laid down many years 
 ago that to treat a disease successfully the cause must always 
 be removed. In those patients in whom the cause is of a consti- 
 tutional nature, there may or may not be local deposits. The 
 mere cleansing of the tooth roots and local treatment ^\dll not 
 always cure such conditions. On the other hand, much harm 
 may be caused (as we have already shown) by local irritation, 
 traumatic lesions, and changes in function w^hich cause the tissue 
 to be readily acted upon by irritants in the blood stream. A 
 large percentage of interstitial gingivitis is influenced or en- 
 tirely due to constitutional causes. Interstitial gingivitis 
 under such circumstances can never be i)ermanently reduced 
 until the cause has been ascertained and remedied. A very thor- 
 ough history of the patient, especially age and condition of the 
 urine, should be obtained. Such data ^^411 assist the specialist 
 greatly in a clear understanding of his method of procedure. 
 
 We have shown that the tooth, so far as this disease is con- 
 
TREATMENT. 311 
 
 cerned, is a foreign body and tlie alveolar process is an endo- 
 transitory structure. When disease, therefore, whether due to 
 local or constitutional causes, once atfects these structures, even 
 if they be restored to comparative health, they are more easily 
 involved than other structures of the body. AVhen inflammation 
 has once taken place in these tissues, whether the disease be due 
 to local or constitutional causes, the operator may apparently 
 restore these structures to health. If, however, the cause is not 
 removed, whether it be local or constitutional, the disease soon 
 returns as it is of a progressive nature. This necessitates fre- 
 quent \dsits of the patient for further treatment. The endo- 
 transitory nature of the alveolar process, after inflammation has 
 once affected the part, naturally causes the disease to become 
 chronic. The obscure constitutional causes and the chronic ten- 
 dency of the disease soon causes the tooth to become loose and 
 finally exfoliated. 
 
 When the disease is taken in hand and continually treated 
 before the bone becomes involved, a fair success may be ob- 
 tained. I have demonstrated that bone absorption around the 
 teeth as one grows older is a natural process which cannot be 
 arrested to any extent. Toxins and irritations assist greatly, 
 dependent always on the resistance of tissue and strength of 
 the irritant. Neglect on the part of the patient to massage the 
 gums properly twice a day and use a proper gum wash, the 
 irritants in the blood and in the mouth, cause the tissue to soon 
 return to their pathologic state when the bone becomes dis- 
 eased, bmng to its endo-transitory nature. Chronic inflamma- 
 tion once set up, "eternal vigilance" on the part of the oper- 
 ator and patient is the onlj^ method that will prevent the disease 
 from progressing with a final destruction of the alveolar process 
 and exfoliation of the teeth. 
 
 The disorder responds quickly to treatment at its outset. 
 Later, its complications and the extent of structure involved, 
 render treatnient very inefficacious, and always insure loss of 
 the tooth. As the general surgeon's duty is to save life, if need 
 be, at the expense of limb or organ, but to save these last if pos- 
 sible, so the dental surgeon's duty is to remove loose teeth, if 
 need be, for the benefit of the gene ''al health, but to save them. 
 
312 INTERSTITIAL GINGIVITIS. 
 
 when possible, for the same reason. The patient, therefore, 
 shoiikl be tohl frankly at the outset of interstitial gingivitis, 
 that it is a condition requiring time for its treatment, and should 
 not be given that prognosis too frequently made of quick cure. 
 To such a prognosis many a case of constitutional disorder is 
 due. The dentist is a practitioner of a surgical specialty, not a 
 mere tooth-puller. The surgical side of dentistry has received 
 too much attention, however; the medical or prophylactic too 
 little. Patients are beginning to pay more attention to the pro- 
 phylaxis of diseases of the teeth and jaws, and need but little 
 encouragement and instruction to see the absolute necessity of 
 early prophylaxis and treatment of interstitial gingivitis. The 
 trend in general medicine is to prophylaxis, and this has un- 
 doubtedly so impressed patients as to open the way for dental 
 prophylactic suggestions. Viewing the question from the narrow- 
 est standpoint of remuneration, the dentist could not fail to profit 
 by instructions to his patients on prophylaxis. He certainly 
 fails in his duty as the member of a learned profession by not 
 doing this. Furthermore, with the known necessity for pro- 
 phylaxis, it is an open question whether the failure to inform 
 the patient of the dangers of the incipient disease could not be 
 successfully pleaded as a basis for a malpractice suit. 
 
 From the etiology of this disease, the treatment would ap- 
 pear simple and easy. 
 
 Early diagnosis is not difficult, since the simple inflammation 
 of the gums is easily recognized by the patient. Bleeding when 
 the toothbrush or toothpick is used can never be mistaken. 
 The dentist wdth his accomplished eye can readily detect the 
 slightest change in color or puffiness around the necks of the 
 teeth or of the festoons between the teeth. Kedness, puffiness 
 and bleeding are pathognomonic of this disease in its incipiency. 
 Few dentists have, hoAvever, given this stage of the disease 
 any thought, albeit they have filled the teeth of their patients 
 from year to year. I have in mind three patients with loose 
 teeth and inflammation extending throughout the peridental 
 membrane and alveolar process, who had been under an old 
 practitioner now retired from practice. The patients had never 
 had the gums treated or even their teeth cleaned. This is not 
 
TREATMENT. 313 
 
 an uncommon occurrence. The excuse usually made by the den- 
 tist is that he cannot get paid for his time. Gingivitis is a dis- 
 ease which the dentist is as much bound to treat and cure as any 
 disease of the mouth and teeth. It is a part of his specialty 
 which should not be ignored. It is claimed that the dental pro- 
 fession is overcrowded. Were this disease treated until the 
 gums were placed in a healthy condition, there would be prac- 
 tice enough for as many more dentists as there are today. The 
 busy dentist of today could attend only to one-half the patients 
 whom he now serves. 
 
 The treatment, then, should be prophylactic in its nature, 
 preventive rather than corrective. The disease and treatment 
 is not unlike an inverted pyramid : the farther from the apex or 
 beginning, the more difficult and hopeless the task becomes. 
 Since the teeth have nothing directly to do wdth this disease, 
 they should be ignored. In the early stages, the gums should 
 receive proper attention. These, like other parts and organs of 
 the body, must be exercised and kept clean to be healthy. The 
 gums should be properly massaged, just as the liver, kidneys 
 or skin are when they are not doing proper work. This can be 
 accomplished by properly made brushes. The ordinary tooth- 
 brush is not adapted to the w^ork under discussion. It will 
 brush the teeth but not reach the gums. What is needed is a 
 massage brush that will miss the teeth to a certain extent, but 
 ^^^ll reach the gums and contract them tight around the teeth. 
 
 Fig. 99. — The Author's Gum ^fASSAGE Brush. 
 
 thus preventing the accumulation of foreign substances. The 
 patient should be instructed with this single idea in view, ''that 
 the gum margin is to be exercised and stimulated and not the 
 teeth, which must be ignored." A brush, properly made for 
 gum massage (Fig. 99), will do sufficient work upon the teeth 
 with the aid of the floss silk and toothpick. It should have 
 
314 INTERSTITIAL GINGIVITIS. 
 
 printed upon the handle, in large letters, ''gum massage 
 brush." The handle should be bent a little more than the "pro- 
 phylactic," so that the end containing the bristles can be 
 brought in contact with the gum, posterior to the central in- 
 cisors, upper and lower, and around the third molar teeth. 
 There should be a tuft of bristles at the point with a space for 
 the teeth. The tuft should be longer than those on the body of 
 the brush. This tuft will reach the gums at all points inside of 
 the mouth and around the molars. The bristles on the body 
 must have spaces between them, so that when the upward and 
 downward movement is given, the bristles will go between the 
 teeth and reach the gum festoons. The bristles must be medium 
 and hard. The quality of bristles must depend, however, upon 
 the condition of the gums. If they be soft and spongy, the 
 medium may be used. If the processes are heavy and thick, the 
 gums swollen and engorged with blood, hard bristles must be 
 used. Soft bristles (although sometimes recommended) should 
 never be used. 
 
 The antique theory that vigorous stimulation is injurious is 
 too much accepted. Barrett,^ for example, says, "massage of 
 the gums with the ball of the finger and by the frequent use of a 
 rather soft brush should be resorted to." Boedecker' remarks 
 that too frequent application of the toothbrush is sufficient to 
 produce papillary hyperplasia. Tomes ^ says, "in my own expe- 
 rience I have found that frequent and vigorous rubbing of the 
 gums with the finger, shampooing them in fact, has often been 
 productive of great advantage, the patient of course being cau- 
 tioned not to rub the actual edge; but even on this point there 
 is difference of opinion, for in a recent paper on the subject, 
 rest and the avoidance of all friction is advocated." Dr. Meyer 
 L. Ehein,* in introducing the "Prophylactic Toothbrush" to the 
 profession, says, in his article on "Oral Hygiene," each brush 
 comes inclosed in an envelope, upon which are printed directions 
 for the intelligent use thereof, and the following caution: 
 * 'Never pass the brush across the teeth, as this movement de- 
 
 1 Dental Cosmos, 1883, page 532. 
 
 ^ Anatomy and Pathology of the Teeth, page 365. 
 
 ' Dental Surgery, page, 704. 
 
 * New England Journal of Dentistry, October, 1884. 
 
TREATMENT. 
 
 315 
 
 stroys the delicate membrane which attaches the gum to the 
 teeth, causing recession of the gum, and ultimate loosening and 
 loss of the teeth. ' ' Citations of this could be multiplied, show- 
 ing the general impression is that the gums should not be stim- 
 ulated to any great extent ; that the finger, a soft cloth, or a very 
 soft toothbrush alone should be employed. The use of the finger 
 is a superstition which is handed down from generation to gen- 
 eration without the slightest critical analysis. If the advocate 
 of this use would try the experiment, he would see how impos- 
 si])le it would be to bring it in contact with all the tissues of the 
 mouth that are involved in this disease; were it possible, the 
 fingers, cloth and soft toothbrush would not accomplish the 
 desired result. 
 
