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Interstitial Gingivitis 
 
 SO-CALLED PYORRHiEA ALVEOLARIS 
 
 EUGENE S. TALBOT, M. D., D. D. S. 
 
 Professor of Dental and Oral Sdrgery, Northwestern University. Woman's Medical School 
 Honorary President of the Dental Section of the Tenth International Medical Congress, 
 Berlin, 1890; Honorary President of the Dental Section of the Twelfth International 
 Medical Congress, Moscow, 1897; Honorary Secretary of the Pan-American Medical 
 Congress, Washington, 1893; Member of the American Medical Assoclation; Fellow 
 OF the Chicago Academy of Medicine; Member of the Chicago Medical Society; 
 Secretary of the Section on Stomatology of the American Medical Asso- 
 ciation; Member of the Chicago Academy of Sciences; Honorary Member 
 OF THE Odontologischen Gesellschaft. Berlin, Germany; Membre 
 Honoraire de l'Association Generale des Dentistes de France; 
 Honorary Member Sociedad Odontologia Espanola; Author of 
 "The Irregularities of the Teeth and their Treatment" 
 Author of " Chart of Typical Forms of Constitutional 
 Irregularities of the Teeth"; Author of "The Eti- 
 ology OF Osseous Deformities of the Head, Face, 
 Jaws and Teeth"; Author of " Degeneracy, its 
 Causes, Signs and Results "; Etc., Etc. 
 
 WITH SEVENTV-THREE ILLUSTRATIONS. 
 
 PiriLADELPHIA : 
 
 AVIIITE DENTAL MA.NT FACT L'HING CO. 
 ISili). 
 
Entered According to Act of Congress, in the Year 1899, by 
 
 Eugene S. Talbot, 
 
 1 the Office of tbe Librarian of Congress at Washington, D. C. 
 
 T K 
 
ALL CO-WOEKERS IN DENTAL SCIENCE, 
 
 This Work, 
 
 As a Slight Tolcen of Appreciation of Their Contributions to Science, 
 
 is Respectfully Dedicated. 
 
PREFACE. 
 
 The great law of medical science, that to know the cause is 
 half the treatment, is as applicable to dentistry as to any other 
 specialty of medicine, and is as aj^plicable 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 ami its treatment, during the past tw(_) 
 decades, no new principle has been advanced whereby the jmrts 
 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 projjhylaxis and 
 treatment, so far as this disease is concerned, is a failure. 
 
 Other specialists restore jjatients to health. Nearly every 
 j)atient with this disease applies to dentists. Most dentists, how- 
 ever, hardly knoAV the disease exists and much less are capable 
 of offering suggestions as to treatment. It seems strange that in 
 America so little original woi'k has been done ujion a disease 
 more to be dreaded than tooth decay. Treatment has been 
 wholly at random, and hence, as a rule, only to limited extent 
 successful. Destruction of the alveolar process and loss of the 
 teeth is so rapidly sure that the necessity for dental scientists to 
 solve the etiology of this very common disease seems imperative. 
 
 Nearly two 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 during appar- 
 ently diverse and sej)arated studies, such as those related to dental 
 and maxillary irregularities and degeneracy, the necessity 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 instances where 
 possible personal elements of error are present, these have been 
 eliminated bv having researches made bv 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- 
 sor of Chemistry, Chicago College of Physicians and Surgeons ; 
 Dr. Vida A. Latham, Pathologist, Northwestern University, 
 Woman's Medical School; Dr. Maximilian Herzog, Pathologist, 
 Chicago Polyclinic Hospital ; Professor Theo. A. Edwin Klebs 
 and Dr. Robert F. Zeit, Pathologists, and Dr. W. L. Baum, 
 Professor of Diseases of the Skin, Post-Graduate Medical School, 
 Chicago ; Dr. G. V. I. Brown, Professor of Oral Surgery, Dental 
 Department, Milwaukee Medical College ; Dr. Frederick Noyes, 
 Histologist, Dental Department, Northwestern University ; Dr. 
 J. G. Kiernan, and to Blomgren Bros. & Co. for electrotyjoes, etc. 
 
 THE AUTHOR. 
 
 103 State Street, Chicago. 
 
CONTENTS. 
 
 I. History ......... 1 
 
 II. iNTRODUC'flON . . . . . . . ■ . 10 
 
 III. Tr.^nsitory Structures — 
 
 The Jaws 20 
 
 The Alveolar Process 21 
 Periosteum and Peridental Me.mbrane . . . 33 
 The Gums and Mucous Membrane ... 42 
 Do Glands Exist in Epithelial and Peridental Mem- 
 brane? ....... -47 
 
 Bone Building and Absorption .... 59 
 
 IV. Theories of Interstitial Gingivitis . . . .65 
 V. Uric Acid and Interstitial Gingivitis ... 68 
 
 VI. Inorganic Salts and Interstitial Gingivitis . . .73 
 
 VII. Heredity and Environment ..... 83 
 
 VIII. Degeneracy and Degenerate Tissues . . . .86 
 
 IX. Neurotic, Diathetic and Degenerate Children . . 89 
 
 X. Interstitial Gingivitis in Dogs . . . . .98 
 
 XL Mercurial Interstitial Gingivitis in Dogs . . 117 
 
 XII. Bacteriology of Interstitial Gingivitis . . .122 
 
 XIII. Scorbutic Interstitial Gingivitis in Man . . . 127 
 
 XIV. Interstitial Gingivitis in Man fro.m Metallic and Other 
 
 Drug Action ........ 142 
 
 XV. Conclusions . . . • . . . . . 146 
 
 Pathogenesis of Interstiti.vl Gingivitis . . .151 
 
 Endarteritis Obliterans . . . . .154 
 
 Absorption of the Alveolar Process . . . 157 
 
 Pyorrhoea Alveolaris from Interstitial Gingivitis . 162 
 Constitutional Effects op Pyorrhea Alveolaris . 167 
 Calcic Deposits . . . . . . .168 
 
 XVI. Treatment . . . . . . . . .172 
 
INTERSTITIAL GINGIVITIS. 
 
 CHAPTER I. 
 
 HISTORY. 
 
 Inflammation of the peridental membrane is probal)!}'' coeval 
 with man. Some of the skulls found earliest in the cave-dwell- 
 ing period exhibit evidences of its j)resence. In some of these, 
 careful observation has shown deposits encroaching npon the 
 roots of the teeth and resultant absorption 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 absorj)tion 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 ]3eriod — 
 those of the Accadians and EgyjDtians — 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 i^eoples. The Greeks, Syrians, Arab- 
 ians, Dravidians and Aryans of India and the early Burmese 
 all suffered from this disorder. In the museum at Constan- 
 tinojjle 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. 
 
 Inflammation of the peridental membranes, it will be evident, 
 is, therefore, not a modern disease ; not a disease confined either 
 to civilized or primitive races, but one which attacked man early 
 
I INTERSTITIAL GINGIVITIS. 
 
 in his evolution. Like most diseases it has been chiefly dis- 
 cussed and analyzed during the past two centuries. 
 
 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), Avhile 
 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 ojiinion 
 systemic disorders like gout, rheumatism, albuminuria, diabetes 
 and anaemia had an influence. 
 
 BonwilP during the same year exjjressed the oj^inion 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) sujDpurative inflammation of the 
 gums and absorption of the gums and alveolar process. 
 
 During the same year Scheff"^ 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, 
 
 ' 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. XXIY. 
 
 ' Wiener Med. Presse, Vol. XVI. 
 
very often obseuve. He doubted, liowever, the influence of 
 rheumatism. 
 
 In 1876 Sirletti'(in a discussion of the jmthology of the 
 disorder, which he called alveolo-dental periostitis) regarded it as 
 due to constitutional conditions, like rheumatism, scrofula, syph- 
 ilis, etc., with local causes as exciting factors. 
 
 In 1877 Rehwnikle," 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 habitual 
 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 exciting 
 cause. 
 
 In another paper during the same year G. A. Mills''' expressed 
 the ojiinion 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 constitutional 
 conditions were, as a rule, without influence, and that local irrita- 
 ting deposits w^ere the cause in twenty-five j^er 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 j^hosphatic diathesis had an 
 influence in the production of the disorder. 
 
 ' Gazzetta Medica di Roma, 1S76. 
 
 -Dental Cosmos, Vol. XIX. 
 
 ■' Ibid., Vol. XXI. 
 
 * Dental Cosmos, Vol. XXI. 
 
 5 Ibid., Vol. XXIII. 
 
 "Ibid., Vol. XXIV. 
 
4 IXTEESTITIAL GINGIVITIS. 
 
 In 1881 (when there seemed to have been many contributions 
 to the literature of the subject) Atkinson ^ exjjressed the opinion 
 that nervous debility 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 Cartwright 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 ^^ajjer, Archovy and Joseph Izklai, of 
 Buda Pesth, ascribed the disorder to minute organisms. Oakley 
 Coles thought that systemic states were the predisjDosing factors, 
 while minute organisms exerted an exciting influence. 
 
 In 1882, L. C. Ingersol ^ 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 was of microbic origin. 
 
 In 1885, A. O. IlaAvls'^ expressed the opinion that the causes 
 were environment with morbid factors, such as malaria, excessive 
 sodium, etc., chloride and mercury. 
 
 In 1886, Reese** expressed the oj^inion 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 opinion 
 that the disorder was of catarrhal origin. Later, in 1886, J. N. 
 Farrar ^ regarded the disorder as a combined result of systemic 
 tendencies and local irritants. There was a joeculiar condition of 
 the system associated with hypersecretion laden with increased 
 earthy deposits. 
 
 ' Dental Cosmos, Vol. XXIV. 
 
 - Transactions of the International Jledical Congress, 1881. 
 
 ■' Dental Cosmos, Vol. XXV. 
 
 * Ibid., Vol. XXVI. 
 
 ■- Ibid., Vol. XXVII. 
 
 ^Independent Practitioner, Vol. VI. 
 
 ' Dental Cosmos, Vol. XXI. 
 
 '* Independent Practitioner, Vol. VII. 
 
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 eases 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 i^eridental 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. 
 
 Of the status of this disease at the close of the year liScSJ, 
 the following analytic picture was drawn by W. X. Sudduth^ : 
 Pyorrhoea alveolaris is a term ajjplied to the secondary stages of 
 a disease that has its inception in a catarrhal stomatitis. Being 
 confined, as a rule, to the margin of the gums surrounding the 
 teeth, it might be called a "gingivitis," were it not for the gen- 
 eral catarrhal tendency shown by the entire mucous membrane 
 of the mouth and nasal passages. The intimate relation between 
 a general catarrhal idiosyncrasy and pyorrhea alveolaris is more 
 than mere coincidence. Its common occurrence in persons who 
 have irregular teeth has also been often noted by Dr. Budduth, 
 who considers that this fact has, besides the matter of uncleanli- 
 ness, a direct bearing upon its pathogeny. It is well known that 
 the irregularities of the teeth present an indication of a degener- 
 ative taint, and that jDcrsons in whom irregularities occur are 
 very prone to catarrhal affections of the resiiiratory organs, 
 including the nasal j)assage. Their skin is usually very suscep- 
 tible to inflammatory affections. Another feature is offensive 
 odor of the saliva of individuals who show this particular ten- 
 dency to catarrhal affections even in j)ersons who take most scru- 
 pulous care of the teeth. In the majority of cases, pyorrhoea is 
 a stomatitis in which the local and constitutional factors in tlie 
 production of the disease are largely dependent uj)ou hereditary 
 catarrhal dyscrasia for their ability to engraft themselves ujion 
 
 American System of ] •entistry. 
 • Dental Cosmos, Vol. XXVIII. 
 ' Sajous' Annual, 1888, Vol. Ill, page 305. 
 
6 INTERSTITIAL GINGIVITIS. 
 
 the tissues. This jjositiou 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 condi- 
 tions ; two were the result of direct irritation of misfitting partial 
 plates, and the remaining three were apparently caused by cal- 
 cific deposits. Patterson remarks that a close examination of the 
 history of the above quoted cases 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 rugge 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 inflammation of 
 other mucous surfaces — first dryness, followed by an increased 
 secretion of mucus. The parts are very sensitive to pressure ; 
 the patient complains pf an annoying, burning sensation. 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 turgid. They present a 
 condition of tumefaction that sometimes rapidly jjasses into 
 hyj^ertrophy ; at other times there is an indurated appearance 
 that may last for some time. Granulation tissue may be pro- 
 duced 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. Bullte are apt to form, which, by rupturing 
 in the process of mastication, give rise to intense smarting. The 
 tongue constantly seeks the surface if it be on the inner side. 
 
 The pathologic changes which take place are, according to 
 Newland Pedley, of England, " hyj)ertrophy of the muco-peri- 
 osteal fold around the teeth, accompanied by dilatation of capil- 
 lary loops, enlargement of the papillae and rapid proliferation of 
 ejiithelial cells. Later the gums become firm and contracted and 
 
display increase of fibrous tissue. The cliauges which go on in 
 the socket have not been as yet satisfactorily worked out. The 
 examination of the jaws of carnivora, apparently affected with 
 ^jyorrhcea alveolaris, leads to the suj)position that osteitis of the 
 alveolar process spreading toward the apex of the socket is pres- 
 ent. Later the 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-lirown tartar. Ultimately 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 exj^lained 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 disj)Osition to catarrhal 
 affections. The next greatest etiologic factor is symptomatic — 
 the local manifestation of a constitutional vice. The most com- 
 mon manifestation is that of syphilis and of its antidotes, mercury 
 and potassium iodide, both of which sometimes find expression in 
 a localized inflammation which may be the starting point for 
 jjyorrhosa 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 l3y 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 jjatients 
 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 with it in mollities 
 ossium and other wasting diseases. Magitot (who views the 
 
INTERSTITIAL GINGIYITIS. 
 
 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 
 Bright's disease and glycosuria, in which latter condition the 
 jjhenomenon 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 well-known fact that these are the very class of 
 people who when irritation is once set uja in their system, present 
 the most aggravated cases, by reason of their superfluous vitality. 
 He says he has occasionally met with cases where the local con- 
 dition was evidently aggravated by constitutional derangement 
 and cure was thereby retarded. The great majority of eases, 
 however, have shown no indication of constitutional predisj)0si- 
 tion, but have j)ointed unerringly to local irritation by means of 
 which the function of the mucous membrane had been destroyed." 
 
 Syphilis and other affections 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 
 attachment 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. 
 
 ' Mioro-Organisms of the Human Mouth. 
 -International Dental Journal, Vol. XIII. 
 'Ibid., Vol. XIV. 
 
HISTORY. 9 
 
 John Fitzgerald/ in 1899, claimed that " The prodnction of 
 pyorrhoea depends upon two factors, a j^redisposing cause and 
 •a local irritation. The predisposing cause may be tubercle, 
 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 obvious, 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 stutly 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. 
 