 No brush should be used whose bristles are softer than the 
 medium; very often these, used once or twice and dipped into 
 water or mouth washes, become so soft as to be wholly unfit for 
 use. It is always a good plan to have two brushes to be used on 
 alternate days. In this way one can dry while the other is being 
 used. The general opinion has been that friction upon the gums 
 was detrimental on account of the resultant tendency to absorp- 
 tion of the gums. AVhile this may exceptionally be true, it is 
 not true of a majority. Should milk, arsenic, iron, strychnine or 
 quinine be entirely abolished as remedies because occasionally a 
 person presents untoward effects? If the alveolar process be 
 very thin over the roots of the teeth, especially the cuspids, the 
 patient must be instructed to use the brush so as not to over- 
 stimulate these particular parts. In such cases the inner alveo- 
 lar process and gum tissues may be stimulated with impunity 
 and with the hardest brush. Again, if the chronic interstitial 
 gingivitis be of long standing, or even if chronic gingivitis has 
 been present for some time, stimulation of the brush "\\ill cause 
 the gums and mucous membrane to recede until hard, sound, 
 healthy bone structure has been secured. Then absorption for 
 the time being will practically cease. In most cases absorption 
 and contraction of the gum tissue will take place to a more or 
 less marked degree. If absorption of the alveolar process has 
 taken place and the gums are puffy, red and swollen, a disease 
 exists, to be cured, regardless of consequences. The alveolar 
 
316 INTERSTITIAL GINGIVITIS. 
 
 process and gums will never return to their original position, 
 but it is a decided advantage to have a healthy mouth, even if 
 the alveolar process and gums have slightly receded. 
 
 I have used medium and stiff brushes in my practice for the 
 last thirty years and have failed to see any ill results. For the 
 past sixteen years I have made constant experiments, with the 
 view of securing the proper shape and stiffness of the bristles 
 and have obtained uniform results in gum treatment. 
 
 Proper employment of the ''gum massage brush" requires 
 skill. Every dentist should train his patient in the method of 
 using the brush. The gingival borders should not only be stim- 
 ulated, but the bristles should be passed in between the gum 
 margin and the tooth so as to remove the debris and exfoliated 
 epithelial scales which have accumulated therein. These are 
 often the cause of the irritation. Unless this is done the gum 
 or epithelial tissue cannot perform its functions or be restored 
 to health. Stimulating astringents and germicidal mouth 
 washes should be employed whenever the gums are massaged. 
 One of the best gum washes is that suggested by Dr. W. H. 
 Whitslar,^ of Cleveland, Ohio, the principal drug of which is 
 sulphocarbolate. This drug may be used in different strengths 
 and in many forms. I use the following: 
 
 Gum Wash. 
 
 Zinc sulphocarbolate gr. 60 
 
 Alcohol oz. 1 
 
 Distilled water oz. 2 
 
 True oil of wintergreen gtts. 8 
 
 The massage should be done three times a day. The patient 
 should be under the care of the dentist at least twice or thrice 
 a week, so that he may direct the treatment. If the teeth are 
 irregular, care and patience are required to reach the festoons 
 between the teeth. After the gums are in perfect health, the 
 patient should visit his dentist at least four times a year, or 
 even oftener if necessary, for inspection. If on inspection the 
 gums be found diseased at any point, the dentist can direct the 
 attention of the patient to the particular locality and the disease 
 be eradicated. By this method and this alone can the gums be 
 
 "Dental Summary, 1907, No. 8. 
 
TREATMENT. 317 
 
 kept in a healthy condition. Each patient must be given specific 
 directions as to the treatment of his or her case. 
 
 When the patient seeks our services, we should decide by a 
 thorough examination whether the disease is due to local or 
 constitutional causes or both. The age of the patient, condition 
 and character of deposits, if any, condition of mouth, jaws and 
 dental arches, condition of urine, occupation and everything 
 pertaining to the patient should be considered. While this ex- 
 amination is being conducted, which requires a few days, the 
 local treatment may be undertaken. This consists of an appli- 
 cation to the mouth, gums, mucous membrane and teeth of a 
 germ destroyer every other day until the parts are in an aseptic 
 condition as far as possible. 
 
 I cannot here too strongly condemn the method of starting 
 the treatment of this disease by scraping the roots of teeth 
 which may or may not have calcic deposits, wounding the soft 
 tissues and infecting them without first rendering them as 
 aseptic as possible. Asepsis is always the first precept of the sur- 
 geon before any kind of an operation. Why should the dentist 
 be exempt from similar methods? It is fortunate for the den- 
 tist that stasis of blood prevents infection to a great extent or 
 serious results might occur. 
 
 This, however, dees not justify the vicious treatment em- 
 ployed, since the method of procedure is wholly unscientific and 
 not in harmony with good practice. 
 
 THE lODIN TREATMENT. 
 
 The operator is not justified in placing his fingers in the 
 filthy mouths of his patients. This is also true of the students 
 in the clinics of our dental schools. It is in the clinic where the 
 student should be taught the object lesson of cleanly mouths 
 before operations. No patient in the clinic or in private prac- 
 tice should be operated upon before a thoroughly aseptic mouth 
 has been obtained. The method is so simple and so easily per- 
 formed that only a few minutes is required before operation 
 may be commenced. This treatment should consist of the free 
 use of iodin applied to the gums and teeth, carrying it well up 
 into the pockets. This will destroy every germ with which it 
 comes in contact. After many years of experimentation, sur- 
 
318 INTERSTITIAL GINGIVITIS. 
 
 geons have come to realize that iodin is the quickest acting and 
 best germicide we now possess. The author, when he began his 
 researches in 1878, commenced the use of iodin and has used 
 it to the exclusion of all other drugs in the treatment of this 
 disease. The results obtained are all that can be desired. 
 
 The official tincture of iodin contains seven per cent of iodin 
 dissolved in alcohol to which is added five per cent of potassium 
 iodid. This preparation, if used often, will cause the membrane 
 to become tender and sore ; it will also, in some patients, destroy 
 the mucous surface. To overcome this difficulty, many years 
 ago, I formulated the following which I have called 
 iodoglycerole : 
 
 Zinc iodid 15 parts or grams 
 
 Water 10 parts or grams 
 
 Iodin ' 25 parts or grams 
 
 Glycerin 50 parts or grams 
 
 As compared with the ordinary tincture of iodin, its astrin- 
 gent and antiseptic properties are greatly increased, the glycerin 
 causes rapid absorption and the irritating effects are reduced 
 to a minimum. The penetrating effect is remarkable. The 
 glycerin thickens the preparation and prevents it from mixing 
 with the saliva and running over the mouth as the ordinary 
 tincture will do. Long, round, wood applicators can be obtained 
 at the drug and instrument houses and on one end cotton is 
 wound; this is saturated with the preparation and the gum 
 margins above and below painted. The jaws are closed, the 
 lips and cheeks distended and the application made as before ; 
 the teeth are also covered; the lips and cheeks are held away 
 from the jaws until the iodin has dried. 
 
 These applications should be made every other day and con- 
 tinued until the patient is dismissed. In a fairly clean mouth, 
 the process of removing the local causes may be commenced at 
 the second appointment or possibly at the first sitting after the 
 iodoglycerole has become dry. In the more filthy mouths, the 
 time to commence operations will depend upon the judgment of 
 the operator and the condition of the mouth under treatment. 
 
 In those patients who are having operations upon the teeth. 
 
TEEATMENT. 319 
 
 although their gums are in fairly good condition, they are treated 
 after each sitting to destroy lactic-acid bacilli and their ferment 
 and all other foreign and undesirable material in the mouth, 
 thus preventing tooth decay. By this method of procedure, I 
 have reduced decay of the teeth from thirty to forty per cent 
 in my patients in the past ten years. While this treatment is 
 being conducted by the operator, the patient should use the gum 
 wash twice a day as directed. After the patient has been dis- 
 missed the gum wash should be used continually once a day. 
 
 Having destroyed all the germs in the mouth including pus 
 germs (except perhaps in so-called pockets out of reach with the 
 iodoglycerole) and contracted the gums, more or less, about the 
 necks of the teeth and on to the bone, exploration of the mouth 
 for local irritants and irregularities may now be undertaken. 
 
 Erupting Teeth, whether the first or second set, should be 
 examined by the operator and the inflamed gums receive the 
 iodoglycerole treatment. This procedure should be continued 
 in the public schools among the poor children as well as at the 
 homes of the well-to-do. If the iodoglycerole gum bath was 
 introduced into the public schools, contagions and infections 
 would be reduced to a minimum. 
 
 MODERN DENTISTRY. 
 
 I have stated that modern dentistry has produced disease of 
 the gums, pericemental membrane, and alveolar process more 
 than any one cause. The education of the student in the dental 
 schools in the mechanics of dentistry has been conducted to the 
 exclusion of the pathology of the mouth. The mechanics have 
 been carried far beyond normal physical tolerance. The dis- 
 covery that pus formation in alveolar, pericemental and blind 
 abscesses and the accumulation of pus about the alveolar proc- 
 ess and roots of the teeth cause many of the diseases of the 
 human body is a just evidence of the necessity of a medical edu- 
 cation of the dentist. Not until the methods of teaching have 
 been reconstructed, can we expect any improvement from the 
 pathologic standpoint in the management of the mouth and teeth. 
 The local causes which bring about interstitial gingivitis have 
 been discussed in Cliapter XVII and every teacher and practi- 
 tioner is familiar with them, hence it is hardly necessary to 
 
320 INTERSTITIAL GINGIVITIS. 
 
 discuss the question here. It is to be hoped that the profession 
 will soon consider the pathology of our specialty and so far as 
 possible correct and prevent local irritations, inflammations and 
 abscesses. 
 
 In passing* this subject, however, there are a few suggestions 
 which may be offered here. There is no excuse for the whole- 
 sale movement of teeth without extraction. The specialist 
 should make a study of the jaws and teeth of each patient to 
 ascertain how much may be accomplished with as little move- 
 ment of the teeth as possible. This is to be frequently accom- 
 plished by the sacrifice of one or more teeth. The health of the 
 patient, as well as the causing of as little inflammation in the 
 alveolar process as possible, should be the foremost thought in 
 the mind of the operator. The frequent use of iodoglycerole is 
 indicated during the operation of correcting irregular teeth to 
 keep down the inflammation. After the retaining bands have 
 been adjusted the iodoglycerole should often be used. 
 
 We have shown that the condition of the alveolar process, 
 especially after it has attained its growth and its endo-transi- 
 tory nature, is a very unfavorable structure for the successful 
 operation for the implantation or transplantation of teeth, par- 
 ticularly so when the peridental membrane is not present. 
 
 Gold Crowns and Bands should only extend to the gum mar- 
 gin and never above it except in extreme cases. 
 
 Artificial Dentures should be so constructed as to produce 
 the least amount of irritation possible. The larger the surface 
 the better the adaptation. Iodoglycerole treatment to the sur- 
 face of the mucous membrane under the plate to destroy germs 
 and reduce inflammation should be frequently applied. 
 
 Individual Teeth wdiose function is not restored from want 
 of proper articulation — too great or not sufficient pressure — 
 must be corrected. Such teeth are liable to become diseased, like 
 any other organ or structure of the body when not properly 
 exercised takes on pathologic changes according to the tissue 
 involved. 
 
 Tartar upon the teeth acts as a local irritant and should 
 always be removed. In some mouths it accumulates rapidly and 
 must be removed as often as once a month ; in other mouths no 
 
TREATMENT. 
 
 321 
 
 tartar is present. The teeth in such patients should be cleaned 
 as often as twice a year. These suggestions, however, are only 
 given out approximately, since the operator must decide by the 
 conditions as they exist how often visits should be made to 
 obtain the best results. Having destroyed the germs in the 
 mouth and about the teeth by the free use of iodoglycerole, the 
 tartar may be removed without fear of infecting the tissues and 
 with a large degree of comfort to the operator on account of a 
 clean mouth. Laceration of the gums in performing this oper- 
 ation is desirable. It removes the excess of stagnant blood from 
 the tissues and greatly assists in restoring normal circulation. 
 Three decades ago, I advocated the following set of scalers: 
 
 They consist of handles, shanks bent at different angles, and 
 three cornered blades, so that they can be used in three direc- 
 tions without removing the fingers from the tooth (Fig. 100). 
 
 Fig. 100. — The Author's Set of Scalers. 
 
 These are all delicately made and tempered very hard. Sharp 
 edges are thus retained. They will reach every point where 
 tartar can collect. After the deposits have been fairly well re- 
 moved, the gums may be syringed with hot water to remove 
 the debris. The gums should then be saturated with iodoglycer- 
 ole and the patient dismissed. Applications should be made 
 every two or three days. The gums w411 contract and healthy 
 circulation follow. The gum massage with the gum w^ash will 
 
322 INTERSTITIAL GINGIVITIS. 
 
 now be used twice a day. After a few treatments and the con- 
 stant use of the massage brush, the gums will contract and other 
 deposits which were not perceptible at the first sitting will now 
 be presented to view. This method of treatment should be con- 
 tinued until the gums and alveolar process are restored to 
 health. The patient should return to the dentist as often as 
 necessary (every month or two) to have the gums examined 
 and for further instructions. 
 
 As has been already shown, chronic interstitial gingivitis 
 may extend only to the peridental membrane, to the periosteum, 
 or it may extend throughout the alveolar process with the ab- 
 sorption of the bone the entire length of the root of the tooth. 
 Pus infection and calcic deposit may or may not take place. In 
 the early stages of this progressive inflammation, the first is 
 probable. If pus and deposits are present they can be treated 
 with signal success according to the symptoms and as herein- 
 after explained. As already suggested, the gum massage brush 
 must be vigorously used to relieve the engorged tissues of blood. 
 Since absorption of the alveolar process depends upon irritation 
 and inflammation, this must be removed as quickly as possible. 
 
 In the treatment of deep-seated interstitial inflammation, 
 iodin or iodin and aconite has always been regarded by physi- 
 cians and surgeons as the best remedy. The gums should be 
 thoroughly saturated twice or thrice weekly, as already sug- 
 gested. If the alveolar process be so absorbed that the tooth has 
 become loose, the case is hopeless. In such unstable tissues, 
 especially when inflammation extends through the process and 
 lacunar, perforating canal absorption and halisteresis is going 
 on, reversal of the order so as to set the osteoblasts to tissue- 
 building is hardly to be expected. The tendency is to destroy 
 and not restore the alveolar process. In such cases the tooth 
 must be fastened to the other teeth perfectly tight to prevent 
 motion in any direction. The movement of the tooth in masti- 
 cation intensifies the irritation, which in time only increases the 
 absorption. Liberal use of iodin and the gum massage brush is 
 all that can be done to reduce the inflammation and absorption 
 as much as possible. The exfoliation is only a matter of time. 
 If the tooth or teeth cannot be retained perfectly tight, no mat- 
 
TKEATMENT. 
 
 323 
 
 ter liow liealthy tlie surrounding tissues may be restored, the 
 irritation produced Ly the loose teeth will soon set up inflam- 
 mation in the surrounding tissues. The sooner the loose teeth 
 are removed the better. In no case can the bone tissue be re- 
 stored, if the matrix or cartilage be destroyed, since in this the 
 osteoblasts are located. If the matrix or cartilage be destroyed, 
 a fibrous union (such as occurs in the case of implanted teeth 
 and the imbedding of foreign bodies in the tissues of the body) 
 only is possible. 
 
 If inflammation has extended into the periosteum, peri- 
 dental membrane and alveolar process, calcic deposits are fre- 
 quently found upon the roots of the teeth. When this has taken 
 place, the calculus must be removed. This should be done with 
 the utmost care, in order that adjacent tissues may not be in- 
 jured, or inflamed parts infected mtli pus germs. Since dead 
 bone is not present, the operator should confine his instrumenta- 
 tion entirely to the root or roots of the teeth, with as little injury 
 as possible to the adjacent tissues. The alveolar process must 
 
 Fig. 101. — Spoon Shaped Excavators for Scaling the Roots of Teeth. 
 
 under no consideration be touched. Eiggs believed that the edge 
 of the alveolar process was always in a state of disintegration, 
 and that it should be so scraped as to get a fresh surface, on the 
 principle of caries of bone. Many dentists are operating in this 
 manner at the present time. I have elsewhere shown simple 
 absorption and not caries is present. Such treatment is wholly 
 unnecessary and contraindicated. The object of the removal of 
 the deposits is to allow^ the fibrous tissue of the peridental mem- 
 brane (after health is restored) to tighten about the root, which 
 cannot be accomplished when foreign substances are present. 
 
324 INTERSTITIAL GINGIVITIS. 
 
 Pushing instruments must never be used, but only such instru- 
 ments as have smooth and round backs, tempered very liard so 
 as to retain sharp edges. These instruments should be small, 
 with small points to reach depressions, and to be as universal 
 as possible. Such an instrument is to be found in the spoon ex- 
 cavator (Fig. 101). The shank can be bent to suit the operator. 
 This is to be carried gently along the length of the root and 
 passed over the deposit with a firm hand, resting the finger upon 
 some other teeth. The drawing motion is invariably to be from 
 the membrane, and toward the crown. Attention was first called 
 to the mutilation and infection of tissues two decades ago, at 
 which time most, if not all, instruments for the removal of deep- 
 seated calcic deposits were used with the pushing movement.^ 
 The deposits are scaled off painlessly. The round blade being 
 larger than the shank, and cutting upon three edges, half of the 
 root in both directions can be circled without removing the in- 
 strument. A similar instrument bent at the shank in the oppo- 
 site direction may be used on the other side. After all of the 
 roots of the teeth have been scaled, the spaces are to be syringed 
 out with warm or hot water. The gums are to be thoroughly 
 saturated inside and out with iodin. The gum massage brush is 
 to be used thrice daily as before. The patient should return 
 twice or thrice a week for further instructions. The contracting 
 gums will assist greatly in revealing the deposit. If deposits 
 still remain on the roots (the appearance of the gums will indi- 
 cate its presence) further use of the scalers is indicated. The 
 delicate instruments and the accustomed sense of touch will 
 reveal the hidden calculus. 
 
 With the precautions already noted, local anaesthesia is 
 unnecessary. The smooth, round surface of the back of the 
 instrument, if carefully inserted, will not produce pain. 
 
 If the gum be painful to the touch, or if the patient be 
 nervous and sensitive, application of iodin may be used, to- 
 gether with massage, for a few days before scaling is resorted 
 to. The sensitiveness will soon disappear, when the instrument 
 may be inserted without difficulty. 
 
 ' Jour. Am. Med. Assoc, Jan. 16, 1897. 
 ' International Dental Journal, April, 1896. 
 
TREATMENT. 
 
 325 
 
 In an article upon -Pyoritoa Alveolaris,'- I showed the 
 ditficulty of removing the deposits upon the roots of the teeth 
 with instruments and made the follomng statement: -From 
 our past experience in the treatment of the disease, the deposits 
 mnst be removed; and right here I would suggest that in the 
 futui^ treatment of this disease a dissolving fluid that is not 
 injurious to the surrounding tissue should take the place of 
 ^ instruments, especially when the disease is extensive." 
 
 I am pleased to state at this time that Dr. Joseph Head in a 
 paper, -A Tartar Solvent, Especially Useful in Pvorrhoea 
 Work,'- m which he demonstrated his experiments upon the 
 action of acid ammonium fluorid as a solvent for calcic deposits 
 c aimed to produce good results without action upon the tooth 
 structure or soft tissue. This preparation, known as -Tarta- 
 sol," can be obtained at any of the dental depots. This or sim- 
 ilar drugs and the method of application must eventually 
 become the proper treatment for the satisfactory removal of 
 deposits upon the roots of the teeth. In this way and this alone 
 can we expect to obtain a clean, smooth root surface. A few 
 years hence, the profession will regard a dentist whose patients 
 have pus oozing from the gums as a prehistoric relic and the 
 patient as an individual whose filth provokes the contempt of 
 his fellows. In this day of antisepsis, the dentist is as account- 
 able for pus infection of his patients as the physician or surgeon 
 There is no more excuse for the dentist's patient being in- 
 fected than the surgeon's. If ordinary antiseptic precautions are 
 taken, pus infection will not often occur. Prevent inflammation 
 ot the gum margin and pus infection cannot follow, no matter 
 how many germs are in the mouth. This is an absolute law of 
 
 bv M-n ""'p ''.'^T- ^' ^"'' ^""^ '"'''''' '''^ '^'' experiments made 
 by Miller, Cx. T. Carpenter and myself on dogs, rabbits, guinea 
 pigs and man. 
 
 The illustrations of the progress of interstitial gingivitis 
 teach that only the mildest treatment is indicated. Harsh treat 
 ment on the inflamed bone or fibrons tissue, either with instru- 
 ments or drug.,, must not be employed. Heroic treatment, such 
 asU,e nubscriminate application of sulphuric and lactic acid and 
 
 s Transactions National Dental Association, 1S<)9, p. 131. 
 