 ' Clinical Journal, March 1, 1899. 
 
CHAPTER II. 
 
 INTRODUCTION. 
 
 The attempt has been made in the 2>reseiit 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. 
 AVhile even erroneous titles may have their meaning so fixed by 
 usage that any danger from the error involved in the title may 
 be j)ractically 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 
 complete disuse. With a view of clearing up this question at 
 the outset by the use of a proper title, I have adopted as a desig- 
 nation 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 path- 
 ology, 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 medical lexicographers, the term is 
 ■emjiloyed in precisely the sense in which it is used in the present 
 Avork. The English surgeon and lexicographer Quain defines 
 interstitial as follows : " Interstitial (inter, between ; and sto, I 
 stand); relating to the interstices 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 connect- 
 ive tissue. In pathology the word is used in connection with 
 absorption when a part is gradually removed without any obvious 
 
INTRODUCTION. 11 
 
 breaking off, and also to indicate the imjjlication of the intersti- 
 tial tissues in morbid processes or their infiltration with morbid 
 l^roduets, as interstitial pneumonia, interstitial hepatitis." 
 
 The Encycloi^tedic Medical Dictionary of the American 
 Foster, states that interstitial has three significations : First, it is 
 applied to a condition disseminated through the substance of an 
 organ or part, and to an inflammation afiecting the connective 
 tissue of an organ ; second, it is also apj)lied to that form of ^ 
 growth which consists in the interposition of new elements 
 between old ones, instead of in addition to the surfaces ; third, it 
 is ajjplied to ijathologic processes occui^ying 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, Foster, 
 and the other lexicographers) to the condition erroneously called 
 jjyorrhoea 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 ex23ulsion of the tooth from its socket." Foster - 
 suggests the substitution of the term ulitis as more j)hilologically 
 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 two terms I have emialoyed convey a 
 fairly correct idea of the j^athologic process involved, and do 
 not imply erroneous views as to etiology, ^^athology, prognosis 
 and treatment. 
 
 The pathologic conception adopted in the present work anent 
 interstitial gingivitis is tlint the discirder is a local inflammatory 
 
 ' Odontalgie. 
 -Foster, op. cit. 
 
12 IXTEESTITIAL GINGIVITIS. 
 
 coiidition of the gums, tending to accelerate their normal ten- 
 dency to disappearance at certain periods of stress, or involution, 
 of which involution the changes jsroduced by old age are a tyjoe. 
 In this early senility of the gums, for such it may be termed, 
 two great types of causes play a part ; the exciting and the pre- 
 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 stronglj^ by Pierce, whose views have been of late so 
 advocated by Kirk.^ The uric acid hypothesis, once very domi- 
 nant in medicine, is now losing its force. The trend of medical 
 oj)inion is to consider it one of the danger signals of auto-intoxi- 
 cation which assumes prominence because of its tendency to 
 excite local irritation. It is but one of a number of local 
 expressions of constitutional defect. This view of the influence 
 of uric acid in etiology the present work will try to demonstrate. 
 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 investigations 
 must be conducted) that there is no specific germ which is capa- 
 ble of jDroducing the disease itself, and furthermore, that the 
 pyorrhoea stage of the disease is merely a complication due to 
 jjyogenic germ infection of the already diseased gums. The 
 views of Galijjpe as to a S23ecific organism will be shown to have 
 failed of sup]3ort 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 jJi'edisposing factor will be 
 shown in the j^resent work to be the nature of the structures 
 affected. This in pathology is called local predisjjosition. The 
 gums, etc., will be shown to be transitory structures in them- 
 selves predestined (as already stated) to certain changes at cer- 
 tain ages. By the influence 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 
 
 ' International Dental Journal, May, 1899. 
 
INTKODUCTIOJf. 13 
 
 been exerted constitutionally through the central nervous system, 
 their local effects being a secondary consequence of this. The 
 same will be shown to be the case with conditions like scurvy 
 (where the constitutional factor is most prominent), and with the 
 great neuroses (paretic dementia, locomotor ataxia, etc.). Here, 
 as in the toxic conditions, one great element considered is the 
 influence of the constitutional conditions upon the nerves gov- 
 erning local blood supply and tissue waste and repair. These 
 influences are significantly illustrated in the various processes 
 described later which tear down and build up. 
 
 The influence of morbid heredity as a direct factor will be 
 shown not to be great. The influence, however, of degeneracy 
 €xj)ressing itself along the lines of least resistance will appear 
 as an ominously important factor. Heredity here, as elsewhere, 
 is a Avarning 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 with great neuroses like paretic dementia 
 and locomotor ataxia, in which guiii 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 pro- 
 cesses, accompanied by diminution of the intensity of others. In 
 the study of this j^hase of the question, the latest researches of 
 dental jjathologists as well as original observation and exjieriment 
 have been employed. 
 
 Among the many questions which the present treatise is 
 believed to settle (so far as exjserimentation can) is the following : 
 The question of the influence and nature of its etiology. It is 
 shown that here, as elsewhere in l^iology, the etiology of morbid 
 conditions has many phases ; that in it exciting and predisjiosing 
 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 
 
14 INTERSTITIAL GINGIVITIS. 
 
 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 sj^ecific nature ; that in it the germ infection occurs 
 as a consequence of existing disease, and is not the cause of 
 the morbid condition, but one of its stages : Pyorrhoea. The 
 experiments made, as well as the pathologic and clinical data, 
 have been obtained from many observers, so that as many control 
 observations should be had as were necessary to eliminate per- 
 sonal elements of error inevitable upon original observation 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. 
 
 The pathologic material for the study of interstitial gingivitis 
 in man is obtained with such difficulty in the recent state as to 
 necessitate research upon animals. This disease was noticeably 
 present among the carnivora, casually inspected in American 
 and EuroiJean zoologic gardens. Cats and dogs were also known 
 to be liable to the disease. As the first step in investigation, two 
 practitioners of comparative medicine, with an extensive hospital 
 practice (Dr. Charles E. Sayre and Dr. Alsoj) E. Flower), were 
 consulted 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 disease. Nearly 
 every dog in the hospital under their care was so affected. These 
 dogs comprised all breeds, from spaniels and terriers to the New- 
 foundland, 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 fingers. 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. 
 
 It should be remembered that the jaw of the dog, like the jaw 
 
INTRODUCTION. 
 
 15 
 
 of man, is undergoing considerable variation. Like man, the 
 dog, having put himself 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 in the 
 
 Fjg. 1. 
 
 wild state and consequently there is less occasion, even for fight- 
 ing purposes, of his jaw's and teeth. 
 
 Independently of conditions of this type, many of the dogs 
 suffered from constitutional disorders. Eight had skin diseases 
 which in the dog are more likely to produce obvious consti- 
 tutional defects than in man. Some were old and blind. Borne 
 had been injured and were under treatment for wounds. Some 
 
16 INTEESTITIAL GIjVGIYITIS. 
 
 were suffering from rachitis, nervous diseases, and were over- 
 bred. Others were constipated or had germ tyj)es of diarrhoea. 
 One had kidney inflammation and bronchitis with high fever. 
 In short, these dogs, being house dogs, presented most of the 
 constitutional diseases to which man is liable. 
 
 The month of a Scotch terrier is shown in Fm, 1. The 
 
 molar and premolar had been removed with the fingers. The 
 cuspids and incisors are quite loose. There are large deposits 
 of tartar. The gum and alveolar process have been absorbed 
 nearly one-half the length of the roots of the teeth. In Fig. 2 
 is seen the mouth of a Boston terrier with the incisors and j^re- 
 molars removed. There is extensive pyorrhoea. There are 
 
rXTRODUC'TIOX. 
 
 17 
 
 •calcic deposits uj)Oii the cuspids and molars. There is recession 
 of the gums and alveolar process. In Fig. 3 is shown the mouth 
 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 deposits about the teeth. In Fig. 4 are shown 
 
 teeth covered with calcic deposit the entire length of the root. 
 These teeth were removed by the fingers from the mouths of tAvo 
 dogs, one of whom was later obtained for scientific study. This 
 was all the material to be obtained from the hospital, since the 
 dogs were pets Avho had been placed under treatment l)y their 
 •owners. 
 3 
 
18 INTERSTITIAL GINGIVITIS. 
 
 Througli 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. jSTinety-five jser cent 
 are mongrel curs leading a street life, hence neither luxu- 
 rious diet nor luxurious care can be charged with any disease 
 in them. They have, at least, plenty of outdoor exercise and 
 fresh air. Many, despite this reversion to the life of their wolf- 
 like ancestors, have skin diseases and are deaf and blind from 
 old age. The bodies were secured after death, at which time 
 examinations 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 
 
 Fici. 4. 
 
 j)ass into an air-tight box. Commpnicating with this box is a 
 stove in which suljihur 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 exam- 
 ined. Such cases as were of interest were placed on one side 
 and the jaws removed from the bodies. Inside of one-half hour 
 the S23ecimens were in a solution to be kejjt until desired for use. 
 Jaws (with interstitial gingivitis in all stages of jDrogress, from 
 simple inflammation of the gums 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 
 
INTRODUCTION. 19 
 
 these dogs at four years of age had the (hsease, eighty per cent at 
 from eight to ten years, ninety-five Y>er cent over twelve years of 
 age. Since I commenced my investigation (four 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- 
 eurialization were picked up in the streets. 
 
 Most of the dogs exhibited at the last three animal dog shows 
 held in Chicago were young, ranging from one to four years of 
 age. About twenty-five per cent would range four years to 
 eight. Three years ago, on a casual examination of their mouths, 
 interstitial gingivitis was found to be common. Occasionally 
 recession of the gums and pyorrhoea alveolaris occurred. During 
 the last two years, on more careful examination, twenty-five j)er 
 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 pyorrhoea alveolaris. In the study of 
 this disease^ therefore, dogs are excellent substitutes, since for 
 l^athologic research they can be obtained at an}"- stage of the 
 disease. 
 
CHAPTER III. 
 
 TRANSITORY STRUCTURES. 
 
 THE JAWS. 
 
 Because of man's advance in evolution and because of the 
 local degeneracies thereon 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 j^eridental membrane, being varial^le 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 jjrocesses with 
 plenty of blood supply and vitality to resist mastication ; teeth 
 short, with large bell crowns to give j^lenty of room between the 
 roots for considerable thickness of the alveolar jDrocess for the 
 nourishment of the jjeridental membrane and supj^ort and pro- 
 tection of the gum tissue — small narrow jaws occur with appa- 
 rently 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 by the following procedure : Drop a j^erpendicular line 
 from the supraorbital ridge, whereu2:)on it will l^e found that 
 the jaws of the jirimitive races protrude beyond the line, as is 
 the case with many j^eoples of Europe and Asia today. 
 
 Mummery, on examination of the skulls of two hundred 
 Britons and Roman soldiers in Hythe Church, Kent, Eng- 
 land, found the narrowest width 2.12 inches, the highest 2.62, 
 Avith an average of 2.50. The width of jaws of 402 British 
 soldiers today is : narrowest 1.88 ; widest 2.63, average 2.28. 
 
TRANSITORY SiTRUCTURES. 21 
 
 The highest Avidth was very rare, only eight measured 2.50. 
 The jaws of the mound-buihlers compared with the existing cliff- 
 dwellers show similar results, the average width is about 2.50 
 inches. Measurements of normal jaws of 855 Italians of Cen- 
 tral Italy were: narrowest 1.88, widest 2.G3, average 2.17. 
 Measurements of normal jaws of 4,935 Americans gave the fol- 
 lowing results : narrowest 1.75, Avidest (only one case) 2.56, aver- 
 age 2.13. While in the highest type of primitive man, the 
 width of the upper jaw from the outer surfaces of the first per- 
 manent molars near tl,ie margin of the gum was 2.50 inches in 
 diameter, the jaws of peop)le now^ living in the same locality are 
 from 0.25 to 0.33 of an inch smaller. The antero-j)Osterior 
 diameter has also shortened from one-half to five-eighths of an 
 inch. 
 
 Standing on the corner of Picadilly Circus and Regent 
 street, London, in the fall of 1897, I examined the faces of 
 10,000 passers-by and found that eighty-three per cent possessed 
 jaws inside of the perpendicular line. Of 3,000 English school 
 children under ten years of age ninety-three per cent possessed 
 jaws inside of the perpendicular line, thus showing a difference 
 of ten per cent in one generation. 
 
 The negroes were formerly, in the 02)inion of anthro2:)ologists,, 
 in the main a long-headed dolichocephalic race with protruding- 
 jaws. Of the Northern negroes, who in the main have white 
 blood, very few have long heads. The same is true of the rela- 
 tions of the jaAvs. The protrusion of the jaws has largely dis- 
 appeared. 
 
 That the jaw is becoming smaller is further shown by the 
 disappearance of the third molar, or the irregularities resultant 
 on its eruption because of want of room, or its erujation with 
 pain for like reason. In the primitive races it is large and 
 well developed. 
 
 THE ALVEOLAR PROCESS. 
 
 The alveolar j)rocesses are sititated upon the superior border 
 of the inferior maxilla and ujDon the inferior border of the 
 superior inaxilla. These bones, considered a part of the maxillary 
 bones often so described by anatomists, should, however, be con- 
 sidered as practically distinct bones — their structure, functions- 
 
22 INTERSTITIAL GINGIVITIS. 
 
 and embryology differ so completely from the structure and 
 functions of the maxillary bones. The superior and inferior 
 maxillae are (unlike the alveolar processes) composed of hard, 
 compact bone structure. The large, powerful muscles attached 
 to them indicate that powerful woi'k is to be accomplished. 
 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 intra- 
 uterine life, calcification of the deciduous teeth commences, and 
 by the twentieth week calcific material is abundantly deposited. 
 Ossification is also rapidly j)rogressing 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 develop- 
 ment. 
 
 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 jDOsition in the jaw. 
 While the alveolar jDrocesses have grown rapidly, they have up 
 to this time developed only sufficiently to cover and protect the 
 follicles while calcification jjroceeds. When the crowns have 
 become calcified and the roots have begun to take in their calcific 
 material, absorption of the borders of the jiroeesses takes j)lace in 
 the order of the eruj)tion of the teeth. When the teeth have 
 erupted, the alveolar j^rocess develops 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 l^ones in 
 the anterior part of the mouth at least, and the upper and lower 
 teeth rest at a point in harmony 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 de2Dends 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 l)order irregular. The crypts of 
 the permanent teeth are located at the apices of the roots of the 
 temporary teeth. The permanent teeth have large crowns which 
 touch each other, forming a line to the jwsterior jjart of the jaw. 
 