326 INTERSTITIAL GINGIVITIS. 
 
 similar drugs in nearly or quite full strength, is not justified by 
 the surgical principles of today. No surgeon would think of mak- 
 ing such an application to inflamed bone in other parts of the 
 body unless he wished necrosis with a desired sequestrum. 
 Much less Avould the intelligent operator use such treatment in a 
 transitory structure which predisposed to destruction. In a 
 number of instances exfoliation of the anterior plate of the alve- 
 olar process has resulted from this treatment, to say nothing c/. 
 the intense pain produced. J. M. Whitney'' has had four cases 
 in his practice in which serious results followed. The first indi- 
 cation is to remove the cause. Instrumentation should be re- 
 sorted to only to remove tartar and calcic deposits. This must 
 be done in such a manner as not to infect the deeper inflamed 
 tissue or carry the products of inflammation into healthy tissue. 
 The treatment of infected tissue within and about the alveoli is 
 not unlike treatment of abscesses and ulceration elsewhere. 
 Such drugs as are used in abscesses and ulcers in other tissues 
 are indicated here in the same strength. If strong drugs be 
 used they should not be permitted to remain in the tissue, lest 
 necrosis of the alveolar process occur. They must be diluted or 
 removed altogether after they have accomplished their purpose 
 Very serious results have occurred from careless use of drugs. 
 When abscesses have formed they should be opened and hydro- 
 gen peroxid — or, which has answered my purpose equally well, 
 hot water — is all that is necessary. More difficult is treatment 
 of ulceration of the tissue near the root of the tooth. Ordinary 
 cases will heal after hot water or hydrogen peroxid have been 
 applied. In some cases the pus germs have followed the inflam- 
 mation along the course of the vessels quite a distance into the 
 interstitial tissue. In such cases they are difficult to reach. A 
 small syringe may be employed, or the drug may be carried to 
 the part on the end of a long, thin orange-wood stick. In all 
 cases the drug must be directly applied to the part in order to 
 have beneficial results. Applications of iodin should be used, 
 as already suggested. Iodin carried to the ulcerated surface 
 often suffices to destroy the pus secretion. Ordinarily one or 
 two applications is sufficient. Occasionally calcic deposits are 
 
 9 International Dental Journal, April, ISHD. 
 
TREATMENT. 327 
 
 located in front of the infected surface and the drug does not 
 reach the part. In such cases the deposit must be removed. If 
 the pus does not cease at the first, second or even third appli- 
 cation, this is not because the drug is not sufficiently strong, but 
 because it does not reach the infected part. Continued applica- 
 tions of iodin externally and internally, carried well up between 
 the roots of the tooth and the alveolar process will, in time, pro- 
 duce the desired result. When pus ceases to flow, antiseptic 
 treatment must stop. The iodin and massage treatment must 
 then be pushed until tlie interstitial inflammation has been re- 
 duced and the gums contracted tightly about the necks of the 
 teeth. 
 
 After the tissues have been placed in a healthy condition, 
 they will require the constant attention of the operator, since, 
 like other tissues of the body when once diseased, favorable con- 
 ditions ^vill cause a recurrence. The patient must return to the 
 operator frequently so that he can advise as to the use of 
 massage. 
 
 When constitutional disorders are the cause of interstitial 
 gingivitis, local treatment will not cure the disease. It is pos- 
 sible to deplete the parts of blood and reduce the inflammation 
 to a minimum. The cause not having been removed, the inflam- 
 mation soon returns. 
 
 When the disease is due to constitutional causes, tartar de- 
 posits rarely occur; scraping the roots, therefore, is useless. 
 Pus germs may or may not be present. The local iodoglycerole 
 treatment, however, is indicated, but the constitutional causes 
 of the disease must be considered by a competent physician. 
 The history of the patient must be looked into, a complete uri- 
 nary examination made and the heart pressure taken. The 
 heart, liver, kidney, bowels, lungs and skin must be placed in a 
 healthy condition ; without this attention local results are impos- 
 sible. Change in climate and food frequently benefit the patient. 
 Loose teeth must be fastened tightl.y to other teeth; this, how- 
 ever, is only temporary, since (as I have already mentioned) the 
 function is lost. Better results can be obtained bv their removal. 
 
328 INTERSTITIAL GINGIVITIS. 
 
 VACCINE TREATMENT OF INTERSTITIAL GINGIVITIS. 
 
 In the treatment of a disease by vaccine, it is positively 
 necessary that the exact nature and identity of the germ or 
 germs producing the disease be known. It is also necessary that 
 the various types of infections as well as the pathologic condi- 
 tion in which the bacteria are present as secondary infections 
 be known. 
 
 This knowledge will prevent the specialist from using a vac- 
 cine which will not inunune the germs which produce the disease. 
 The technique of this treatment is of so much importance 
 that I cannot express my views better than to quote from an 
 article, ^'The Principles of Bacterin Therapy," by Dr. J. Favil 
 Biehn," "The corresponding bacterins are indicated in all bac- 
 terial infectious diseases ; but since the bacterins have a spe- 
 cific action only, it is absolutely essential to know the particular 
 organism or organisms causing the disease under treatment and 
 to give the corresponding bacterins. Thus, for instance, bacil- 
 lus-coli bacterins are of value only in diseases caused by the 
 bacillus coli ; they are practically valueless in diseases caused by 
 other organisms. Hence, there are no bacterins for such ail- 
 ments as boils, furuncles, and the like, for these conditions are 
 not always produced by the same organism or group of organ- 
 isms. In one case streptococci, in another case staphylococci 
 (either albi or aurei) may be the etiological cause. The first 
 form will be benefited only by the bacterins containing strepto- 
 cocci, while the second responds only to one containing staphylo- 
 coccus albus, etc. However, a mixed bacterin may be employed, 
 and will prove beneficial, provided it contains the specific organ- 
 isms responsible for this particular diseased condition. 
 
 "Therefore, unless the exact etiologic cause is determined 
 mid the corresponding bacterins are administered, failure will 
 surely result. It is quite necessary, in case several pathogenic 
 bacteria are acting together in producing a disease, that the cor- 
 responding bacterins for all of them be utilized ; and further, if 
 the infection should change as a result of the invasion of other 
 organisms unless a bacterin for these organisms is also used, a 
 complete cure may not be obtained." 
 
 10 American Journal of Clinical Medicine, February, page 157. 
 
TREATMENT. 329 
 
 A careful study of the researches in this work mil show that 
 interstitial gingivitis is due to local and constitutional irritants 
 and toxins and not to infections. 
 
 The operator must not lose sight of the fact that it is the 
 inflammatory condition which causes the absorption of the alve- 
 olar process, and the exfoliation of the teeth and not the pus 
 stage. The pus formation is the result and not the cause of the 
 disease. 
 
 While it is possible that a vaccine may be made, of the pus 
 germs which cause the secondary state of the disease (pyorrhoea 
 alveolaris), which may possibly render these germs innocuous 
 and stop the flow of pus, such treatment can, according to our 
 present knowledge, hardly be expected to reduce the primitive 
 stage (interstitial gingivitis) so much to be deplored. It is barely 
 possible that in the future specific germs may be discovered 
 which may cause the inflammatory stage. When this has been 
 accomplished, a vaccine may be produced which will be a posi- 
 tive method of treatment. Until then the vaccine method of 
 treatment should be used with discretion. 
 
BIBLIOGRAPHY 
 
 The following books and monographs 
 of the author have been drawn on largely 
 for material in compiling the present 
 work. 
 
 Books 
 
 The Irregularities of the Teeth, First 
 Edition, 1888. 
 
 The Irregularities of the Teeth, Sec- 
 ond Edition, 1890. 
 
 Chart of Typical Forms of Irregu- 
 larities of the Teeth, 1891. 
 
 A Study of the Degeneracy of the 
 Jaws of the Human Race, 1892. 
 
 The Etiology of Osseous Deformities 
 of the Head, Face, Jaws, and 
 Teeth, Third Edition, 1894. 
 
 Degeneracy: Its Signs, Causes and 
 Results (London), 1898. 
 
 Interstitial Gingivitis or So-called 
 Pyorrhoea Alveolaris, 1899. 
 
 Irregularities of the Teeth, Fourth 
 Edition, 1901. 
 
 Quiz Compend of Irregularities of 
 the Teeth, 1901. 
 
 Irregularities of the Teeth, Fifth Edi- 
 tion, 1903. 
 
 Developmental Pathology; A Study 
 in Degenerative Evolution, 1912. 
 Monographs 
 
 Education, Dental Colleges — The 
 Dental Cosmos, 1876. 
 
 Mercury, Chemical and Physiolog- 
 ical Action of Fillings on the Sys- 
 tem — The Dental Cosmos, 1879. 
 
 Preparation of Nerve Canals for 
 Treatment and Fillings — The 
 Dental Cosmos, 1880. 
 
 Gold Crowns — The Dental Cosmos, 
 1880. 
 
 Screws for Artificial Crowns — The 
 Dental Cosmos, 1881. 
 
 Treatment and Filling of Approx- 
 imal Cavities — The Dental Cos- 
 
 mos, 1881. 
 The Regulation of Teeth by Direct 
 
 Pressure — The Dental Cosmos, 
 
 1881. 
 Dental Regulating Apparatus — The 
 
 Dental Cosmos, 1885. 
 Spreading the Dental Arch — The 
 
 Dental Cosmos, 1886. 
 Regulating Individual Teeth — The 
 
 Dental Cosmos, 1886. 
 Pyorrhoea Alveolaris, ist Paper — 
 
 The Dental Cosmos, 1886. 
 
 12. The Etiology of Irregularities of the 
 
 Teeth— The Dental Cosmos, 1888. 
 
 13. Arrest of Development of the Maxil- 
 
 lary Bones, due to Race Crossing, 
 Climate, Soil and Food — The 
 Dental Cosmos, 1888. 
 
 14. Development of the Inferior Maxil- 
 
 la by Exercise and Asymmetry 
 of the Lateral Halves of the 
 Maxillary Bones — The Dental 
 Cosmos, 1888. 
 
 15. Asvmmetrv of the Maxillary Bones 
 
 — The Dental Cosmos, 1888. 
 
 16. The Alveolar Process — The Dental 
 
 Cosmos, 1888. 
 
 17. The Origin and Development of 
 
 the V and Saddle Arches and 
 Kindred Irregularities of the 
 Teeth— The Dental Cosmos, 1889. 
 
 18. The Above Concluded — The Dental 
 
 Cosmos, 1889. 
 
 19. Classification of Typical Irregular- 
 
 ities of the Maxillae and Teeth — 
 The Dental Cosmos, 1889. 
 
 20. Statistics of Constitutional and De- 
 
 velopmental Irregularities of the 
 Jaws and Teeth of Normal, Idiot- 
 ic, Deaf and Dumb, Blind and 
 Insane Persons — The Dental Cos- 
 mos, 1889. 
 
 21. Fallacies of Some of the Old Theo- 
 
 ries of Irregularities of the Teeth 
 with Some Remarks of Diagnosis 
 and Treatment — The Dental Cos- 
 mos, 1890. 
 
 22. The Teeth and Jaws of a Party of 
 
 Cave and Cliff Dwellers — The 
 Dental Cosmos, 1890. 
 
 23. The Differentiation of Anterior Pro- 
 
 trusions of the Upper Maxilla 
 and Teeth, International Medical 
 Congress, Berlin — The Dental 
 Cosmos, 1890. 
 
 24. Mouth-Breathing not the Cause of 
 
 Contracted Jaws and High Vaults 
 — The Dental Cosmos, 1891. 
 
 25. Management of Dental Societies — 
 
 The Dental Cosmos, 1891. 
 
 26. Studies of Criminals — The Alienist 
 
 and Neurologist, 1891. 
 
 27. Scientific Investigation of the Cra- 
 
 nium and Jaws — The Dental Cos- 
 mos, 1891. 
 
 28. Evidence of Somatic Origin of Ine- 
 
 briety — Journal of Inebriety, 1891. 
 
BIBLIOGKAPHY. 
 
 331 
 
 29. A Study of the Degeneracy of the 
 
 Jaws of the Human Race — The 
 Dental Cosmos, 1892. 
 
 30. Empj-ema of the Antrum — Journal 
 
 of the American Medical Asso- 
 ciation, 1893. 
 
 31. The Vault in its Relation to the 
 
 Jaw and Nose — The Dental Prac- 
 titioner and Advertiser, 1894. 
 
 32. Stigmata of Degeneracy in the Aris- 
 
 tocracy and Regicides — Journal of 
 the American Medical Associa- 
 tion, 1894. 
 
 33. The Degenerate Ear — Journal of 
 
 the American Medical Associa- 
 tion, 1895. 
 
 34. Pyorrhoea Alveolaris, 2nd Paper — 
 
 International Dental Journal, 
 1896; The Dental Cosmos, 1896. 
 
 35. Dental and Facial Evidence of Con- 
 
 stitutional Defect — The Interna- 
 tional Dental Journal, 1896. 
 
 36. H. H. Holmes — Journal of the 
 
 American Medical Association, 
 1896. 
 
 37. Pyorrhoea Alveolaris, 3rd Paper — 
 
 Journal of the American Medical 
 Association, 1896. 
 
 38. Degeneracy of the Teeth and Jaws 
 
 — Journal of the American Medi- 
 cal Association, 1896. 
 
 39. Oral Hygiene — International Medi- 
 
 cal Congress, Moscoiv, 1897. 
 
 40. Autointoxication in its Medical and 
 
 Surgical Relations to the Jaws 
 and Teeth — Journal of the Amer- 
 ican Medical Association, 1897. 
 
 41. Pyorrhoea Alveolaris in Me-curial 
 
 and Lead Poisoning and Scurvy, 
 4th Paper — Journal of the Ameri- 
 can Medical Association, 1898. 
 
 42. Degeneracy in its Relation to De- 
 
 formities of the Jaws and Irregu- 
 larities of the Teeth— r//^ Chica- 
 go Dental Revieiv, 1898. 
 1.3. A Study of the Stigmata of Degen- 
 eracy among the American Crimi- 
 nal Youth — Journal of the Ameri- 
 can Medical Association, 1898. 
 
 44- Irregularities of the Dental Arch — 
 
 1898. 
 
 45- A Study of the Deformities of the 
 
 Jaws among the Degenerate 
 Classes of Europe — The Interna- 
 tional Dental Journal, 1898. 
 
 46. Inheritance of Circumcision Effects 
 
 — Medicine, 1898. 
 
 47. What Became of the Dauphin Louis 
 
 XVII? A Studv in Dental Juris- 
 prudence — Medicine, 1899. 
 
 48. Interstitial Gingivitis due to Auto- 
 
 intoxication — The International 
 Dental Journal, 1900. 
 
 49. Traitement de la Pyorrhie Alveo- 
 
 dentaire — XIII International Med- 
 ical Congress Proceedings, Paris, 
 1900. 
 
 50. The Intervention of Therapeusis in 
 
 Anomalies of Position and Direc- 
 tion of the Teeth — XIII Interna- 
 tional Medical Congress Proceed- 
 ings, Paris, 1900. 
 
 51. Limitations in Dental Education — 
 
 Journal of the American Medical 
 Association, 1900. 
 
 52. Interstitial Gingivitis from Indiges- 
 
 tion Autointoxication — Journal of 
 the American Medical Associa- 
 tion, 1900. 
 
 53. Interstitial Gingivitis as a Promi- 
 
 nent Obvious Early Sympton of 
 Autointoxication and Drug Poi- 
 soning— Chicago Medical Society 
 Proceedings, 1901. 
 
 54. Peridental Abscess — Proceedings 
 
 Xe^v York State Dental Society, 
 1901. The Chicago Dental Re- 
 i>ieiv, 1 90 1. 
 
 55. Oral Manifestations and Allied 
 
 States — Journal of the American 
 Medical Association, 1901. 
 
 56. Degeneracy and Political Assassina- 
 
 tion — Medicine, 1901. 
 
 57. The Higher Plane of Dentistry — 
 
 Revue de Stomatologic, Paris 
 1902. 
 
 58. Juvenile Female Delinquents — The 
 
 Alienist and Xeurologist, 1901- 
 2-3- 
 59- The Stigmata of Degeneracy — The 
 Medical Examiner and Practi- 
 tioner, 1902. 
 
 60. Deformities of the Bones of the Nose 
 
 and Face — The Laryngoscope, 
 1902. 
 
 61. Evolution of the Pulp — Journal of 
 
 the American Medical Associa- 
 tion, 1902. 
 
 62. Why Dentists do not Read — The In- 
 
 ternational Dental Journal, 1903. 
 
 63. How Far do Stomatologic Indica- 
 
 tions Warrant Constitutional 
 Treatment? — The International 
 Dental Journal, 1903. 
 
 64. Syphilitic Interstitial Gingivitis — 
 
 The International Dental Journal 
 1903. 
 
 65. Gum Massage— r//^" International 
 
 Dental Journal, 1903. 
 
 66. The V^asomotor System of the Pulp 
 
 — Journal of the American Medi- 
 cal Association, 1903. 
 
 67. Recognition of the D. D. S. Degree 
 
 by the American Medical Asso- 
 ciation — Dental Journals, 1903. 
 
 68. What the Physician or Surgeon 
 
 should know of Dentistry — Iltt- 
 nois Medical Bulletin, 1903. 
 
332 
 
 INTERSTITIAL GINGIVITIS. 
 
 69. Pathogeny of Osteomalacia or Senile 
 
 Atrophy — Journal of the Ameri- 
 can Medical Association, 1904. 
 
 70. Constitutional Causes of Tooth De- 
 
 cay — The Dental Digest, 1903. 
 
 71. Interstitial Gingivitis or So-called 
 
 Pyorrhoea Alveolaris — The Dent- 
 al Summary, 1903. 
 
 72. Buccal Expressions of Constitutional 
 
 States — Medicine, 1903. The 
 
 Dental Digest, 1903. 
 
 73. Endarteritis Obliterans and Arterio- 
 
 sclerosis of the Alveolar Process 
 — The Dental Digest, 1903. 
 
 74. Pathology of Root Absorption and 
 
 Alveolar Abscess — The Dental 
 Digest, 1904. 
 
 75. The Relations of the Nose and Geni- 
 
 talia — Medicine, 1904. 
 
 76. Pulp Degeneration — Journal of the 
 
 American Medical Association, 
 1904. 
 
 77. Criminal Responsibility and Degen- 
 
 eracy — British Medical Associa- 
 tion, Section on Psychological 
 Medicine, 1904. 
 
 78. Anatomic Changes in the Head, 
 
 Face, Jaws and Teeth in the 
 Evolution of Man — Fourth Inter- 
 national Dental Congress, St. 
 Louis, Mo., 1904. 
 
 79. Constitutional Causes of Tooth De- 
 
 cay, Erosion, Abrasion and Dis- 
 coloration — Fourth International 
 Dental Congress, St. Louis, Mo., 
 1904. 
 
 80. Etiology of Cleft Palate — Fourth 
 
 International Dental Congress, St. 
 Louis, Mo., 1904. 
 
 81. Scorbutus or Interstitial Gingivitis 
 
 — Medical Nen.vs, 1904. 
 
 82. Negro Ethnology and Sociology — 
 
 Illinois Medical Bulletin, 1905. 
 
 83. Gonorrhoeal Ulcero-Membraneous 
 
 Stomatitis — The International 
 Dental Journal, 1905. 
 
 84. Evolution of the Central Nervous 
 
 System — The Dental Digest, 1905. 
 
 85. Study of the Pithecanthropus Erectus 
 
 or Ape-Man — The International 
 Dental Journal, 1905. 
 
 86. Advance and Retrogressive Evolu- 
 
 tion — The Dental Digest, 1905. 
 
 87. Underlying Factors of Development- 
 
 al Pathology or Suppressive Evo- 
 lution — The Dental Digest, 1905. 
 
 88. Laws Governing Eugenesis : A 
 
 Thirty-five Years Study of Devel- 
 opmental Pathology — The Dental 
 Era, 1905. 
 
 89. Developmental Pathology and Tooth 
 
 Decay — The Dental Cosmos, 1905. 
 
 90. Errors in Dental Education — The 
 
 Dental Cosmos, 1906. 
 
 91. Interstitial Gingivitis due to Autoin- 
 
 toxication: Etiology — The Dental 
 Digest, 1906. 
 
 92. Interstitial Gingivitis due to Autoin- 
 
 toxication as Indicated by the 
 Urine and Blood Pressure Diag- 
 nosis — The Dental Digest, 1906. 
 
 93. Therapeusis and Treatment of In- 
 
 terstitial Gingivitis due to Auto- 
 intoxication — The Dental Digest, 
 1906. 
 
 94. Acid Autointoxication and Systemic 
 
 Disease the Cause of Erosion and 
 Abrasion — Proceedings of the 
 Neiu York State Dental Society, 
 1907. 
 
 95. Alcohol in its Relation to Degener- 
 
 acy — Journal of the American 
 Medical Association, 1907. 
 
 96. Acid Intoxication or Acidosis: A 
 
 Factor in Disease — Neiv York 
 Medical Record, 1907. 
 
 97. Stomatology in its Medical Aspects 
 
 — Extrait du Bulletin of the Inter- 
 national Association of Stomatol- 
 ogy, Bruges, 1908. 
 
 98. Swan Songs and Degeneration of 
 
 American Dental Colleges — The 
 Dental Cosmos, 1908. 
 
 99. The Care of the Teeth — Illinois 
 
 Medical Bulletin, 1908. 
 
 100. Etiology of Face, Nose, Jaw and 
 Tooth Deformities — Journal of 
 the American Medical Associa- 
 tion, 1909. 
 
 loi. Bone Pathology and Tooth Move- 
 ment — Journal of the American 
 Medical Association, 1909. 
 
 102. Acidosis, Indicanuria, Internal and 
 
 External Secretions: the Effects 
 upon the Alveolar Process and 
 Teeth — The Dental Cosmos, 1908. 
 
 103. Sense and Nonsense as taught in 
 
 American Dental Schools — The 
 Dental Cosmos, 1909. 
 
 104. Treatment of Interstitial Gingivitis 
 
 — The Dental Cosmos, 1909. 
 
 105. Progress of Stomatology in Europe — 
 
 The Dental Cosmos, 1909. 
 
 106. Hard Teeth and Soft Teeth— The 
 
 Dental Cosmos, 1909. 
 
 107. Progress of Stomatology in Hungary 
 
 — American Journal of Clinical 
 Medicine, 1909. 
 
 108. Local Manifestations of Systemic 
 
 Diseases — XFI International Med- 
 ical Congress, Budapest, 1909. 
 