TRANSITORY STRUCTUEES. 23 
 
 These teeth, as they erupt, entirely absorb the alveolar j^i'ocess 
 which surrounded the temporary teeth, and as the new set comes 
 into place a new j^i'ocess is Ijuilt up around them for their sup- 
 port. The permanent teeth require a deeper alveolar process to 
 sujjjjort their roots, which are much longer than those of the 
 temporary 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 opposite side. 
 It is harrow in front, and gradually enlarges until it reaches the 
 tuberosity, where it becomes rounded. 
 
 The process is composed of two j^lates of bones, an outer and 
 an inner, Avhich are united at intervals by sej)ta of cancellous 
 tissue. These forni the alveoli for the reception of the roots of 
 the teeth. In some cases the buccal and labial surfaces of the 
 roots of healthy teeth extend nearly or quite through the outer 
 bony plate and are covered by the peridental and mucous mem- 
 branes only. 
 
 This plate is continuous with the facial and zygomatic surfaces 
 of the maxillary bone. The inner plate is thicker and stronger 
 than the outer, and is fortified by the palate bones. The external 
 jilate is irregular upon the outer surface, prominent 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 dental 
 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 nourishment. 
 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 suscej^tible 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. 
 
 The sockets for the incisors and cuspids are conical and nuicli 
 larger than any of the other single sockets. The alveolar pro- 
 cess is longer and thinner than at any of the other teeth. The 
 3 
 
24 INTERSTITIAL GIXGIVITIS. 
 
 sockets for the bicusj^ids are flattened upon their anterior and 
 posterior surfaces, and near the apices tliey are frequently bifur- 
 cated. The sockets of the molars are large at the openings. 
 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 nourishment is 
 requ^ired. 
 
 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 widely 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 well- 
 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 sujiport 
 the tissues. 
 
 The sockets are lined with a thin j^late of compact, bony sub- 
 stance, 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 nourishment of 
 the teeth. 
 
 The bony plate has upon its inner surface the elastic periden- 
 tal membrane, which acts as a cushion for the teeth, while it is 
 surrounded by a spongy bone. 
 
 The teeth are held firmly in their alveolar sockets by the peri- 
 dental 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 
 
TEANSITORY STEUCTUEES. 
 
 25 
 
 root and those bent or irregular, receive support from all sides 
 by reason of their irregularity. Fig. 5 (a section of the jaw of a 
 cat) illustrates the relative position of the teeth, peridental mem- 
 brane and alveolar process to each other. 
 
 After the removal of the permanent teeth the alveolar process 
 is entirely absorbed. Fig. 6 shows how the absorption takes 
 place. The teeth have all been removed from the superior max- 
 illa and the alveolar process has been entirely absorbed. The 
 
 Fig. 5. — Ground Section of Jaw and Teeth of Cat. (Andkews.) 
 
 molars on the lower jaw having been extracted, absorption of 
 the alveolar jDrocess 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 protect the 
 teeth in their crypts during development and after eruption. 
 After the temporary teeth are in place the alveolar process 
 remains unchanged (except l\y gradual enlargement in harmony 
 with the growth of the maxillary bones) until about the sixth 
 year, when the second set ap]Dears. The crowns of the perma- 
 
26 
 
 INTERSTITIAL GINGIVITIS. 
 
 nent teeth require more space than those of the temj^orary set ; 
 and the alveolar process must necessarily enlarge to accom- 
 modate them. This enlargement of the alveolar process is 
 caused chiefly by foi'mation of the crowns of the permanent 
 teeth before eruption, and to a limited extent only by growth of 
 
 the maxillary bones. These may cease develoj^ment at any 
 period of the life of the individual, or continue as late as the 
 thirty-sixth year. As diameter of the crowns of tlie permanent 
 teeth form a larger circle than that of the maxillary bones, the 
 
 alveolar process must necessarily increase its diameter and pre- 
 sent large spaces between the roots of the teeth for the devel- 
 oj)ment 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 
 
TRANSITORY STRUCTITRES. 27 
 
 sliould not eruj^t, or if it should be extracted early, the process 
 would not be developed at that point. In my collection of 
 models 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 were 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 vas- 
 cularity of the process may be such that hypertrophy results. 
 Excessive development of the alveolar process is frequently 
 observed by every practitioner in connection with the anterior 
 inferior teeth. When the articulation is normal, occlusion 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. 7. This model is taken from the jaw 
 of a jDerson thirty-seven years of age, but this excessive develop- 
 ment 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 case under observation the incisors and cuspids,, 
 together with their alveolar process, are situated upon the 
 external surface, while the biscupids, molars and their alveolar 
 process are located upon the inner border of the jaw. In 
 another case, the alveolar process failed to cover the roots of the 
 biscuspids and molars upon the outer surface, the teeth having 
 forced themselves into a larger circle through the alveolar process 
 by the contact of the crowns. The roots in this case can easily 
 be outlined by the finger through the mucous membrane, the 
 outer plate of the alveolar process barely, if at all, covering them. 
 Tomes ^ illustrates a case of faulty development of the outer 
 plate of the alveolar process, exposing the crown of the tem- 
 porary teeth. This occurred in a hydrocephalic. I have a 
 number of models showing the anterior alveolar process project- 
 ing beyond the normal position through the forward movement 
 
 ' Dental Surgei')', page 44. 
 
28 INTERSTITIAL GINGIVITIS. 
 
 of the molars. This may be due to a natural 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 simjjly by the force consequent upon absorp- 
 tion and deposition of bone. This is noticeable in the sjDaces 
 between the centrals, when the alveolar 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 j)roducing a full, round arch uj)on one side of the 
 jaws, and a perfectly flat or straight arch upon the other. Occa- 
 sionally both u^Jj^er and lower alveolar processes are carried for- 
 ward 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 ujjper 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 
 subsequent change. Owing to this the teeth of the su^Jerior 
 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 j^rocesses to be carried in, while the anterior teeth of the 
 lower jaw are held inside of the superior anterior teeth, thus car- 
 rying 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 j)rocess, but they should also antag- 
 onize properly. The teeth may be compared to the bricks in an 
 arch. Remove a brick and the arch falls to pieces. It is fre- 
 quently 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 absorj^tion and depo- 
 sition of bone, demonstrating the fact that the process changes in 
 .shape and substance. Ziegier' says absence of functional use is 
 a frequent cause of j^remature lacunar absorption of the bone. 
 
 ' A Text-Book of Special Pathological Anatomj', page 145. 
 
TRANSITORY STRUCTURES. 
 
 29 
 
 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 sup- 
 port, 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 body, however, the 
 absorption of the alveolus progresses to a greater extent because 
 of the unstable condition of the structures. 
 
 From what has already been said of the vascularity of the 
 alveolar process, it is evident that hypertrophy of tlie tissue may 
 
 V^,.^^J|;'i'^'i -i^iiA'Msm 
 
 Fig. 8. 
 
 ensue from an unbalanced nervous system and from simple irri- 
 tation of varying degree. The irritation consequent upon the 
 eruption of the teeth, together with the excessive blood supply, 
 are both primal causes of overbuilding of tissue, i. e., hyperplasia. 
 
 The ragged roots of the temporary teeth, produced by absorp- 
 tion of the gases from the putrescent pulps, and the pressure of 
 the permanent crowns against the tissues, produce sufficient 
 stimulation to excite physiological action. Tissue-building gener- 
 ally 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 hypertroijhy of the process result. 
 
 In cases of hypertrophy of the alveolar process, enlargement 
 is associated with the inner plate of the alveolar process. In 
 cases coming under my ol)servation the inner plate in most is the 
 
30 
 
 ESfTERSTITIAL GINGIVITIS. 
 
 part of the alveolar process affected (Fig. 8 case). The outer 
 plate, although quite irregular from the arrangement of the teeth, 
 is usually normal in thickness. This disparity 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 i^osterior 
 or descending palatine arteries furnishing the ossific material. I 
 have observed but few cases where hypertrophy has extended to 
 and included the outer plate. When the outer plate becomes 
 involved the alveolar process assumes a very thick condition. 
 Occasionally hyjjertrophy will affect one side only or one distinct 
 
 Fig. 9. 
 
 locality (Fig. 9). In this case 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 develop- 
 ment 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. 
 
 Under the microscope, two systems of Haversian canals are 
 seen in the alveolar process. Kolliker' describes these as follows : 
 
 "The Haversian canals are of two kinds. One with the 
 regular lamellae system surrounding it, and the other, the so-called 
 
 ' Handbuch der Gewebelehre, page 272. 
 
TRANSITORY STRUCTURES. 81 
 
 Volkmann's cauals, containing the perforating vessels from Von 
 Ebner, which have no surrounding h^nlell3e, but simply penetrate 
 through the layers of bone. Volkmann's canals are present in 
 all tubular bones in old and young. While especially 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. 10). 
 They run partly transversely or obliquely, and also partly longi- 
 tudinally, through the lamellae. jNIany of these canals open in 
 
 iViTA^C''/ 
 
 
 ■h^ 
 
 
 rKXF'BSt^ '"^ 
 
 r^ 
 
 Fig. 10. — Section of Bone Showing Blood Vessels of Von Ebner. 
 
 the outer or inner surfaces of the substantia (compact substance), 
 and also here and there in the Haversian canals, and form alto- 
 gether usually a, wide-meshed irregular network. In their struc- 
 ture 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 structures without any lumen, or like 
 those far from rare obliterated true Haversian canals first 
 described by Tomes and de Morgan. The contents of the 
 Volkmann canals are the same as the Haversian canals." 
 
 Fig. 10 is a cross section of the medulla of a calcified human 
 
32 
 
 INTERSTITIAL GINGIVITIS. 
 
 liumeiTis slightly eularged. The outer lamellse contams a large 
 number of Volkmann's canals running longitudinally and trans- 
 versely and extending through the outer jjlate of bone into the 
 periosteum. Fig. 11, the cross section of the section seen in 
 JFig. 10, shows these canals more highly magnified. The Haver- 
 ,sian canals are large round spaces (Fig. 12), containing a single 
 artery and vein. The fine hair-like spaces running from these 
 large spaces are the canaliculi. The dark sj^ots circulating each 
 Haversian canal are the lacunte. The canaliculi 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 lamellae. The lacunae seem to be about uniformly 
 
 -Section of Bone (Hichee Macmficvtion) Sh 
 Von Ebner. 
 
 ivG Blood Vessels of 
 
 •distributed throughout the bone. The spaces between the 
 lacunae and canaliculi are filled with lime salts. 
 
 A longitudinal section of bone (Fig. 13) 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 with each other at certain intervals. The 
 
TRANSITOKY STEUCTITEES. 
 
 33 
 
 foregoing deseriptiou, with illustrations from Kolliker, is essen- 
 tially that of the minute anatomy of the alveolar j^roeess. 
 
 THE PERIOSTEUM AND PERIDENTAL MEMBRANE. 
 
 The periosteum is a fibrous tissue covering the outer surface 
 of the alveolus. The peridental membrane is composed of 
 similar structures covering the roots of the teeth and lining 
 
 
 Fig. 12. — Transverse Section of the Diaphysis of the Htmercs Magnified 350 
 
 Times. 
 a, Haversian Canal. Dark spaces, Lacunar. Hair-like spaces, Canaliculi. 
 
 the inner wall of the alveolus. They are both derived from 
 the mesoblastic layer. For this reason there can be very little 
 difference 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, white 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 
 ]ieridental membrane. The coarser fibers run parallel with the 
 
34 IXTEESTITIAL GINGIVITIS. 
 
 alveolar process (J) over the border and extend as far as the- 
 union of the ej^ithelial 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. 
 
 The fibers of the periosteum, therefore, are continued 
 throughout the process from the periosteum on the one side 
 
 
 Fig. 13. — Longitudinal Section of Bone Magnified 100 Times. 
 a, Haversian Canals, h, Lacuna seen from the side, c, Canaliculi. 
 
 to the jDeridental membrane on the other. This is also illus- 
 trated in the mouths of persons, where (after wearing artificial 
 dentures for a short time) heat produces absori^tion 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 process- 
 at the Haversian canals. The plexus of blood vessels is much 
 
 ' American System of Dentistry, page 663. 
 
Fig. 14 — Longitudinal Section of Tooth, Alveolar PfiOfEss, Peridental Memhrane and 
 Periosteum. Nokmal Tissue. Sheep. 
 B, Dentine. C, Cementum. E, Epithelial Tissue. G, Submucons 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 7a. A. A. obj. Zeiss. Micro-photographs, reduced one-third. 
 
 Fig. 15. — Ceoss Section of Tooth, Alveolae Peocess, Peridental Membrane and 
 Periosteum. Normal Tis.sde. Dog. 
 
 B, Dentine. C, Cementum. D, Pulp. H, Periosteum. J, Alveolar Process^ 
 K, Capillaries. M, Fibrous Tissue. U, Nerve Tissue. C T, Connective Tissue. 
 
TRANSITORY STRUCTURES. 37 
 
 larger projiortionately in connection with the alveolar process 
 than with other bones of the body, owing to its transitory 
 nature. 
 
 The peridental membrane 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 s^^ace 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 temjDorary teeth are shed,. 
 is restored with the eru23tion of the second set, and when the per- 
 manent teeth are extracted it disappears with the alveolar 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 comj)rises nearly all 
 or quite all of that portion of the jaw which eventually 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 j)aper. 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 crosswise ^penetrating the cementum, on the one 
 hand, and the alveolar process on the other. In a general way, 
 since the fibers extend through the alveolar wall, they are more 
 closely adherent to the bone than to the cementum, 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 regularly 
 into a board (the "fibers of Sharpey " Fig. 14), but vary as to 
 quantity in different localities. In some localities they jjenetrate 
 in large quantities and almost surround a piece of alveolar pro- 
 cess, while a few fibers penetrate but a short distance. In some 
 
 ' Anatomy. 
 
 - American System of Dentisti-y, page 668. 
 
38 INTERSTITIAL GIN^GIYITIS. 
 
 places, they caii 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 Avliich jaass 
 into the alveolar process are numerous blood vessels. Others run 
 diagonally, and still others lengthwise, all making up a tissue 
 which holds the tooth in position in the jaw. The fibers enter 
 the peridental membrane at all j^oints of the process, from its 
 margin to the apex of the roots. The elasticity of this membrane 
 is so great that in correcting irregularities 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 mem- 
 brane 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 jjro- 
 cess occurs, the fibrous tissue retains the shape of the process. 
 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 peridental mem- 
 brane or fibrous tissue. 
 
 Two kinds of structures are present in the alveolar j^rocess — 
 a dense, compact, hard structure (comjjosed of lime salts), 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 j)ro- 
 cess (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 sup^jly of the peridental membrane is situated in the 
 
X 75. A. A. obj. Zeiss. Micro-pliotographs. reduced one-third. 
 
 Fig. 16. — Cross Sehiin of Tooth, Alveolar Process and Peridental Memdi!ane. 
 Injected Blood Vessels. Normal. Dog. 
 