 109. How Shall the Stomatologist be Edu- 
 
 cated ? — International Association 
 of Stomatology, Budapest, 1909. 
 
 110. Scope of Developmental Pathology 
 
 — The Alienist and Neurologist, 
 Feb. 1910. 
 
 111. Rip Van Winkles in American Dent- 
 
 al College Faculties — The Dental 
 Cosmos, 1910. 
 
BIBLIOGRAPHY. 
 
 333 
 
 112. The Scope of Developmental Pathol- 
 ogy in its Relation to Oral Mani- 
 festations — International Ameri- 
 can Congress of Medicine and 
 Hygiene, 1910. 
 
 1x3. Oral Hygiene in American Dental 
 Schools: — The Dental Cosmos, 
 1910. 
 
 114. The Acidemic Condition — The Med- 
 
 ical Standard, 1910. 
 
 115. lodin as an Astringent, Antiseptic, 
 
 Disinfectant and Germicide in the 
 Treatment of Mouth Diseases — 
 Journal American Medical Asso- 
 ciation, 1910. 
 
 n6. How Shall the Stomatologist be Ed- 
 ucated? — Journal American Med- 
 ical Association, 1910. 
 
 117. Care of the Mouths of School Chil- 
 dren — The Dental Summary, 
 1910. 
 
 ti8. The Quality of Service Rendered — 
 The Dental Summary, 1910. 
 
 119. What are Dentists as a Profession 
 doing to Advance their Specialty? 
 — The Dental Summary, 1910. 
 
 120. Treatment to Alleviate the Conta- 
 
 gions, Infections and Local Dis- 
 eases of School Children — The 
 Dietetic and Hygienic Gazette, 
 1910. 
 
 121. Developmental Pathology: A Study 
 
 in Degenerative Evolution — Pro- 
 ceedings of the First District 
 Dental Society of New York, 
 1910. 
 
 122. The Future of Dentistry — Sunday 
 
 Editorial in The Chicago Tribune. 
 1911. 
 
 123. Some Bacterial and Non-Bacterial 
 
 Diseases — Dental Summary, June 
 1912. 
 
 124. The Relation of Rheumatic Arthri- 
 
 tis to Pvorrhoea Alveolaris — 
 Clinical Medicine, November, 
 1912. 
 
 125. Degeneracies, the Result of Alcohol 
 
 and other Narcotics — Read before 
 Society for the Study of Alcohol 
 and Other Narcotics, at Washing- 
 ton, D. C, Dec. 11-12, 1912. 
 
 126. Interstitial Gingivitis and Pyorrhoea 
 
 Alveolaris — Journal American 
 Medical Association, 191 3. 
 
INDEX OF AUTHORS 
 
 Page 
 
 Adami 123 
 
 Alexander, H. C. B 173 
 
 Allbright 3 
 
 Allen, Harrison 22 
 
 Andrews, R. R 88 
 
 Arkovy 4 
 
 Atkinson 4 
 
 Barker 272 
 
 Barrett 314 
 
 Bauman 239 
 
 Beaumont 203 
 
 Bernard, Claude 203 
 
 Bichat 201 
 
 Biehn, J. Favil 328 
 
 Billings, Frank 298 
 
 Black 5, 42, 50, 52, 53, 56, 57 
 
 Boak, G. D 213 
 
 Boedecker 314 
 
 Bondurant 207 
 
 Bonwill 2 
 
 Bouchard, H. H 184, 239 
 
 Braconnot 239 
 
 Bremer, L 228 
 
 Brown 2 
 
 Brown-Sequard 271 
 
 Brubaker, A. B 90 
 
 Bui lard 227 
 
 Calve, Marshall 2 
 
 Carpenter 104, 108, 109, 283, 289 
 
 Carter 239 
 
 Cartwright, Hamilton 4 
 
 Chittenden, Prof. Russell H 242 
 
 Christian 202 
 
 Clowes 3 
 
 Coles, Oakley 4 
 
 Collins, J 86 
 
 Congdon, Ernst 90 
 
 Coplans, Mayer 219, 220 
 
 Croftan, Alfred C 70 
 
 Cruveillier 207 
 
 Davis, David J 308 
 
 Dickinson, Howship 78 
 
 Dray, Arthur R 21 
 
 Ebner, Von 62 
 
 Eisenhart 277 
 
 Enderlein 76 
 
 Essig, C. J 3 
 
 Evans, W. A 106 
 
 Farrar, J. N 4 
 
 Fauchard, H. A 2 
 
 Fitzgerald, John 10, 90, 295, 296 
 
 Flower, Alsop E 126 
 
 Foster 14 
 
 Gallippe 4, 16, 104 
 
 Geddings, H. D 75 
 
 Gilmer 305 
 
 Page 
 
 Gmeiin 239 
 
 Goadby, K. B 220, 302 
 
 Gubler 239 
 
 Hafner 215 
 
 Hammarsten 87 
 
 Hartzell, T. B 306 
 
 Hassal 239 
 
 Head, Joseph 325 
 
 Hektoen 156, 265 
 
 Herschell 296 
 
 Hertwig 62 
 
 Herzog 108 
 
 Hodgen 233 
 
 Hogben 173 
 
 Howell 177 
 
 Hunter 298, 301 
 
 Ingersoll, L. C 4 
 
 Izklai, Joseph 4 
 
 Jacobson 75 
 
 Jaffe 239 
 
 Joirac, M 2 
 
 Jourdain 2 
 
 Jurgensen 194 
 
 Kaecker, L 2 
 
 Kaufmann 66, 275, 276 
 
 Kiernan 271 
 
 Kirk 124, 184, 206 
 
 Klebs 122 
 
 Koch 16 
 
 Kolliker 35, 37, 62, 279 
 
 Krabler 194 
 
 Kuh, Sidney 273 
 
 Kuttner 282 
 
 Libman, E 309 
 
 Macauley 242 
 
 Magitot 2, 8, 57, 61, 64, 206 
 
 Mailhol 14 
 
 Malassez 4 
 
 Malenfant 79 
 
 Marinesco 271 
 
 Mendel 228 
 
 Metchnikoff 236, 239, 258 
 
 Miller 9, 102, 103, 104, 105, 286 
 
 Mills, G. A 3 
 
 Minot 38, 58, 62 
 
 Moorehead, Frederick 299 
 
 Morgan, de 36 
 
 Meyer 233 
 
 Mummery 2i 
 
 Murchison 202 
 
 Murrell 228 
 
 Nasse 271 
 
 Nencki 239 
 
 Niles, N. S 3 
 
 O'Neill, Eugene F 21 
 
 Osier 300 
 
INDEX OF AUTHORS. 335 
 
 „ , f*2g^ Page 
 
 Parker 213 Sirletti 3 
 
 Patterson, J. D 4, 6, 9, 103 Stadeler 239 
 
 Pedley, Newland 7, 8 Starr, A. R 5 
 
 Pierce, C. N 9, 16, 90, 91, 206 Stevenson yg 
 
 P'tres 273 Stewart 297 
 
 Planer 238, 239 Suckdorf 237 
 
 Prout 203 Sudduth, W. X 6, 8, 9, 105 279 
 
 Purdy 257 Sutton, Bland 8 
 
 Quain 13 Talbot, E. S 5, 10, 11, 12, 104, 182 
 
 Ravvls, A 4, 233 186, 191, 197, 324 
 
 Recklinghausen, von 277 Thoma 122 
 
 •^eese 4^ Thompson 202 
 
 Reeves 90 Tiedemann 239 
 
 Rehwinkle 3 Tomes 36, 314 
 
 Rennert 232 Tuke 203 
 
 Rhein, M. L 9, 90, 104, 105, 206, 314 Turck 272 
 
 Riggs, John T 2 Vaillard ..273 
 
 Robin 57, 60, 61, 64, 206, 239 Valentine 271 
 
 Roger, G. H 239 Vaughn 195 
 
 Rokitansky 282 Vignas 237 
 
 Rosenovv, Edward E 309 Virchow 282 
 
 Rush 228 Waldeyer 62 
 
 Salisbury, J. H 79, 91, 93 Walker 4, 21 
 
 Salkowsky 239 Waller .'271 
 
 Salter 52 Ward, Charles 22 
 
 Sayre, Charles E 126 Wesener 91, 92 
 
 Scheele 87, 89 Whitnev, J. M '326 
 
 Scheff 2 Whitslar, W. H 316 
 
 Scheheotskey 78 Wood, James 227 
 
 Schieff 239 Wright, A. E 219 
 
 Schmidt 78 Zawadsky 76 
 
 Selmi 235 Ziegler 32, 212, 276 
 
 Senator 239 Ziemssen 194 
 
 Shambaugh, G. E 299 Zilz 300 
 
INDEX OF SUBJECTS 
 
 Abscess, Alveolar, 290. 
 
 Alveolar, Production of, 290. 
 
 Formation, Description of, 117. 
 
 Pericemental, 297. 
 
 Peridental, 123. 
 Abscesses, Location of, 287. 
 
 Treatment of, 326. 
 Acid Autointoxication and Mouth Acidity, 
 250. 
 
 Excess of System, Disposal of. Through 
 Salivary Glands, 254. 
 
 States, 198. 
 Alcohol, Constitutional Effects of, 226. 
 
 Effect of, on Alveolar Process, 224. 
 Altitude, High, Effect of, on Alveolar 
 process, 216. 
 
 High, Effect of on Teeth and Gums, 215. 
 Alveolar Abscess, 290. 
 
 Production of, 290. 
 Alveolar-Process, abnormal, 30. 
 
 Absorption of, 25, 28, 121, 189, 205, 271, 
 
 Absorption of, and Calcic Deposits on 
 
 Roots of Teeth, 275. 
 Absorption of, Caused by Excessive 
 
 Brushing of Teeth, 189. 
 Absorption of, in Asthma, 205. 
 Absorption of, in Bright's Disease, 205. 
 Action of Poisons on, 223. 
 And High Blood Pressure, 208. 
 And Lessened Blood Alkalinity, 256. 
 And Poisons in Circulation, 209. 
 Arrested Development of, 30. 
 As End Organ, 70, 118, 121, 236. 
 As Transitory Structure, 236. 
 Atrophy of, 197. 
 Blood Vessels of, 177. 
 Changes in Function of, 184. 
 Effect of Acid States on, 199. 
 Effect of Constitutional Disturbances on, 
 
 207. 
 Effect of Diabetes on, 207. 
 Effect of Exanthemata on, 205. 
 Effect of High Altitude on, 216. 
 Effect of Interstitial Inflammation on, in 
 
 Dog's Tooth, 137. 
 Effect of Nutritional Disturbances on, 
 
 233- 
 
 Effect of Picking Teeth on, 190. 
 
 Effect of Pregnancy on, 200. 
 
 Effect of Tobacco, Alcohol, Tea, Coffee, 
 Drugs and Poisons on, 224. 
 
 Effect of Toxins on, 223. 
 
 Endarteritis Obliterans and Arterioscle- 
 rosis of Vessels in, 266. 
 
 Exfoliation of Anterior Plate of, 326. 
 
 Growth of, 24. 
 
 Alveolar-Process, Hypertrophy of, 30, 33. 
 In Phosphorus Poisoning, 121. 
 In Tuberculous Monkey, Absorption of, 
 
 155- 
 inflammations of, 113. 
 Injury to, by Bridgework, 188. 
 Injury to, by Gold Crowns, 188. 
 Nerve Supply in, 123. 
 Obliteration of Arterioles in, 266. 
 Osteomalacia of, 197, 200, 277. 
 Overlapping Fillings Cause of Injury to, 
 
 189. 
 Structure of, 25. 
 Toxemia and, 199. 
 Transitory Nature of, 69, 96. 
 Under the Microscope, 35. 
 Wasting of, and Facial Hemiatrophy, 
 208. 
 Antimony as Cause of Interstitial Gin- 
 givitis, 173. 
 Arsenic as Cause of Interstitial Gingi- 
 vitis, 173. 
 Arteries, Changes in Walls of, in Disease, 
 261. 
 Irritations of Walls of, 263. 
 Arteriosclerosis and Nerve End Oblitera- 
 tion, Degeneration, 261. 
 Of Alveolar Blood Vessels, 266. 
 Asthma, Absorption of Alveolar Process 
 
 in, 205. 
 Atmospheric Pressure and Bleeding From 
 
 Gums, 215. 
 Atrophy from Disuse, 237. 
 Autoinfections, 236. 
 Autointoxication, 236, 244. 
 Factors in, 201. 
 In Interstitial Gingivitis, 235. 
 In Neurotics and Degenerates, 242. 
 Indicanuria as Source of, 258. 
 Urinary Signs of, 247. 
 Bacillus Coli Communis as Inhabitant of 
 
 Mouth, 296. 
 Bacteria Infesting Mouth, 296. 
 Bacterial Experiments in Interstitial Gin- 
 givitis, 104. 
 Infection of Man, 236. 
 Thrombosis in Peridental Membrane, 
 162. 
 Bacteriology of Interstitial Gingivitis, 104. 
 Bile, Composition of, 75. 
 Blood, Alkalinity Effect of Lessened, 256. 
 Analysis of, 73. 
 
 From Portal Vein, Toxicity of, 240. 
 Pressure, High, and Alveolar Process, 
 
 210. 
 Pressure, High, and Gingivitis, 208. 
 
INDEX OF SUBJECTS. 
 
 337 
 
 Blood, Vessels of Gums Alveolar Process 
 
 and Pericemental Membrane, 177. 
 Body Equilibrium, Maintenance of, on Re- 
 stricted Diet, 242. 
 Heat, 196. 
 
 Refrigeration of, 212. 
 Temperature and Climate, 211. 
 Bone Absorption, 66. 
 
 Absorption in Inflammation, 120, 124. 
 Building and Absorption, 64. 
 Brass-Worker's Ague as Cause of Inter- 
 stitial Gingivitis, 172. 
 Bridgework, Injurious Effect of, on Aveo- 
 
 lar Process, 188. 
 Bright's Disease, Absorption of Aveolar 
 
 Process in, 205. 
 Bromides as Cause of Interstitial Gingivi- 
 tis, 173. 
 Cachexia, 198. 
 
 Calcic Deposit: See also Tartar. 
 Calcic Deposits on Teeth: See also Serum- 
 
 al Deposits. 
 Calcic Deposits on Teeth. 10, 83, 280. 
 
 Deposits, Removal of, 323. 
 Calcification, Causes of, 282. 
 Calcospherites, 50, 162. 
 Catarrh Coexistent with Pyorrhoea Alveo- 
 
 laris, 103. 
 Cementoblasts in Dog's Tooth, 140. 
 Children, Neurotic and Degenerate, Erup- 
 tion of Teeth in, 182. 
 Climate and Scurvy, 218. 
 Coca, Abuse of, 229. 
 Cocain, Effect of, on Gums, 230. 
 
 Effects of Use of, 229. 
 Coffee, Nervous Symptoms of, 227. 
 Criminals, Chest Formation of, 205. 
 
 Tuberculosis in, 205. 
 Crowns and Bands, 320. 
 Degeneracy of Tissues, 100. 
 Degenerates, Autointoxication in, 242. 
 Dental Arches, Irregular, 102. 
 Pulp: See also Tooth. 
 Pulp, n8. 
 
 Shelf, Development of, 58. 
 Shelf, Embryology of, 62. 
 Dentistry as Cause of Interstitial Gingivi- 
 tis, 182. 
 Modern, Diseases Caused by, 319. 
 Dentures, A.rtificial, 320. 
 Digestive-Apparatus, Evolution of, 237, 
 240. 
 In Differing Types, 241. 
 Diabetes, Effect of, on Alveolar Process, 
 
 207. 
 Diabetic Patients, Uranalysis in, 251. 
 Drug Poisons, Nervous Effects of, 231. 
 Drugs, Effect of, on Alveolar Process, 224. 
 Nervous Symptoms Due to Use of, 228, 
 
 Poisonous Effects, First Noted in Gums, 
 230, 234. 
 Dyphodontia, 12. 
 Emotions and Their' Physical Effects, 201. 
 
 And Trophoneuroses, 271. 
 
 Violent, and Nutrition, 204. 
 
 Enamel Organ, 59. 
 Endarteritis, Causes of, 263. 
 
 Definition of, 263. 
 
 Obliterans and Nerve End Degenera- 
 tion, 261. 
 
 Obliterans in Alveolar Blood Vessels, 
 266. 
 Environment in Interstitial Gingivitis, 95. 
 Epithelial Debris, 60. 
 Evolution of Digestive Apparatus, 237, 
 
 240. 
 Exanthemata, Effect of, on x'\lveolar 
 
 Process, 205. 
 Face, Evolution of, 113. 
 Facial Hemiatrophy and Wasting of 
 
 Alveolus, 208. 
 Faeces, Salts in, 76. 
 Fever, Cause of, 195. 
 Fever, Definition of, 194. 
 Fevers, Trophic Changes After, 206. 
 Gum Margin, Irritation of, 182. 
 
 Massage, 314, 316. 
 
 Wash, 316. 
 Gums, Bleeding From as Effect of At- 
 mospheric Pressure, 215. 
 
 Bloodvessels of, 177. 
 
 Effect of High Altitude on, 215. 
 
 Effect of Poisons on, 199, 230. 
 
 First Structure to Indicate Certain Sys- 
 tematic Defects, 250. 
 
 Inflammation of, in Scurv\", 209, 220. 
 
 Irritation of, 66. 
 
 Signs of Drug and Metal Poisoning in, 
 114. 
 
 Structure of, 40. 
 
 Ulceration of, 271. 
 Gingival Glands, 52. 
 
 Organs, 52, 90. 
 Gingivitis, Philology of, 14. 
 Gold Crowns and Destruction of Alveolar 
 
 Process, 188. 
 Gout, Deposits in Tissues in, 79. 
 Halisteresis, Definition of, 276. 
 Heat, Difference Between that of Sun and 
 
 Shade Heat, 213. 
 Heredity in Interstitial Gingivitis, 95, 96. 
 Horses, Cause of "Cribbing" in, 126. 
 Hygiene in the Tropics, 213. 
 Hypophysis Cerebi, Disorders of, and Body 
 
 Changes, 34. 
 Indican, Effects of Administration of, 239. 
 
 In Organism, Effect of, 258. 
 Indicanuria and Neurasthenia, Relation- 
 ship of, 257. 
 
 As Source of Autointoxication, 258. 
 Infection, Susceptibility to, and Low Tem- 
 perature, 212. 
 Inflammation, Active, Illustration of, 114. 
 
 And Bone Absorption, 120. 
 
 Behavior of Blood in, 115, 120. 
 
 Leucocytes in, 115. 
 
 Nervous System in, 122. 
 
 Production and Course of, 114. 
 
 Without Gingivitis, 112. 
 lodoglycerole, 318. 
 Insane, Disturbances of Teeth in, 207. 
 
338 
 
 INDEX OF SUBJECTS. 
 
 Instruments to be Used in Removing Cal- 
 cic Deposits, 323. 
 Intermarriage, Effect of, on Teeth, 97. 
 Interstitial, Foster's Definition of, 14. 
 
 Quain's Definition of, 13. 
 Interstitial-Gingivitis and Constitutional 
 Diseases, 236. 
 
 And Higli Blood Pressure, 208. 
 And Inorganic Salts, 73. 
 
 And Irregular Arches, 102. 
 
 And Uric Acid, 87. 
 
 And Pericementitis, 176. 
 
 And Poisons in Circulation, 209. 
 
 Animal Research on, 125. 
 
 Antimony as Cause of, 173. 
 
 Arsenic as Cause of, 173. 
 
 Autointoxication in, 235. 
 
 Bacteriologic Researches in, 104. 
 
 Brass-worker's Ague as Cause of, 172. 
 
 Bromides as Cause of, 173. 
 
 Contagiousness of, 6. 
 
 Caused by Regulation of Teeth, 190. 
 
 Choice of, in Preference to Pyorrhoea 
 Alveolaris, 13, 15. 
 
 Condition of Urine in, 247. 
 
 Constitutional Causes of, 8, 84, 194, 327. 
 
 Definition of, 112. 
 
 Degenerate Tissues in, 100. 
 
 Differential Diagnosis of, 221. 
 
 In Defective Children, 103. 
 
 In Dogs, 126. 
 
 In Dogs, Technique of Examination for, 
 131. 
 
 In Human, Autopsy Findings, 156. 
 
 In Man From Drugs, 170. 
 
 In Pregnant Women, 8, 176. 
 
 In Soldiers in the Tropics, 213. 
 
 Infectivity of, 17. 
 
 Influence of Climate in, 211. 
 
 lodin Treatment of, 317, 322. 
 
 Irregular Teeth and, 6. 
 
 Laboratory Experiments in, 105. 
 
 Local and Constitutional Causes of, 104, 
 
 175- 
 Local Causes of, 5, 84, 104, 112, 175, 182. 
 Mercurial, in Dogs, 150. 
 Method of Extension of, to Aleovolar 
 
 Process, 276. 
 Drug and NIetal Poisons in Etiologv of, 
 
 84. 
 Etiology of, 84. 
 Frequency of, in Animals, 126. 
 Heredity and Environment in, 95. 
 History of, i. 
 In Animals, 7, 8. 
 In Children, 82. 
 