 B, Dentine. C, Cfmentum. I, Peridental Membrane. J, Alveolar Process. K, Capillaries. 
 L, Haversian Canals. 
 
X To. A. A. 011.1. Zeiss. .Micro-photoifrapUs. reduced one-third. 
 
 Fig. 17.— Cboss Section of Tooth, Alveol.\k Process and Pehidextal Membrane. 
 Injected Blood Vessels. Normal. Dog. 
 
 B, Dentine. C, Cementum. I, Peridental Membrane. J, Alveolar Process. K, Capillaries. 
 L, Haversian Canals. 
 
TRANSITORY STRUCTURES. 41 
 
 center of the structure. This has not been my experience. 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 largest amount 
 is requii-ed to supply the alveolar process. The system 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 vessels 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 with the fibrous 
 tissue through the Haversian canals and these in turn permeate 
 the entire bone. As age advances, however, the bone Ijecomes 
 more dense, and the Haversian canals become smaller and (under 
 certain conditions) cease to exist. When disease takes place, 
 either at the gingivus or at the apex of the root, the supply of 
 blood being thus cut off", the tissues receive sufficient nourishment 
 through the alveolar wall. Since the structures are in a transi- 
 tory state, being destroyed an(^ rejjaired so frequently, it is evi- 
 dent 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 bicuspids.'" 
 
 ' Periosteum and Peridental Membrane, Pase 94. 
 
42 INTEESTITIAL GINGIVITIS. 
 
 When irritation and inflammation take j)lace in the peridental 
 membrane, the cementoblasts build up cement substance, just as 
 the osteoblasts do in the alveolar process and the odontoblasts do 
 in the pulp chamber. tSometimes they are attached to the root 
 of the tooth, Avhich produces what is called exostosis or cenien- 
 tosis. They may remain unattached, floating in the fibrous tissue. 
 These are very common in connection with interstitial gingivitis. 
 
 GUMS AND MUCOUS MEMBRANE. 
 
 The tooth, according to Minot,' is a j^apilla which projects 
 into the epidermis, and ossifying in a particular way, changes into 
 ivory around the soft core or pulp. To the laajnlla the epidermis 
 adds a layer of enamel. The tooth proper unites with a small 
 Y>\ate 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 primitively organs of 
 the skin and widely developed over the surfaces of the body. As 
 the mucous membrane is practicall}^ a continuation of the skin, it, 
 in accordance with the law of individuation, 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, leav- 
 ing a free space between the membrane and the teeth through its 
 entire length. 
 
 It consists of two layers (Fig. 18), the epithelium (A) and 
 corium (B), sej^arated by the basement membrane (C). The 
 epithelium is composed of the epithelial cells : First, one row of 
 columnar cells (B) 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 squamous 
 cells (G) ; and fifth, four or five rows of flattened dead cells (H), 
 which were originally the columnar cells upon the basement 
 membrane. The young new cells are the columnar cells which 
 jaass from one stage to another, changing their shapes until they 
 
 ' Embryology, page 481. 
 
TRANSITORY STRUCTURES. 
 
 4a 
 
 eventually become dead cells and are exfoliated from the surface 
 of the tissue. The basement membrane (C) is made up of fillers 
 running longitudinally, from papillae, which allow the tunica 
 propria containing blood vessels and nerves to pass up into the 
 epithelium structure. 
 
 The corium (B) (which lies below the basement membi-ane) 
 is composed of alveolar connective tissue, white yellow fibrous 
 connective tissue, muscular fibers, nerves, blood vessels and 
 lymphatics. It is made up of the tunica propria and the 
 submncosa. 
 
 Fig. is. — Diagrammatic Illustkatio.v of the Epithelium and Submucous Laykus ok tiik 
 Mucous Membrane. 
 
 A, Epithelium. B, Coriuni. C, Basement Membrane. D, Columna Cells. E, Prickle 
 Cells. F, Six-sided Cells. G, Squamous Cells. PI, Flattened Dead Cells. 
 
 . The tunica jDropria (beautifully shown in Fig. 19) consists 
 of interlacing connecting fibers interspersed with much elastic 
 fibrous tissue. This tissue penetrates the epithelial layer in the 
 
44 INTERSTITIAL GINGIVITIS. 
 
 form of cone-sliaped papillfe, varying in length with the thick- 
 ness of the epithelium. This layer being the thickest at the 
 gum margin (E), these j^apillse 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 j^erios- 
 teum and peridental membrane (M), so that it is difficult to 
 determine the mucous capacity line of demarcation separating the 
 different structures. The submucosa is composed of fibrous 
 connective tissue of a much less compact variety. This structure 
 is attached to the bones through the j)eriosteum and peridental 
 membrane. In this structure the glands, Ijlood 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 infiammation commences in 
 interstitial gingivitis. Numerous veins accom2)any 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 j^apilla in connection with the capillaries. 
 The terminal nerve fibers come in contact with the muscular 
 fibers, so that there is direct communication by blood vessel and 
 nerve throughout the mucous membrane from the nose, stomach 
 and lungs. The gum tissue is very thick and made wp of fibrous 
 tissue running in three or four directions, rendering it dense, 
 tough and hard. The membrane 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 verti- 
 cally, those which radiate and are fan-shaped, and those which 
 are horizontal. 
 
 The mucous membrane, like the alveolar process and peri- 
 dental membrane, is comjDOsed of very unstable tissue. It 
 changes its structure, blood vessels and nerve system as often 
 
X 75. A. A. obj. Zeiss. Mici'O-pliotographs, reduced one-third. 
 
 Fig. 19. — Longitudinal Section of Tooth and Gum Tissue. Dog. 
 
 D, Dentine. E, Epithelial Tissue. G, Submucous Membrane. K, Capillaries. M, Fibrous 
 Tis.'ue. V, Violent Inflammation. AA, Point of Union of Epithelial Tissue and Peridental 
 Membrane. RR, Space Pocket from '\^'a^t of Union of the Epithelial Fold. 
 
46 INTERSTITIAL GINGIVITIS. 
 
 as the other structures. Its blood vessels and nerve system are 
 continually renewing connective tissue, periosteum and jaeridental 
 membrane. 
 
 A difference is noticed in the structui'e of the papillary layer 
 in man and the lower animals, such as the dog, the sheej) 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 
 paj^illfe are narrow, long and more closely set together. Blood 
 vessels and nerves are not so numerous and close together in man 
 as in animals. 
 
 DO GLANDS EXIST IN THE MUCOUS AND PERIDENTAL 
 MEMBRANES ? 
 
 A somewhat widespread ojiinion locates sj)ecial 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 knowl- 
 edge as to the etiology of interstitial gingivitis, and in part to the 
 fact that certain constitutional conditions, such as mercurial and 
 potassium iodide 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 example : " That part 
 of the gingival margin that lies in against the neck of the tooth 
 is of a different structure from its other parts. Here it is clothed 
 with a very soft, round or polygonal gland-like epithelium that 
 suggests the formation of a giand, 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 Avhich are always found 
 in the saliva (Salter) and are usually called mucous-corj)uscles. 
 It is well known that certain glands have the power of the selec- 
 tion and excretion of certain j^oisons, and in this way of elimi- 
 nating them from the system, and that if the substance be in 
 large amount, hyjDersemia, or even inflammation, may result. It 
 is also known that mercury and potassium iodide will produce 
 inflammation of the free margins of the gums, and Salter has 
 found that these cells are in greater abundance under these cir- 
 cumstances ; also that the cells taken from the o-ingival border 
 
 ' American System of Dentistry, pages 955-956. 
 
X 75. A. A. obj. Zeiss. Micro-photographs, reduced one-third. 
 
 Fig. 20. — Longitudinal Section of Gum. Nor.m.il Tissue. Sheep. 
 
 C, Cementum. E, Epithelial Tissue. G, Submucous Membrane. K, Capillaries. 
 M, Fibrous Tissue. A A, Point of Union of Epithelial Tissue and Peridental Membrane. 
 Nm, Naysmith's Membrane. Sg, So-called Glands of Serres. 
 
48 IJiTTEESTITIAL GINGIVITIS. 
 
 and submitted to chemical tests after the person has taken potas- 
 sium iodide, 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 with the peri- 
 dental membrane at the neck of the tooth. Black' (in an 
 article beautifully illustrated by Frederick Noyes) seems to 
 identify these with the so-called glands of Serres, or gingival 
 glands (Fig. 20). He speaks of them as glands in various 
 places throughout the article ; for example, " But little can now 
 be said of the function of the network of glands of the periden- 
 tal membrane, beyond what is indicated by their form, location 
 and histological characters. With the knowledge of their posi- 
 tion and general character, clinical observation leads to the con- 
 clusion that they are readily disturbed by certain drugs, notably 
 by mercury and iodin ; and that they are often disturbed by 
 .substances poisonous 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 very certain that the 
 disease which I have described as phagedenic pericementitis has 
 its seat in these glands." Black, however, does not seem quite 
 certain of the validity of his position, since he further remarks, 
 ""Though definitely lobulated, this l3ody does not seem to possess 
 the characters of a gland, and I should not sup2')0se 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 ajipear at all." 
 
 In many slides of sections from canine jaws and human,- the 
 same jDCculiar arrangement of structure was observed, although 
 not in so marked a degree. In the immature herbivora (calf and 
 
 ^ Dental Cosmos, February, 1S99. 
 
 - The material obtained for rnaking slides from man, other tlian the scurvy cases, 
 ■fl'as 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. 
 
^t^XS^Tv 
 
 w;- 
 
 
 .V 
 
 «;^ 
 
 w 
 
 D. 
 
 \ 
 
 X 75. A. A. obj. Zeiss. Micro-photographs, reduced one-third. 
 
 iFiG. 21.— Ceo.¥s Section- of Tooth and Peridental Membrane. Norm.\l Tissue. Sheei'. 
 
 C, Cementurn. D, Dentine. I, Peridental Membrane. TV, Epithelial Debris. 
 
X 300. No. 2 projection ocular. D. D. obj. Zeiss. Micro-photographs, reduced one-third. 
 
 Fig. 22. — Cross Section of Tooth and Peridental Membkane. Noemal Tissue. Siiebp.- 
 
 C, Cementum. D, Dentine. I, Peridental Membrane. W, Epithelial Debris. 
 
TRANSITOEY STRUCTURES. 51 
 
 lamb) these jieculiar 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 
 scurvv, and exhibit marked inflammation with liroken-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 cur^-e 
 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 
 2)0cket is closed up (Figs. 48, 44, 51). Again it remains open 
 (Figs. 19, 32, 50, 53). Frequently this peculiar type of 
 structure is absent, showing that the fold of gum tissue either 
 has been absorbed in 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 invariably starts on the lingual or palatine and 
 labial surfaces where this structure does not appear. In the 
 slides of the scurvy case there does not aj^pear the slightest 
 evidence of anything resembling glandular structure. Hence 
 it would seem safe to conclude that the glandular structure does 
 not occur in this locality. It is by no means impossible that in 
 the peculiar epithelium in this locality, epithelial cells undergo 
 changes which to some observers simulate glandular structure, 
 but on histologic analysis are distinguishable trom it, resemliling 
 in this the crypts of the head of the penis. 
 
 In cross sections of the peridental membrane, with a low 
 2)ower may be seen dark bodies arranged along the margin of the 
 cementum in the peridental membrane (Fig. 21). They are 
 more numerous, however, near the o-inoiyal liorder than at the 
 
52 
 
 IN^TEESTITIAL GINGIVITIS. 
 
 root extremity. These bodies are more numerous and better 
 defined in the sheep than in the calf, and more ajiparent in the 
 canine jaw than in the human. Under higher power (Fig. 22) 
 they may be distinctly demarcated as epithelial cells arranged 
 
 
 ** 
 
 ' -Sfc^ 
 
 ' ^':' 
 
 «*; ■; 
 
 ss» \ 
 
 ik 
 
 «^ 
 
 i 
 
 j 
 
 -■•"t 
 
 IBI^ 
 
 X 560. No. 2 projector ocular. One-twelfth obj. Zeiss. 
 
 Fig. 23. — Ceoss Section of Tooth and Peridental Membrane. Normal Tissue. 
 
 Sheep. 
 
 C, Cementum. D, Dentine. I, Peridental Membrane. W, Epithelial Debris. 
 
 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. 23) it will be seen that these masses of cells are 
 polygonous, never prismatic. They hence are similar in shape 
 
TRAXSITORY STRUCTURES. 53- 
 
 to the epithelial cells situated above the columnar cells. 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 (p.m non. of a gland that there should 
 be an oj)ening 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 
 characteristics of glands. They do not have (as Robin and 
 IMagitot remark) a columnar or prismatic cell wall. It is not 
 difficult to understand how epithelial cells are scattered in dif- 
 ferent shapes and sizes throughout the peridental membrane. 
 Epithelial cells have the property of multiplying and develop- 
 ing 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 grows into the der- 
 mis and then the dermal tooth papilla is develoj)ed. The first 
 indication of the develo23ment of tooth germs in mammals 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 ejDithelium. 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 
 
 ' Dental Cosmos, February, 1899, pages 112-118. 
 -Dental Follicle, page 116. 
 ' Embryology, pages 581-90. 
 
54 INTERSTITIAL GINGIVITIS. 
 
 side, so that the second set of germs is develoj^ed for tlie perma- 
 nent teeth. The end of the shelf, toward the articulation of the 
 jaws, is prolonged without retaining the direct connection with 
 the ej^ithelium and from this jji'olongation arise the enamel 
 organs for the three permanent molars. Wherever a tooth-germ 
 arises the dental shelf is locally enlarged, and the local enlarge- 
 ment 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 sej^arate fragments ' which may persist throughout 
 life and lead to various pathological structures. While the per- 
 manent 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 forma- 
 tion, the fully developed enamel organs have several bands or 
 threads by which they are connected with the dental shelf jirojier. 
 
 After the shelf has developed somewhat, its line of connection 
 wdth the ejjithelium of the gum becomes marked by a superficial 
 groove, as may be seen in the human embryo of eight to ten 
 weeks. This groove was formerly supjjosed 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, while 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 lower ends, but remain each connected by a nar- 
 row neck with the oveidying ei^idermis. The expanded end is 
 the enamel germ proper ; it very soon assumes a triangular out- 
 line, as seen in sections, owing to the flattening of its under side, 
 and at the same time it moves somewhat toward the lips. Mean- 
 while the shelf continues growing on the lingual side of each 
 ingrowth to j^roduce 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 
 
 ' Including the epithelial debris of Robin and Magitot. 
 
TRANSITORY STRUCTURES. 55 
 
 form the outline of the dental papilla, and is beginning to develop 
 fibrilla? 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 prol^ably 
 determined by the growth of the enamel organ. 
 