 Modern Dentistry as Cause of, 182, 186. 
 Nature of Structures Involved in, 112. 
 Pathognomonic Symptoms of, 312. 
 Persons with Predisposition to, 124. 
 Point of Commencement of, 56. 
 Predisposition to, 100. 
 Pregnancy and, 8, 176. 
 Recovery From, 286. 
 In the Human, Researches on, 156. 
 Scorbutus in, 85. 
 
 Interstitial-Ciingivitis, Scurvy in, 218. 
 Symptoms of, 7. 
 Syphilis in, Etiology of, 8, 9. 
 Tartar as Cause of, 112. 
 Theories of, 84. 
 Tooth Eruption and, 182. 
 Treatment of, 310. 
 Trophic Disturbances in, 86. 
 Uncleanliness as Cause of, 186. 
 Vaccine Treatment of, 328. 
 With Intestinal Fermentation, 244. 
 Intestinal Putrefaction and Toxins in the 
 
 Blood, 239. 
 Jaw, Arrested Development of, 95. 
 
 Effect of Phosphorus Poisoning on, 120. 
 Excessive Development of, 95. 
 Variation in Dogs, 127. 
 Jaws, changes in, 238. 
 Deformities of, 242. 
 Evolution of, 19, 113. 
 
 Irregular in Neurotics and Degenerates, 
 96. 
 Kidney Disease, Absorption of Alveolar 
 
 Process in, 205. 
 Laboratory Experiments in Interstitial 
 
 Gingivitis, 105. 
 Lymph, Salts in, 76. 
 
 Mallet, Excessive Use of as Cause of In- 
 flammation of Peridental Membrane, 
 187. 
 Maxillary Necrosis, 271. 
 Metabolic Disturbances and Their Effects, 
 196. 
 
 Mental States, Physical Effects of, 201. 
 Mouth Acidity and Acid Autointoxication, 
 250. 
 
 Infection and Glandular Affections, 297. 
 
 Toxins Generated in, 199. 
 Mucous-Membrane, Glands, in, 50, 57. 
 
 Irritation of, 66. 
 
 Of Mouth, 38. 
 
 Of Mouth, Blood Vessels and Nerves of, 
 40. 
 
 Under Microscope, 53. 
 Nerve End Degeneration, Endarteritis, 
 and Arteriosclerosis, 261. 
 
 Exhaustion in Parents, Effect of, on 
 Child's Teeth, 97, loi. 
 
 Supply in Alveolar Process, 123. 
 Nerves, Effects of Toxins on, 273. 
 Nervous System in Inflammation, 122. 
 Neurasthenia and Indicanuria, Relation- 
 ship of, 257. 
 Neurotics, Autointoxication in, 242. 
 Nutrition, Causes of Arrest of, 223. 
 
 Disturbances of. Effect of, on Alveolar 
 Process, 223. 
 
 Modification of, by Emotions, 204. 
 Opium, Nerve Effects of, 228. 
 Osteoclasts, 279. 
 Osteomalacia, 197. 
 
 Of Alveolar Process, 197, 200, 277. 
 
 Varieties of, 276. 
 Pancreatic Juice, Composition of, 76. 
 Paretic Patients, Urine in, 252. 
 
INDEX OF SUBJECTS. 
 
 339 
 
 Pericemental Membrane, Bloood Vessels 
 
 of, 177. 
 Pericementitis, 175. 
 
 And Interstitial Gingivitis, 176. 
 
 Artificial Production of, 176. 
 
 Author's Researches on, 176, 178. 
 
 Causes of, 176. 
 
 Due to Syphilis, 176. 
 
 Effect of on Surrounding Tissues, 176. 
 
 In Human, Research on, 175. 
 
 Phagedenic, 53. 
 Peridental Abscess, 123. 
 Peridental-Membrane, 27, 42, 45. 
 
 Bacterial Thrombosis in, 162. 
 
 Blood Vessels in, 49. 
 
 Cells in, 65. 
 
 Condition of, in Pyorrhoea, 289. 
 
 Cross Sections of, 57. 
 Peridental-Membrane, Degeneration of, 
 From Drugs, 172. 
 
 Effect of Interstitial Inflamm.ation on, in 
 Dog's Tooth, 137. 
 
 Excessive Use of Mallet Cause of In- 
 flammation of, 187. 
 
 Glands in, 50. 
 
 Hard Bodies in, 50. 
 
 Infection of, 96. 
 
 Irritation of, 66. 
 Periostitis, Suppurative, 162. 
 Periosteum, 42. 
 
 Perspiration, Inorganic Salts in, 76. 
 Phosphorus Poisoning, Effect of, on Jaws, 
 
 120. 
 Poison, Scant Elimination of, by Skin, 242. 
 Poisons, Action of, on Alveolar Process, 
 223. 
 
 Classification of, 223. 
 
 Effect of, on Gums, 230. 
 
 Elimination of, 243. 
 Polyphyodontia, 12. 
 
 Potassium Bromide as Cause of Intersti- 
 tial Gingivitis, 173. 
 Pregnancy, Elimination of Poisons in, 243. 
 
 Urinary Acidity in, 244. 
 Purin bodies, 88. 
 Pyorrhoea-alveolaris, 96, 124, 285. 
 
 And Irregular Arches, 102. 
 
 Bacteria in, 106. 
 
 Catarrh Coexistent Vi^ith, 103. 
 
 Constitutional Effects of, 295. 
 
 Description of, 285. 
 
 Development of, 285. 
 
 In Animals, 106, 129, 131. 
 
 In Dog's Teeth, Technique of Examina- 
 tion for, 131. 
 
 In the Human, 106. 
 
 In Troops, 220. 
 Rachitis, Association of. With Scurvy, 218. 
 Saliva, Composition of, 78. 
 Salivary Calculi, Composition of, 79. 
 
 Concretions, 98. 
 
 Glands, Effect of Tobacco on, 225. 
 Salivation in Scurvy, 221. 
 Scalers, Description of Author's, 321. 
 Scurvy and Armies, 218. 
 
 And Climate, 218. 
 
 Scurvy, and Food, 219. 
 
 And Inflammation of Gums, 209. 
 
 And Interstitial Gingivitis, 236. 
 
 Causes of, 218. 
 
 Differential Diagnosis of, 220. 
 
 In Interstitial Gingivitis, 218. 
 
 In Institutions, 221. 
 
 Rachitis with, 218. 
 
 Salivation in, 221. 
 
 Symptoms of, 220. 
 Sedentary Habits, Effects of, 89. 
 Serumal Deposits: See also Calcic De- 
 posits. 
 Serumal Deposits on Teeth, Analysis of, 
 
 .79- 
 Skin, Scant Elimination of Poisons by, 242. 
 Status Epilepticus, 201. 
 Submaxillary Gland, 185. 
 Submucous Membrane, Proliferation of 
 
 Epithelial Cells in, 58. 
 Syphilis and Interstitial Gingivitis, 236. 
 Tabes Dorsalis, Urine in, 252. 
 Tartar: See also Calcic Deposit. 
 Tartar, 184, 320. 
 
 And Malnutrition, 185. 
 Salivary, Formation of, 184. 
 Solvent For, 325. 
 Tea-tasters, Nervous Symptoms in, 226. 
 Teeth: See also Tooth. 
 Teeth, Calcic Deposits on, 280, 323. 
 
 Cavities in, and Overlapping Fillings, 
 Cause of Injury to Alveolar Process, 
 189. 
 Change of Position of, 31. 
 Effect of Acid States on, 199. 
 Effect of High Altitude on, 215. 
 Eruption of, 64, 319. 
 Eruption of, and Interstitial Gingivitis, 
 
 182. 
 Eruption of, in Neurotic and Degenerate 
 
 Children, 182. 
 Evolution of, 113. 
 
 Examination of, for Uric Acid, 90. 
 Excessive Brushing of, and Bone Ab- 
 sorption, 189. 
 Decay of, 196. 
 Deformities of, 242. 
 
 Degeneration of, Due to Evolution, 238. 
 Devitalization of Pulps of, 188. 
 Disturbances of, in the Insane, 207. 
 Falling Out of, and Trophoneuroses, 
 
 271. 
 Description of, 285. 
 Individual, Correction of, 320. 
 In Inmates of Institutions, 221. 
 Irregular, 186. 
 Loosening of, 271. 
 Method of Eruption of, 64. 
 Milk, Formation of Papilla; for, 58. 
 Of Defective Children, 103. 
 Picking of, Efl^ect of, on Alveolar Pro- 
 cess, 190. 
 Proper Way of Brushing, 313. 
 Result of Wedging Apart of, 193. 
 Regulation of, and Interstitial Gingivi- 
 tis, 190. 
 
340 
 
 INDEX OF SUBJECTS. 
 
 Teeth, Sliape of Crowns of, 27, 29. 
 
 Sockets of, 26. 
 Temperature, Sudden Changes in, Consti- 
 tutional Effects of, 215. 
 
 Effect of Lowering of, 211. 
 Tissue Degeneration in Internal Organs, 
 
 196. 
 Tobacco, Constitutional Effects of, 224. 
 
 Effect of, on Alveolar Process, 224. 
 
 Effect of, on Salivary Glands, 225. 
 
 Mental Effects of, 225. 
 Tooth: See also Teeth. 
 Tooth Brush, Best Kind to Use, 
 
 Destruction, Role of Friction 
 
 Teeth and Foreign Bodies in, 250. 
 
 Germs, Development of, in Mammals, 
 58. 
 
 Pulp, Death of, 196. 
 Toxins, Effect of, on Alveolar Process, 
 
 523. 
 Toxins Producing Trophic Changes, 223. 
 Transitory-Structures, 19, 24. 
 
 Arrested Development of, 113. 
 Trophic Changes Caused by Toxins, 223. 
 Trophoneuroses and Emotions, 271. 
 
 313- 
 of 
 
 Lips, 
 
 Tropics, Hygiene in, 213. 
 Tuberculosis and Interstitial Gingivitis, 
 236. 
 
 Effect of, on Alveolar Process, 207. 
 
 In Criminals, 205. 
 Ulceration, Location of, 289. 
 Uric-Acid and Interstitial Gingivitis, 87. 
 
 Crystals on Teeth, Inaccuracy of Dry 
 Distillation Test for, 92. 
 
 Laboratory Examination of Teeth for, 
 90. 
 
 Poisoning, 89. 
 
 Tests for, on Teeth, 90, 91. 
 Urinary-Acidity in Pregnancy, 244. 
 
 In Senility, 255. 
 
 In various diseases, 254. 
 Urine, Examination of, in Interstitial Gin- 
 givitis, 247 
 
 In Diabetic Patients, 251. 
 
 Inorganic Salts in, 77. 
 
 In Paretic Patients, 252. 
 
 In Tabetic Patients, 252. 
 
 Report of 394 Examinations, 247. 
 
 Toxins in, 201. 
 Wallerian Degeneration, 271. 
 
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