 The follicle is merely an enveloj^e 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 fibrillte 
 are less numerous than in the former. A rich network of capil- 
 lary vessels is developed in the follicle and apj^ears in part as a 
 series of villous-like growth into the enamel organ. The follicle 
 develops first over the lower part of the papilla, then over the 
 enamel organ, the neck of which aborts and the follicle closes 
 over, comj)letely separating the enamel organ from its parent 
 epidermis. The enamel organ changes greatly in ajjj^earance. 
 The layer of cylinder cells is well preserved over the concave 
 surface, but only where the epithelium is in contact with the den- 
 tal papilla. In the neck the cells become irregular in form. 
 Over the convex surface the cells become lower and cul)oidal. 
 They ultimately atrophy and flatten out. The cells in the center 
 of the enamel organs undergo a peculiar metamorphosis. They 
 remain united together b}^ 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 
 cord, the follicular wall and the round bodies of lamina epithel- 
 ium 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 
 Avhence 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 
 
 ' See their Memoir on the Genesis and Development of the Dental Follicle in 
 Jour, de Physiologie de Brown-Sequard, 1860. 
 5 
 
56 INTERSTITIAL GINGIVITIS. 
 
 the opinion tliat 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 
 remains of the cord of the primitive follicles may be fonnd, even 
 after the formation of the follicles of the permanent teeth, and 
 it is j)robably 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 a 
 
 -__ ^^_^^^,/ I 
 
 Fig. 24. — Section through the Incisive Portion of the Lower Jaw of an Ovine 
 Embryo, Measuring 82 Millim- (3 J Inches) in Length. Magnified 260 Diaji., 
 after Dhs. Ch. Legros and E. Magitot. ■ 
 
 D, Oral Epithelium. C, Lowest Laj'er of Cells in the Stratum Malpighii. 
 F, Epithelial Cord. K, Bourgeon of the Secondary Cord. I, Follicular AVall. 
 H, Dental Bulb. 
 
 correspondingly earlier stage ; and we think it safe to say that, 
 as a general rule, the complete absorption occurs toward the 
 period of erujstion." 
 
 The embryology of the dental shelf, which has been sum- 
 marized by Minot from Waldeyer, KoUiker, Von Ebner' and 
 O. Hertwig, indicates the source of the structures which have 
 been mistaken by Black for the limiting walls of glands. 
 
 ' Handbuch der Zahnheilkunde, 1890, pages 209-262. 
 
TEANSITOKY !^TRUC'TURE8. 57 
 
 After the epithelial cordis of the temporary and permanent 
 sets of teeth have been demarcated from their follicles, the proc- 
 ess of cell building proceeds like the process of cord building. 
 These buds, according to Charles Robin and Magitot,' are given 
 oif at the upper border of the follicle and below the ejjithelium 
 of the gum. " In fact, as soon as the epithelial lamina loses its 
 connection with the follicle, by the rupture of the cord, the epi- 
 thelial cells composing it become greatly increased in number at 
 the severed point. The multip)lication of cell-elements results 
 
 ji|@ 
 
 Fig. 25. — Vertical Tr.vnsversb Section through the Ixcisive Region of the 
 Lower Jaav of Ho.ai.^s Foltits Measurixg 38 Centimetres (15} Inches), M.-iG- 
 
 NIFIED 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, E[jithelial Globule. L, Enamel Organ of 
 the Permanent Tooth. 
 
 in the formation of irregular buddings, which wander in different 
 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 
 connective is absorbed, thus isolating an ejjithelial mass." 
 
 This budding occurs at different points along the cord (Fig. 
 24) at the end and upon the outer surface of the follicular wall 
 (Figs. 25 and 2B) at the point where the cord is severed from the 
 
 'Loc. cit., 1860. 
 
58 ■ IXTEESTITIAL GIXGIVITIS. 
 
 enamel organ. These gradually diminish as they descend upon 
 its sides. Doubtless the epithelial cord remains in the periosteal 
 and submucous tissue throughout life. Fig. 27 represents evident 
 sections of epithelial cord in a man sixty-eight years of age, and 
 Fig. 28 in a dog eight years. In the photographs of the scurvy 
 cases and of dogs will be seen evidences of the persistence of 
 epithelial debris late in life. The position already cited from 
 
 ^WM^S'M 
 
 
 
 ,.-. V 
 
 Fig. 26. — Fkoji the Loiver Jaw of ax 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. 
 
 Hobin and INIagitot as to its early disappearance would hence 
 apj^ear to be too strongly taken. 
 
 Robin and ^lagitot claim that this budchng jjrocess 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 ap]3ear 
 in the fibrous tissue of the middle and outer surfaces. The bone 
 dej^osit gradually takes the form of the jaw, filling in and 
 encroaching upon the fibrous tissue, forming a Ijony wall on the 
 
TKANSITORY STRUCTURES. 
 
 59 
 
 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 tissue 
 hiterally, 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 narrow space 
 
 X 50. One-half-in. obj. No, Oc. 
 
 Fig. 27. — Cross Section of Epithelial Cord. M.\x. 
 
 I, Peridental ^Membrane. W, Epithelial Debris or Cord. EO, Endarteritis Obliterans. 
 
 of the peridental membrane, and owing to the position of the 
 debris at the upper part of the follicle, it would be natural 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 maroin of the bone tissue, and 
 
60 
 
 INTERSTITIAL GINGIVITIS. 
 
 tliroughout 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 
 
 X 5fi0. No. 2 projection ocular. One-t^\'elfth obj. Zeiss. 
 
 Fig. 28. — Cross Section Epithelial Cokd. Dog. 
 
 I, Peridental Membrane. W, Epithelial Debris or Cord. U, Nerve Tissue. 
 
 local or constitutional, they will continue their process of con- 
 struction. Hence, the frequency of hyperti-ophy of the process, 
 and in disease the calcification of the j^eridental membrane. 
 
 On the other side of the membrane, next the root surfaces, 
 
TRANSITORY STRUCTURES. 61 
 
 may be seen other cells Avliicli l^uild up aucl destroy the cemen- 
 tum; these are called cemeutoblasts 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 2;)eri- 
 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 
 bone and tooth structure due to unstal:»le nervous tissue, and from 
 the slightest irritation. 
 
 The gums, mucous membrane, alveolar process and peridental 
 membrane, owing to their transient nature, are influenced by the 
 slightest irritation. This influence is the result of both constitu- 
 tional and local causes. It consists of an irritation in the periph- 
 eral nerves which sets the osteoblasts and osteoclasts at work 
 to build up or tear down the alveolar process. This influence 
 may be only sufficient to stimulate these cells to action without 
 inflammation. This is noticed in the advance toward old age, in 
 long, lingering debility, in the development of bone, especially 
 the tearing down and the building up of the inferior maxillary 
 backward. It may be noted in mild or intense iuflanimation of 
 the peridental membrane, due to more acute forms of disease, to 
 scurvy, mercurial, lead and iodide poisoning, or to local irrita- 
 tion. So sensitive are these structures that in neurotics 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 producing that 
 pathologic condition called hypertrophy of the alveolar process ; 
 one of the most marked evidences of an unstable nervous 
 system. 
 
 The breaking down of the tissues by the osteoclasts nuiy lie 
 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 
 
 ' Pathologische Anatomie. 
 
62 
 
 INTERSTITIAL GUNGIVITIS. 
 
 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 commonest form of bone destruction is by lacunar 
 absorjDtion. This process occurs not only under physiologic 
 conditions, but is extraordinarily frequent in pathologic states, 
 e. g., in the various types of atrophy. They form on the 
 smooth, su]jerficial 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. 
 29). There are no alterations of the bone substance that would 
 
 
 ^^^^if^0^P^^^^^^'^'^-%^' ' 
 
 ^^^m- 
 
 a, Bone Trabecule, b, Tubercle with Granulation Tissue, c, Broken-down Tissue. 
 d, Blood Vessel, e, Osteoclasts. /, Fat Cells. 
 
 indicate a jarimary line of absorption (Plummer). The con- 
 fluence of these lacunae form larger cavities. 
 
 " The second form of bone absorjDtion, 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 the lamellse (general 
 lamellae) which contain vessels (perforating vessels). These are 
 often associated with the Haversian canals and gradually pass 
 
TRANSITORY STRUCTITRES. 
 
 63 
 
 into them, but unlike tliem, are surrounded witli circular 1am- 
 ellee. Under ^^athologic conditions the conception of these j^er- 
 forating canals is somewhat widened. On the one hand 
 Volkmann's canals are spoken of when reference is made to the 
 
 b a e c 
 
 a, Large Spaces Resulting from Absorption of the Trabecule. 6, Decalcified Bone, 
 c and d, Decalcified Bone and Atrophied Trabecuhe. e. Haversian Canals. 
 
 vessels or vascular connective tissue penetrating from one medul- 
 lary space in the spongy substance, or from one Haversian canal 
 in the comjiact substance, to another, in such a way that a passage 
 is made from one part of the bone to the other ; Volkmann's- 
 canals also include irregular ampula-formed dilations or cavities- 
 
•64 INTEESTITIAL GINGIVITIS. 
 
 (Fig. 30). By confluence of these are j^i'oclucecl cavities or irreg- 
 ularly outlined canals penetrating the bone substance. These, if 
 they emj^ty into the medullary space, become filled with cells. 
 
 " 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 (halister- 
 esis) and the remaining substance (bone cartilage) is then further 
 ■dissolved, passing through a temporary fibroid stage. This 
 destruction of the decalcified and interfibrillse decomposed bone 
 is produced as a rule without osteoclasts. The decalcified border 
 zones of the trabeculse appear with sim^jle carmine (coloring) or 
 by double stains." 
 
CHAPTER IV. 
 
 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 
 advocates as strongly the constitutional theory. In a general 
 way, etiology may be divided into exciting and j)redisj)Osing. 
 Etiology may also dej^end ujjon an element dependent on the 
 exciting cause, an element dependent on the constitution of the 
 individual attacked, 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. The local causes assigned 
 are acute inflammation of the mucous membi'anes, catarrhal 
 states, germs or fungi, irregular teeth, lactic acid, jDOcket dis- 
 ease, hfemorrhagic 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 cases. Many 
 ■of the assigned causes could lie comjiressed into fewer etiologic 
 influences. Thus meat-eating and the uric acid states are too 
 intimately connected to be regarded as different causes, from a 
 constitutional standpoint. As has been already pointed out, uric 
 acid acts, when it acts at all, like lactic and other acids, as a local 
 irritant rather than as the constitutional condition (as many sup- 
 pose) 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 monotony of 
 diet. It is a constitutional disorder, peculiarly apt to have its 
 local expression in the gums long ere the general constitutimial 
 
66 I^TTEESTITIAL GINGIVITIS. 
 
 symptoms are manifest. The germs and fungi etiologists, on tlie 
 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 w^ell 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 jDrod- 
 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 
 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 feecal 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 
 vaso-motor (blood vessel) system. Many trophic disturbances,, 
 as J. Collins ^ remarks, are j)robably due to vaso-motor changes,, 
 and it is not possible to separate by any sharjjly deflned line the 
 vaso-motor from the trojjho-neuroses. At the same time, it 
 should be distinctly remembered that there exist troj)ho-neuroses 
 in which there are no appreciable vaso-motor change as in many 
 
 ' Nervous Diseases, by Dr. F. X. Dercum. 
 
THEOEIEf!! OF INTEESTITIAL GINGIVITIS. 67 
 
 cases of acromegaly and hypertrophies. On the other hniul, 
 there are any amount of vaso-motor disturbance which are ))y 
 no means trophic in character. Trophic disturbance, which may 
 play a very important part at the onset of interstitial gingivitis, 
 is neurotic oedema due to nerve irritation. While this is most 
 frequent on the face, lips, tongue, pharynx, forehead and genital 
 organs, it also apj^ears on the gums. The oedema reaches its 
 full development 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. 
 
CHAPTER V. 
 
 URIC ACID AND INTERSTITIAL GINGIVITIS. 
 
 Wliat John Fitzgerald' calls tlie giagival organs, possess, as- 
 lie 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 hyperfemia, 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 directioUr 
 but of late this trend is changing. 
 
 During the past two decades uric acid has assumed again the 
 j)rominence in pathogeny which it once had when called sup- 
 pressed gout. It is not surprising, therefore, to find that Reeves, 
 Pierce, Kirk, Rhein and others claim a uric acid etiology for 
 interstitial 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 jjhosphate. 
 Destructive distillation gave a strong ammonic 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 was present. 
 
 The great deficiency in the experiments thus described is the 
 small number of cases examined and the lack of proper control 
 
 ^ The Clinical Journal, March 1, 1899. 
 
 -International Dental Journal, Vol. XV, pages 1, 217, 501. 
 
UEIC ACID AND INTERSTITIAL GINGIVITIS. G9" 
 
 experiments. These elements have so frequently led to errors in 
 dental pathology that I determined upon a series of investigations 
 in two different laboratories, whose results were rej)orted some 
 years ago.^ The Columbus Medical Laboratory was selected for 
 one series of experiments in special cases. The laboratory of the 
 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 were 
 sent to the laboratory last named from three institutions in 
 Chicago which make a specialty of extraction. These teeth liad 
 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 extracted. 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 sjDecimens obtained from the institu- 
 tions just mentioned, and were therefore without history. The 
 tests employed were the hydrochloric acid, the dry distillation, 
 and the nuirexid, these being the tests recommended by Pierce. 
 The examinations in the Columbus Medical Laboratory were 
 made by J. A. Wesener, and those in the laboratory of the 
 Northwestern University Women'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 was found the needle-shaped crystals, and 
 one in Avhich there Avas 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 remaining 
 eighty gave a decided reaction. By the murexid test, four gave 
 a slight murexid color, but remainder gave no reaction. Special 
 examination 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 distilla- 
 tion tests for ammonia. Two gave a slight reaclfion by the 
 murexid test. In examination of the teeth of three uric-acid 
 diathetic women, over forty years of age, uric acid was not 
 
 'Dental Cosmos, April, 1896, page 310. Journal of the American Medical Asso- 
 ciation, January 16, 1S97. 
 
70 INTERSTITIAL GINGIVITIS. 
 
 detectible either by the niurexid 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 
 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 j^ositive with the dry distillation test. All are nega- 
 tive Avith 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 was uric acid and gouty histories gave nega- 
 tive 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 jDroduce 
 ammonia. By the murexid test only twelve out of the two 
 hundred and fifteen gave a jDOsitive 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 resemble 
 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 
 ap2:)lication. 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 
 
URIC ACID AND INTERSTITIAL GINGIVITIS. 71 
 
 of uric acid. If crystals be present they by no means settle the 
 existence of uric acid. When the faintest quantity possible of 
 uric acid is mixed with tartar from teeth and subjected to crystal- 
 lization, the results are always negative. If subjected to the 
 murexid test, the results are always positive. The dry distilla- 
 tion 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 Rush 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 selected 
 as carefully as possible, removed from the tooth, and jjlaced in a 
 small porcelain crucible. A drop of pure nitric acid was added 
 and the mixture evaporated on the water bath. AVhen dry, the 
 evaporation was repeated with another drop of nitric acid, and 
 the crucible allowed to cool. When cool, the color produced by 
 the nitric acid was observed, and then a glass rod, wet with 
 ammonia water, was brought near the deposit, and any color ^^ro- 
 duced was noted. If no color was observed, the ammonia was 
 allowed to flow over the residue. A j^ellow 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 vfith 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 were 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 [)er cent of ui'ic acid. As a 
 result of the different experiments, iu tlie first two liuudred and 
 fifteen cases five per cent uric acid was found. In the second 
 
 G 
 
72 INTERSTITIAL GINGIVITIS. 
 
 three hundred cases, four per cent, and in the third four hundred 
 and thirty-five cases, six per cent was found. In an examination 
 of nine hundred and fifty cases by different chemists at different 
 periods, five to six per cent give j)Ositive results as to uric acid by 
 the chemic 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 gingi- 
 vitis, since the deposits were examined after the teeth ha,d been 
 removed. Any other irritation may have been the exciting 
 cause. Uric acid acts, when at all, solely as a local irritant. 
 
CHAPTER VI. 
 
 INORGANIC SALTS AND INTERSTITIAL GINGIVITIS. 
 
 The foods which enable the body to repair its waste, to build 
 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 j)urely mechanical manner. After having 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, however, not 
 received the attention from physiologic chemists that their 
 importance demands. They are, as a rule, found in greater or 
 lesser quantity in all foods that are taken into the body. They 
 do not serve as a source of energy, but as the other foods are 
 needed for the develojjment of the tissues, so the inorganic salts 
 are needed for the building of bone tissue and the repair of 
 waste. This is accomplished by the soluble salts in the blood. 
 Human blood has the following comj)Osition : 
 
 ANALYSIS OF HUMAN BLOOD (C. SCHMIDT). HOWELL'S 
 PHYSIOLOGY. 
 
 Man. Woman. 
 
 25 Years. 30 Years. 
 
 Water 788.71 .... 824.55 
 
 Solids 211.29 .... 175.45 
 
 Proteids and Extractives 191.78 .... 157.93 
 
 Fibrin 3.93 1.91 
 
 HcTsmatin (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. 
 
 CI 1.75 
 
 Kjo 3.091 
 
 NAju 0.470 
 
 SOg 0.061 
 
 205 ••••• I.ODO 
 
 CaO 
 
 M<„ 
 
 Blood Plasma. 
 
 CI 3.536 
 
 Kjo 0.314 
 
 NA2„ 3.410 
 
 SO3 0.129 
 
 P205 0-1^5 
 
 CaO 
 
 M90 
 
 These acids and bases exist, of course, in tlie 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 Pliosphate 0.633 
 
 Sodium Carbonate 0. 341 
 
 Calcium Phosphate 0. 094 
 
 Magnesium Phosphate 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 corjjuscle 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 j^lasma of the blood j^ass- 
 ing l^y 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 
 turn open into definite lymphatic vessels. These vessels unite 
 
PKK' ACID AND INTERSTITIAL GINGIVITIS. 75' 
 
 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 propoi'tion 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 with them. 
 
 The chemical composition of the human bile, according to 
 Jacobson,' is as follows : 
 
 Water 977 . 40 
 
 Sodium Glycocholate 9 . 94 
 
 Cholesterin 0.54 
 
 Free fat 0.10 
 
 Sodium palmitate and sterrate 1 . 26 
 
 Lecitine ^ . . . . . 04 
 
 Other organic matter 2 . 26 
 
 Sodium cliloride 5 . 45 
 
 Potassium chloride 0.28 
 
 Sodium phospliate 1 . 33 
 
 Lime pliosphate 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 
 
 Magnesiimi traces 
 
 'American System of Dentistry. 
 
 -Transactions South Carolina Medical Association, ISSO. 
 
76 IXTEESTITIAL GINGIVITIS. 
 
 SecKetions of the 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 . 5.3 
 
 ■ The comjiosition of the normal human pancreatic juice has 
 not been determined comjjletely 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 pai-ts 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 varying from 2 to 3.5 parts per thousand. 
 The elements of the sweat which are of imjjortance from an 
 excretory standpoint are water, inorganic salts and urea or related 
 nitrogenous compounds. " 
 
 Inorganic salts from the faeces are made up of the salts of 
 sodium, jDotassium, calcium, magnesium and iron. According to 
 Enderlin' the following represent the composition of the material 
 matter in the fseces : 
 
 SALTS SOLUBLE IN WATER. 
 
 Sodium chloride and suljihate 1.37 
 
 Sodium phosphate 2 . 63 
 
 SALTS 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 projDortion, according as the fluid is more or less rich in 
 
 ' Gamgee, Physiological Chemistry of the Animal Body. 
 
URIC ACID AXD INTERSTITIAL GINGIVITIS. 77 
 
 water. The salts are much more abundant than the organic 
 solids. 
 
 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 j^art is derived directly from the salt taken in the food. 
 The phosphates occur in combination with Ca and Mg, but chiefly 
 as acid phosphates, of Na or K. The acid reaction of the urine 
 is caused by these latter. The phosj^hates are produced in part 
 from destruction of phosphorus-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 
 
 Solids , 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 
 
 Magnesium .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 phos- 
 phate and carbonate with urate of ammonia. ' 
 
 ' American Text-Book of Physiolog}'. 
 - Landolt, Ph\'siology. 
 
78 INTERSTITIAL GINGIVITIS. 
 
 Each oue of these compounds is nearly in a j^ure state. A 
 stone may be composed entirely of one salt or it may be comjiosed 
 of two, three or four, each compound forming sej)arate consecu- 
 tive layers through the stone. One examination made by How- 
 shij) Dickinson' showed eighty-nine per cent lime carbonate and 
 the rest lime oxalate and phosphate of lime. 
 
 The deposits upon the teeth are derived j^artly 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 phosp)hate 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 ujaon 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 little car- 
 bonate and trace of fluorine.... 77.21 .... 81.18 
 
 100.00 .... 100.00 
 
 Another analysis made by Scheheoetskey resulted thus : 
 
 Water and organic matter 22. 07 
 
 Magnesium j)hosphate 1 . 07 
 
 Calcium phosphate 67 . 18 
 
 Calcium carbonate 8.13 
 
 Calcium fluoride 1.55 
 
 100.00 
 ' Renal and Urinary Afl'ections. 
 
URIC ACID AND INTERSTITIAL GIN(iIVITIS. 
 
 79 
 
 Malenfant found that salivary calculi (located in Wharton's 
 duct) was composed of: 
 
 Lime jjhosphate 27 
 
 Magnesium phosf)hate 1 
 
 Basic lime phosjDliate .... 60 
 
 Alcohol and muriatic acid 4 
 
 Ptyalin 2 
 
 Loss 6 
 
 100 
 The following are results of analysis of salivary calculi by 
 various observers : 
 
 
 
 Weight. 
 
 
 
 
 
 100 Parts. 
 
 
 
 Bivra. 
 
 Lecanu. 
 
 Besson. 
 
 
 ■1 
 
 2 
 
 3 
 
 Bird. 
 
 Calcium carbonate. . . 
 
 81.2 
 
 79.4 
 
 80.7 
 
 13.9 
 
 30 
 
 15 
 
 2 
 
 Calcium phosphate . . . 
 
 4.1 
 
 5.0 
 
 4.2 
 
 38 2 
 
 75 
 
 55 
 
 75 
 
 Magnesium phosjahate 
 
 
 
 
 5.1 
 
 
 1 
 
 
 Soluble solids 
 
 Organic matter 
 
 6.2 
 7.1 
 
 4.8 
 8.5 
 
 5.11 
 8.3| 
 
 38.1 
 
 5 
 
 25 
 
 23 
 
 Water and loss 
 
 1.3 
 
 2.3 
 
 1.7 
 
 6.3 
 
 
 
 
 Deposits in the tissues in gout are made uj) of soda and lime 
 urates. In order to compare the calcic dejDosits in other parts of 
 the body with the serumal deposits upon the teeth affected with 
 interstitial gingivitis, thousands of teeth were obtained from three 
 dental offices which make a practice of extracting teeth. From 
 these one thousand were selected at two different times, making- 
 two thousand teeth containing dejiosits direct from the tissues. 
 These were submitted to a chemical analysis by J. H. Salis- 
 bury, 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 iliflference 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 dissolved in nitric acid and the solution preci23itated 
 with ammonium molybdate. The precipitate was washed, dis- 
 solved in ammonia precipitated by magnesia mixture and the 
 
-80 INTERSTITIAL GINGIVITIS. 
 
 13recipitate of ammonia magnesium jjhospliate, washed, dried, 
 ignited and weighed. 
 
 " In B, calcium and magnesium were estimated as follows : 
 The ash was dissolved iu hydrochloric acid and the acid just 
 neutralized with ammonia water and sodium acetate added. It 
 Tvas 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 
 jjhosjihate added, and the precipitate of magnesium-ammonium 
 23hosphate collected, washed, dried, ignited and weighed. In 
 case the phos^^horic 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 comjDOsition of the serumal tartar 
 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 serumal tartar, October 24, 1898, shows it to 
 iave the following composition : 
 
 Water 4.48 
 
 Organic matter 27.00 
 
 Calcium phosphate 72 . 73 
 
 Magnesium phosphate 4.91 
 
 99.12 
 
 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 person 
 and differ in jDcrsons of like age, on the same diet. No matter 
 how careful the chemist may be in analysis, no two results will 
 be exactly alike. For this reason, in tartar and calcic deposit 
 
URIC ACID AND INTERSTITIAL GINGIVITIS. 81 
 
 upon the roots of teeth, two different analyses of the same deposits 
 are cited. It is evident that while slight differences occur in the 
 table, these are due chiefly to the character of the secretions. 
 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 s^jace disorder, adenoids, arrest of the 
 facial bones. They are neurotics and degenerates. 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 hypertrop)hy of the alve- 
 olar process take place and large deposits 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 same 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 
 neurotic, degenerate, 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 
 
82 INTERSTITIAL GINGIVITIS. 
 
 interstitial gingivitis, ranging from simple inflammation of tli e 
 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 mani- 
 fested 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 process and 
 contraction of the gums. 
 
 In cases where large collections of tartar are dej30sited ui^on 
 the teeth of children there is also an excess of excreta through 
 the kidneys. Examination of urine in such cases will reveal 
 always from four to eight times more deposit than tlie 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 trojjhic disorders of nutrition and the tissues take 
 on disease more readily than healthy individuals earlier in life. 
 AVhen 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, 
 deposits do not take place. As is elsewhere shown,' calcic 
 dej)Osits on the roots of teeth are a result of inflammation and 
 pus infection and not the cause. 
 
 ' International Dental Journal, April, 1896. 
 
CHAPTER VII. 
 
 HEREDITY AND ENVIRONMENT. 
 
 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. In the first type the morbid condition is directly inher- 
 ited ; in the second, a deficiency is due to the morbid condition 
 which may or may not express itself in a tendency to the morbid 
 condition of which it is the offshoot. Heredity further should be 
 separated from congenital states which result from the operation 
 of germs or toxins during a particular pregnancy wherein these 
 pass through the j)lacenta to the foetus. A child may l^e Ijorn of 
 a tuberculous mother with a tendency to tuberculosis, but the 
 tubercle bacili may also directly infect it through the placenta so 
 that it is born with tuberculosis. The first is the inheritance of 
 the weakened organism of the mother. The second is a condition 
 of intra-uterine infection. 
 
 The reported cases of direct heredity of the pyorrhoeic stage 
 of interstitial gingivitis may afford instances of one or the other of 
 these categories. As has elsewhere been shown, transitory organs 
 are peculiarly apt to be weakened by heredity both in their 
 structure and in their resistance to morbific germs and agencies. 
 These weaknesses are especially apt to l)e shown dui'ing the 
 period of systemic stress connected with the first and second 
 dentition. Such weaknesses may be the outcome of general 
 nerve exhaustion on the part of the parents (the mother espe- 
 cially), and constitutes transformed heredity, which is far more 
 frequent than direct. This transformed heredity may be more 
 intense than the constitutional deficiency of the innnediate 
 ancestry. On the other hand, the conservative influence of 
 several generations may so oft'set the evil results of the defects in 
 the parents that the inheritance of defect is slight, if at nil 
 existent. 
 
 ' Talbot : Degeneracj' ; Its Signs, Causes and Effects. 
 
84 INTEESTITIAL GINGIVITIS. 
 
 This last type of heredity is called atavism (or " throw-back,"' 
 by the breeders). It is more likely to work for good than evil, 
 albeit the evil effects are more generally looked for. Because of 
 this atavism a serious nervous defect in a parent might express 
 itself only in an increased tendency to disease on the jjart of 
 transitory structures. The periods of stress are times in the life 
 of man when certain great life functions are developing or under- 
 going retrogression. These periods of development or evolution 
 are marked by the two dentitions and the development of the 
 sexual organs, which might more aptly be called the third den- 
 tition, since ere its close the wisdom tooth appears, if at all. The 
 periods of retrogression are when the great sexual functions are 
 undergoing involution or when the whole body is undergoing 
 senile change. These jj^i'iocl'^ often constitute an etiologic 
 moment for the production of disease even when potent heredi- 
 tary defect is absent, albeit at these periods such defect is apt 
 to ajDpear. 
 
 Another possibility to be considered in this connection as 
 complicating the diagnosis of heredity in disease is environ- 
 ment, understanding by this term all the external conditions that 
 can favor the develojiment of a disorder. Family habits and 
 surroundings are apt to be alike -for every member. If anything 
 in the environment especially favors the breaking out of a disease 
 in one member, the cause is equally apt to be, effective with 
 another, provided the individual idiosyncrasy is similar. This 
 may give rise to a suspicion of heredity, since conditions of life, 
 family habits and intimate household surroundings favor the 
 occurrence of a disorder in several members or generations of the 
 same family. Habits are often transmitted by imitation from 
 parents to offspring. These may be direct exciting or predis- 
 posing causes of an affection, especially if it be more or less 
 favored by their existence. 
 
 That constitutional conditions of hereditary origin favor the 
 occurrence of interstitial gingivitis is undeniable, but this does 
 not prove that gingivitis itself is hereditary. They favor its 
 occurrence as they favor other morbid conditions, by lessening 
 resistance, or by preparing the way. The gingivitis is only one 
 of the many accidents that are thus facilitated. So far as sali- 
 vary concretions are to be regarded as an exciting cause, heredity 
 
HEREDITY AND ENVIROXMEXT. 85- 
 
 may be disregarded, since these (thougli varying widely in dif- 
 ferent indivitluals in the amount of the deposit, and consequently 
 the irritation produced) are dependent upon more remote con- 
 stitutional or local conditions without direct connection with the 
 heredity. 
 
 The varieties (charged to lithasmia or arthritic conditions 
 notoriously hereditary) are of accidental origin rather than essen- 
 tially connected with constitutional conditions that happen to 
 furnish the irritant. 
 
 Local uric acid jjoisoning ' is, as I have elsewhere show^n, 
 occasionally associated with gingivitis. The coexistence illus- 
 trates the lowered vitality of the system, rather than the 
 etiology. 
 
 The same is true of all the other neurotic, rachitic and degen- 
 erative conditions, hereditary or otherwise, that are met with, 
 associated with gingival inflammation. They all favor the 
 occurrence of the disease by causing a weakened power of resist- 
 ance predisposing to the attack of any irritation. The mouth, 
 resistant as it ordinarily is, is at all times open to irritation. When 
 resistance is impaired it gives way at its most vulnerable point, 
 and the gingival margin is one. Interstitial gingivitis is favored 
 or hindered, like other disorders of its kind, by constitutional 
 conditions which may or may not be inherited, and which bear 
 toward it the relations only of predisposing and accessory 
 causes. 
 
 ' Dental Cosmos, 1896, page 312. 
 
CHAPTER VIII. 
 
 DEGENERACY AND DEGENERATE TISSUES. 
 
 One of the most important factors of predisposition is that of 
 degeneracy, either local or general. Three possibilities of life 
 await, as has been elsewhere pointed out,^ each living being : 
 either it remains primitive and unchanged, or it progresses 
 toward a higher type, or it backslides and retrogresses. The 
 factors underlying the stable state force the animal to remain as 
 it is ; these underlying the progressive tendency make it more 
 elaborate, while the factors of degeneration tend to simplify its 
 structure. Degeneracy is, therefore, a gradual change of 
 structure by which the organism becomes adapted to less varied 
 and less complex conditions of life. It is a reverse of develop- 
 ment which proceeds from the indefinite and homogeneous to the 
 definite and heterogeneous with a loss of explosive force diie to 
 the acquirement of inhibitions or checks. In proportion to the 
 depth of degeneracy does it affect the earlier simpler, or later 
 complicated, acquisitions. The opposite process of progression is 
 a gradual change of structures 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 suppression of form corresponding to the 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 accomj)ani- 
 ment to the elaboration in all the other organs. During the period 
 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. As the 
 teeth and jaws are among the most variable structures in the 
 body, they are peculiarly apt to be affected by either general 
 degeneracy, which affects the l^ody as a whole, and has local 
 
 ' Talbot : Degeneracy ; Its Causes, Signs, and Results. 
 
DEGENERACY AND DEGENERATE TISSUES. 87 
 
 expressions or local degeneracy by wliicli the ]:)0(ly l^enefits. 
 The foctors jjroclucing degeneracy act by causing nervous exhaus- 
 tion in the first generation. This implies a practical degenera- 
 tion in function, since tone is lost. 
 
 Every nerve cell has two functions ; one connected with sensa- 
 tion or motion, and the other with growth. If the cell be tired 
 by excessive work along the line of sensation or motion, the func- 
 tion as regards 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 system of nerves (the sympathetic ganglia) which, while 
 under control by the spinal cord and brain, act independently. 
 If these nerve centers become tired, the organ fails to perform its 
 functions, the general system becomes both poisoned and ill-fed, 
 and nervous exhaustion results. In most cases, however, the 
 brain and sijinal cord are first exhausted. The nerves of the 
 organs are thus allowed too free play, and exhaust themselves 
 later. This systemic exhaustion has local expression in the 
 testicle in the male, in the womb and ovaries in the female. 
 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 weakened in their function. Practically the 
 neurasthenic in regard to his organs has taken on a degenerative 
 function, albeit not degenerating in structure, since the rest- 
 lessness of the organs is a return to the undue expenditure of 
 force which occurs in the lower animals in proportion as it is 
 unchecked by a central nervous system. Through the influence 
 of various exhaustion agencies the spinal cord and the l>rain lose 
 the gains of evolution and the neurasthenic is no longer adjusted 
 to environment. Since the reproductive organs suffer partic- 
 ularly, children, born after the acquirement of nervous exhaus- 
 tion, are more or less checked in development as the influence of 
 atavism is healthy or not — have degenerations in the structure 
 of their organs which in the parent were represented Ijy neuras- 
 thenic disorder in function. As the ovaries of the neurasthenic 
 woman generally exhibit prominently the effects of the nervous 
 exhaustion, the offspring of these do not retain enough vigor to 
 23ass through the normal process of develoimient. 
 
OO INTERSTITIAL GINGIVITIS. 
 
 The action of degeneracy, considered as a local factor of con- 
 stitntional origin, may be exerted to preserve embryonic con- 
 ditions in adult life. Such preservation may result in the 
 breakdown of tissues which would otherwise withstand germs or 
 other causes of disease external to the tissues. Given this con- 
 dition of local degeneracy, a local predisj)Osing factor is added 
 to both the exciting causes and the constitutional predis]30sing 
 factors. So long as the teeth and transitory 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, the degenerate types find this factor adding dangers to 
 their evolution. In the degenerate the struggle for existence 
 between the organs 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 mem- 
 brane. This in degenerate children often fails so to develop 
 that the bactericidal function of mucus does not appear. This 
 hereditary feebleness of the mucous membrane is j^eculiarly apt 
 to occur in the nose, throat and gums, but other mucous mem- 
 branes are not exemjjt. 
 
CHAPTER IX. 
 
 NEUROTIC, DIATHETIC AND DEGENERATE CHILDREN. 
 
 Miller, as elsewhere stated, found a little over thirty-three 
 and one-third per cent on examination of twenty-six rachitic 
 children under twelve years who manifested interstitial gingivitis. 
 Considering that most of these manifested symptoms of inherited 
 congenital or acquired constitutional defect, such a small propor- 
 tion is rather remarkable. The fact suggests one of two explana- 
 tions — either the children in the institute visited by Doctor 
 Miller took better care of their teeth and gums than is usual 
 with 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 gingivitis was 
 found in all its stages, from simjale 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 encountered in office jaractice usually have 
 jaw deformities and teeth irregularities. Patterson has had 
 under observation thirty-eight cases of well-marked pyorrhoea, 
 thirty-three of which coexisted 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. 
 
 Luxury and modern degeneracy are generally charged with 
 the production of diseases later found to have attacked man 
 in prehistoric periods. This has been the case with interstitial 
 gingivitis. 
 
 R. R. 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 jieople accus- 
 tomed to luxury — good livers, people about middle age who 
 over-eat and under-work." 
 
90 IXTEE8TITIAL GINGIVITIS. 
 
 No method of living can be regarded as a cause of this 
 disease, excej^t so far as it affects the general system, thus j^i'O- 
 dueing trojahic changes. There is probably a slight difference 
 in liability to interstitial gingivitis between ^^eople of sedentary 
 habits and active outdoor workers, as well as between animals 
 domesticated or in cai^tivity 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, climate, 
 or mode of life, have suffered with the disease. Examinations of 
 animals in the American and European zoological gardens show 
 that it is not confined to any class of animals. Dogs and cats, 
 wdiether housed or I'unning at large, suffer with it. 
 
 The question how far this region is affected by toxic agents 
 introduced into the system is an open one ; still it seems probable 
 that they exert some influence. In chronic phosphorus 2>oison- 
 ing the jaw is j)articularly and seriously involved. This has 
 laeen attributed chiefly to the entrance of phosphorus into the 
 deeper tissues through carious teeth or through solutions of con- 
 tinuity of tissue due to tartar. , In the case of other poisons this 
 local factor is not so evident. Mercury has among its first 
 effects a soreness of the teeth with loosening of them in their 
 sockets. Here it appeai-s that the alveolus was one of the first 
 special points of attack independent of any traumatism or 
 abrasion of the soft tissues. In a similar way the toxins of 
 scurvy directly attack the alveolus. Its fleshy covering is later 
 involved in the progress of the disease. This sometimes extends 
 to comjjlete loosening and falling out of the teeth. Here an 
 irritation of a toxin from within the organism has a point of 
 -election, a structure that from its constitution or other reason is 
 particularly vulnerable to attack. Another constitutional dis- 
 order in which the alveolus is early affected is diabetes. The 
 ■exact pathology of this is uncertain, 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 jDassed the line of morbidity, alveolar impli- 
 cation is often very marked. This may l^e one cause of the 
 
NEUROTIC, DIATHETIC AND DEGENERATE CHILDREN. 91 
 
 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 auto-intoxications and trophic 
 disorders as- well, since the balance of the nervous system has 
 been disordered. Some (the paretic and organic dements) 
 exhibit especial tendencies to trophoneurotic disturbances affect- 
 ing the teeth. In states of depression and stupor, circulatory 
 disturbances predispose to these. 
 
 The constitutional results of acute and chronic infections are 
 apt to produce auto-intoxication 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 symmet- 
 rical and unacconq^anied by exfoliation or necrosis of the osseous 
 system elsewhere. Tuberculosis does not spare the alveolar pro- 
 cess. The well-developed disorder known as Riggs's disease has 
 been charged by Robin and Magitot to the direct influence of the 
 arthritic (gouty and rheumatic) process, and declared a special 
 form of arthritic manifestation. 
 
 The alveolus is clearly vulnerable to the toxins of many 
 infectious diseases. It is also quickly affected by some of the 
 autotoxic influences of disordered metabolism. Its vital resist- 
 ance to these agencies is less than that of other tissues. It is the 
 earliest sacrifice when these toxins or all toxins disturb the har- 
 mony of the organism. 
 
 Another cause for implication of these parts than the action 
 of toxins exists. Whenever tissue waste, whether local or gen- 
 eral, exceeds rej)air there is trophic change. This latter depends 
 directly upon disordei'ed local or general nervous functions. 
 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 neurotic atrophies where the direct inter- 
 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 probabl}^ thus exerted in many cases 
 
 'American Journal of Insanity, 1892. 
 -Kiernan, Journal of Nervous and Mental Diseases, 1878. 
 
 " Salter : Transactions of Pathological Society, London, 18.59-60, Vol. X[, page 309. 
 Lucas, Lancet, 1887, page 692. 
 
92 INTERSTITIAL GINGIVITIS. 
 
 rather than by direct infection. Where no cause has been ascer- 
 tained, examination directed to this factor wouki 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 perhaj)S the most prominent instance of 
 this ty23e of trophic failure affecting the part. Even simple 
 anaemia may thus rise to alveolar wasting. 
 
 The second form of trophic failure in the alveolus is less 
 prominent siiice it generally coexists with overshadowing disturb- 
 ance elsewhere which masks it to a certain extent. C Cruveilier' 
 noticed its occurrence associated with paraplegia and invokes a 
 nervous influence in its causation. In facial hemiatro23hy local 
 Ts^asting of the alveolus has ap2oeared before the disorder had 
 involved generally the jaws. This may sometimes be due to a 
 local cause, but its occurrence and association with other neviro- 
 trophic symptoms is suggestive. 
 
 The causes which, acting locally, produce direct interstitial 
 gingivitis, are the toxic effects of mercury, lead, brass, uric 
 and other acids, potass, iodide, and other agencies acting in a 
 similar manner, and scurvy. It is not the intention to enter into 
 an elaborate discussion of the toxic action of these drugs, but in 
 a general way to show the similarity in action and results upon 
 the tissues. Scurvy, a disturbance of metabolism, produces the 
 same train of symptoms as the metals. 
 
 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 
 system ; later occur nausea and vomiting, tremor in the arms and 
 hands. Besides local nerve inflammation (neurites), mercurial 
 and brass poisoning jaroduces j^aralysis 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 the teeth. The central nerve system dis- 
 turbance affects all other structures. Inflammation of the 
 mucous membrane of the mouth, as well as of the gums, and of 
 
 ' Bilk. Soc. de Chir. Paris, 1870, pages 30 and 31. 
 
NKUROTK', DIATHETIC AXD DEGENERATE CHILDllEX. 93 
 
 the alimentary canal, frequently occurs with sloughing of tissue. 
 The kidneys become involved, and are unable to carry off the 
 eifete matter. 
 
 The cachexia, which resembles that of scurvy, is characterized 
 by great debility, anaemia, emaciation, aloi^ecia, atrophy and 
 coarseness of the nails, with pain in the muscles and joints. 
 
 ]\Iercury is eliminated by all excretory organs for which it 
 has a great affinity. The soluble salts pass out by the bowels. 
 So long as the excretory organs of the body eliminate mercury, 
 the tissues are not effected. Small closes are eliminated, but con- 
 tinuation of dosage soon involves the nervous system, and after- 
 w^ards the tissues of the body, esi^ecially the jaws. The first 
 effect of mercury upon dogs is to produce vivacity and animation. 
 This lasts for two or three days, when the limbs begin to trem- 
 ble. The kidneys and bowels act at first freely. At the end of 
 seven or eight days paralysis agitans occurs. There is constant 
 trembling, whether when 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 remark- 
 able. 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 concerned. 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 with 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 system, repeated small doses distributed over a long period 
 are not so eliminated on account of the thickness and occlusion 
 
 ' Twentieth Century Practice of IMedicine, Vol. Ill, page 935. 
 
94 INTERSTITIAL C4INGIVITIS. 
 
 of the walls of the capillaries, producing endarteritis ohliterans, 
 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 
 length of time. Its effects are not manifest until the central and 
 jDcripheral nervous 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 slightly 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 
 sulphite) is always in the tissue outside of the blood vessels. 
 Plumbism 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 
 imjDeded circulation resultant on a thickening of the coats of the 
 vessel, producing occlusion. A bluish line upon the gums indi- 
 cates 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 troj^hic changes ; upon 
 the capillaries a thickening of the inner coat results in endar- 
 teritis obliterans. Brass j^roduces, as Hogben^ has shown, sim- 
 ilar effects to mercury and lead ; 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 infrequent 
 occurrence. 
 
 Scurvy is due to poor food and hygiene. Insufficient alter- 
 nation of food, impure air, want of bodily exercise, ennui and 
 uncleanliness combine the causes of this disease. Previous to 
 the introduction of canned goods, sailors on long voyages,, 
 prisoners and others under confinement were subject to scurvy. 
 Lunatics, idiots or j^eople who have had a long sickness, are now 
 
 ■ Birmingham Medical Review, 1887. 
 
NEUKOTK', DIATHETIC AND DEGENERATE CHILDREN. 95 
 
 most prone to it. AntEinic convalescents from protracted fevers 
 suffer from it. 
 
 In the British Arctic Expedition of 1875-76 over forty-eight 
 per cent of the men suftereil from scurvy. When the j^otato 
 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 i-ate 
 in the late civil war. It occurs among the Klondyke miners. 
 
 In public institutions for degenerate children it is very 
 prevalent. I have observed it in both American and European 
 institutions. 
 
 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 p)i"oprietary infant foods are 
 prone to scurvy. They lose their appetites, become pallid, per- 
 spire freely, have diarrhoea, the mouth becomes sore with inflamed 
 mucous membrane and gums. Purpura and hfemorrhages of 
 mucous membrane are common with pain and swelling of the 
 joints. 
 
 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 Rawls, of Cincinnati, Ohio, believed that an 
 excess of salt in the system produced gingivitis. Languor, 
 depression, anaemia, with a rise of temperature, and enlarged 
 joints with soreness are the first symjjtoms. 
 
 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 ansemia, vascular weakness and altered compo- 
 sition of the blood, oedema is connnon both in the lungs and in 
 the submucous and subcutaneous tissue, especially the feet and 
 legs. The gums begin to swell with redness and fibrous thicken- 
 ing of the deeper layer, which cause protrusion, especially in 
 
 1 Medical Chir. Trans., London, Vol. CXVI, 1883. 
 - Practitioner, London, February, 1894. 
 
96 INTERSTITIAL GINGIVITIS. 
 
 the cases of degenerates. The blood vessels, especially the capil- 
 laries, become thickened, in some cases they are occluded, or ero- 
 sion and ulceration occurs. The patient becomes decidedly pale 
 and markedly debilitated. The skin is dry and blanched. Gen- 
 eral 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 j^ale 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. 
 
 Factors acting through local trophic disturbances are not 
 only local disorders but also constitutional diseases, especially 
 those which prevent elimination of effete matter (Bright's dis- 
 •ease, diabetes, etc.) skin eruptions, lung affections, auto-intoxica- 
 tion (gout, etc.) and conditions like pregnancy, amenorrhoea, 
 dysmenorrhea, etc. The physiologic processes of nutrition, 
 growth and repair are regulated by local nerves which, as 
 already pointed out, because of this function are called trophic. 
 These are under control of both spinal and brain centers. Dis- 
 orders of the local nerve or of the higher centers may produce 
 trophic change. Such disoi'ders affect more decidedly provi- 
 sional structures, since the growth, nutrition and repair of these 
 is normally unstable. The alveolar process is an outgrowth of a 
 permanent portion of the skeletal structure, provoked and main- 
 tained by the existence of what are really dermal appendages 
 and not true bones. It is a provisional structure, almost unique 
 of its kind in adult life, which has apjiarently little independent 
 vitality. This is in part due to mechanical causes, since its 
 .slender structure unsupported by the teeth offers little resistance 
 to impacts from without, to which its situation renders it esi^e- 
 cially liable. There is more than this to be considered in reckon- 
 ing the special vulnerability of the alveolus. It is protected by 
 a thin layer of fleshy tissue only, which itself is peculiarly liable 
 to injuries, thus exposing the bone to infection. There is, more- 
 
NEUROTIC, DIATHETIC AND DEGENERATE CHILDREN. 97 
 
 over, no cavity of the body that is more ojjen to germs than the 
 mouth, and some of these that are considered especially viru- 
 lent are its constant residents. Access of germs and accidental 
 pathogenic factors to the alveolus is constantly afforded by cari- 
 ous teeth, the irritation of tartar deposits, etc. Its liability to 
 disease is thus indefinitely increased. As it is not very resistant 
 to morbid influences, the infections have thus free play, hence 
 supjxirative disease is more readily induced. 
 
 Great practical importance, as Hirt ' remarks, must be attrib- 
 uted to the changes in the hair and teeth which are observed in 
 tabetics (locomotor ataxia). The teeth become loosened without 
 pain and fall out without appearance of inflammation ; the tooth 
 being seemingly intact. This Hirt ascribes to disturbance in the 
 nutrition of the jaw ; an ati'ophic change connected with a lesion 
 of the nucleus of the trigenimus. The fact that this condition is 
 often connected with laryngeal crisis tends, in Hirt's opinion, to 
 support the view of Buzzard^ that the center for bone nutrition 
 lies quite close to the vagus. Similar facts have been observed 
 by C. L. Dana in America. ^ The conclusion is obvious that dis- 
 turbance of the nerve centers governing nutrition, growth and 
 repair exerts the same influence on the alveolus, jaws and teeth 
 as similar disturbances do upon the skin, hair, mucous mem- 
 branes and bones elsewhere. 
 
 These structures, which have previously become affected by 
 disease, although the patient has been restored to health, readily 
 become the seat of interstitial gingivitis. This is illustrated in 
 those persons who have been affected with scurvy, salivation, etc. 
 
 ' Handbuch der Nerveiikrankheiten, 1896. 
 -British Medical Journal, February 19, 1886. 
 ^ Diseases of the Nervous System. 
 
CHAPTER X. 
 
 INTERSTITIAL GINGIVITIS IN DOGS. 
 
 The technique of the examinations of interstitial gingivitis 
 and jjyorrhoea alveolaris in dogs was as follows : After fixing 
 and hardening in two per cent formalin, alcohol, or Miiller's 
 fluid, the tissues were decalcified in a five per cent alcoholic solu- 
 tion of nitric acid, imbedded in celluloidin and stained in various- 
 ways, the principal ones being hfematoxylin 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. 31 is a longitudinal section of a cuspid tooth with the 
 alveolar process in situ. A illustrates the enamel of the tooth, 
 (E) the ej)ithelium passes from the outer margin to the lower 
 border, then folds upon itself and extends down the 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 infiammation may be seen extending along the 
 border of this layer. It can also be observed extending down 
 the capillary blood vessels into the submucous tissue (SI and G). 
 
 Fig. 32 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 ejiithelium is 
 shown at the neck of the tooth. This structure passes downward, 
 folds outward and upon itself (AA) and returns two-thirds of 
 the distance toward the gingival border, leaving a pocket (RR). 
 The ejjithelium (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 Liga- 
 ment," Black) may be seen at H, inserted firmly into the 
 
X 75. A. A. obj. Zeiss. Micro-photog^raph, reduced one-third. 
 
 Fig. 31.— Longitudinal Section op Tooth and Glut Tissue. Slight Gisgivitls. Dog. 
 
 A, Enamel. B, Epithelial Tissue. G, Submucous Membrane. M, Fibrous Tissue. 
 SI, Slight Inflammation. 
 
X 75. A. A. obj. Zeiss. Micro-photograpli, reduced one-third. 
 
 Fig. 32.— Longitudinal Section of Tooth and Gu.m Ti.ssue. Chronic Interstitial 
 Gingivitis. Dog. 
 
 A, Enamel. E, Epithelial Tissue. G, Submucous Membrane. H, Periosteum. 
 K, Capillaries. V, Violent Inflammation. AA, Point of Union of Epithelial Tissue and Peri- 
 dental Membrane. ER, Space Pocket from want of Union of Epithelial Fold. 
 
f 
 
 
 
 h 
 
 ':^- ' 
 
 
 > 
 
 «»' 
 
 ~ll 
 
 w.-,,, 
 
 % 
 
 
 "• 
 
 ** . 
 
 . -v 
 
 V 
 
 
 ^-^ 
 
 psfc ■ 
 
 H-- 
 
 < 
 
 /^^ ■ 
 
 
 
 ■■'?• 
 
 
 -■J 
 
 ffii^^'. 
 
 .,3sv 
 
 'y:.i^^'fe.x 
 
 X 75. A. A. obj. Zeiss. Micro-pholograph, reduced one-third. 
 
 Fig. 33. — Longitudinal Section of Alveolar Process and Peridental Membrane. Slight' 
 Interstitial Gingivitis, Extending into Alveol.ik Process. Dog. 
 
 J, Alveolar Process. L', Inflammation Extending through Enlarged Haversian Canals. 
 ■V, Inflamed Peridental Membrane. 
 
X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 
 
 Fig. 34. — Longitudinal Section of Alveolar Proces.s 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 IVIembrane. I', Inflamed Peridental Membrane. L', Inflam- 
 mation Extending through Enlarged Haversian Canals. 
 
INTERSTITIAL GINGIVITIS IN DOGS. 103 
 
 ceiuentuiu and extending outward and downward. Just below 
 (A A) may be seen the interlacing of the coarser fibers of the peri- 
 osteum with the finer fibers of the submucous tissue. Chronic 
 i-ound-cell infiammation may be seen extending from the jiapil- 
 lary layer through the capillaries into the interstitial tissue of 
 the submucuous 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. 33 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 submucous 
 tissue, the fibrous tissue of the periosteum into the peridental 
 membrane and into the alveolar process. Round-cell inflamma- 
 tion may be seen in the blood vessels extending through the 
 Haversian canals (L^). 
 
 Fig. 34 is a similar section from another tooth showing chronic 
 inflammation extending throughout the jjeridental membrane (I) 
 and alveolar process (J). The Haversian canals (L) are well 
 outlined by the iiiflammatory progress. Marked inflammation 
 has resulted at V and also at the margin of the- alveolar process. 
 
 Fig. 35 is a section of the ^jeridental 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 through the Haversian canals, 
 producing the type of absorption of the trabeculiB known as 
 halisteresis ossium. Lacunar absorption has also occurred (O). 
 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. 36 is a section from another locati(jn of the alveolar 
 23rocess witli a greater amplification, showing the inflanunatory 
 
 8 
 
104 INTERSTITIAL GINGIVITIS. 
 
 process extending through the alveolar process. Endarteritis- 
 obliterans may be seen in different localities (EO). Three forms- 
 of absorption are evident in this figure : Enlarged areas arising 
 from absorption of the trabeculse (halisteresis ossium) due to the 
 inflammatory process. The vessels of Von Ebner precede perfo- 
 rating canal absorption (BB), distributed over the entire field, also 
 the result of the inflammatory j)rocess and lacunar absorption (O) 
 which may result from inflammation. As long as the fibrous tissue 
 remains in these large areas to retain the osteoblasts, new bone 
 tissue may be produced under favorable conditions. On the 
 other hand, when this tissue and the osteoblasts are destroyed, the 
 alveolar process cannot be restored. 
 
 Fig. 37 shows a section of the alveolar process from another 
 dog. Here lacunar and other absorption (halisteresis ossium) are 
 well shown. Thirty-seven osteoclasts (O) may be counted in the 
 field while destruction of bone by halisteresis (Q) is rapidly 
 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 
 extended 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 alveolar 
 process come away with the peridental membrane attached to the 
 tooth. Fig. 66 was obtained in this manner. In the upper left- 
 hand corner may be seen eight or ten new osteoclasts (O) in an 
 enlarged Haversian canal, at work isolating one piece of the 
 alveolar process from the other. 
 
 Fig. 38 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 were originally the location of Haversian 
 canals and which have thickened walls and a tendency to oblit- 
 eration. The light color shows decalcification, the dark normal 
 bone. At P may be seen perforating canal absorption. At FGr 
 
A. A. oDj. z,eiss. Micrii-photOfii-aph, reduced one-third. 
 Fig 35.- Longitudinal Section of Tooth, Alveolae Process and Peridental ME^tBRiNE 
 Violent Eound-Cell Inflammation of Peridental Membrane, Extending through the 
 Haversian Canals into the Alveolar Process. 
 
 C.Cementnm. .T,- Alveolar Process. K, Capillaries. L, Haversian Cana]=; NLar<.e 
 Spaces arising from Absorption of the Trabecuhe, starting in the Haverskn Canals (HaliS 
 MS). O, Lacunar Absorption. V, Violent Inflammation. B V, Blood Vessels ori-rinalh- Havir 
 EXiS^veSa^a^:^ ^^^'"^"*^^ ^^^■»'^--- ^■' I"«a,nmation^.SS'\.l^^^^; 
 
X 150. D. D. obj. Zeiss. Micro-photograph, reauced one-third. 
 Fig 36.-LONGITUDINAL Section of Alveolar Process. Chronic Infla>>m..vtion Extending 
 
 THROUGHOUT, SHOWING H ALISTERE3IS, PERFORATING CaNAL AND LACUNAR ABSORPTION. DOG. 
 
 J Alveolar Process N, Large Spaces arising from Absorption of the TrabeculEe, starting 
 in the Haversian Canals (Halisteresis). 0, Lacunar Absorption. P, Perforating Canal 
 Absorption. BB, Blood Vessels of V. Ebner preceding Perforating Canals. EO, Endarte- 
 ritis Obliterans. 
 
X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-thirti. 
 Fig. 37.— Longitudinal Section of Alveolar Process. Chronic iNFL.iM.M.iTioN Extending 
 
 THROUGHOUT, SHOWING HaLISTERESIS AND LACUNAR ABSORPTION. DoG. 
 
 J, Alveolar Process. L, Haversian Canals. N, Large Spaces arising from Absorption of 
 the Trabeculs;, 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. 
 
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 X 75. A. A. obj. Zeiss. Mioro-pliotograph, reduced one-third. 
 
 Fig. 38. — Tean.svekse Section, Alveolae Process. Chronic Inflammation Extending 
 throughout. dog. 
 
 J, Alveolar Process. N, Large Spaces arising from Absorption of the Trabecute, starting 
 in the Haversian Canals. P, Perforating Canal Absor]3tion. Q, Halisteresis Ossium or 
 Decalcified Bone. X, Remains of Calcified Bones. EO, Endarteritis Obliterans. EG, Fat 
 Globules. 
 
X rri. A. A. obj. Zeiss. Jlicro-pholo^'i-aph. reduced ouelliird. 
 
 Fig. 39. — Cross Section of Tooth, Alveolae Process and Peridental BIembrane. Chronic 
 Inflammation of Peridental Membrane and Absoriiion of the Root of Tooth. Dog. 
 
 B, Dentine. C, Cementum. D, Pulp. I', InHamed Peridental Membrane. K, Capillaries. 
 S, Root-absorptioD. 
 
X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 
 Fig. 40. — Lokgitudin.-vl Section of the End of the Root of a Tooth, Alveolar Process 
 
 AND PeEIDENT.1L MeMBEANE, SHOWING ClIRONIC INFLAMMATION OP THE PERIDENTAL MeM- 
 
 bkane. Exostosis of the Root of the Tooth and Lacunae Absorption. Dog. 
 
 C, Cementum. 
 
 D, Pulp, with 3 Foramina. J, Alveolar Process. O, Lacunar Absorption. 
 P, Perforating Canal Absorption. CC, Cementosis. 
 
X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 
 
 FiG. 41. — Cross SEcrroN op Inflamed Peridental Membrane. Dog. 
 
 II, Inflamed Peridental 3Ienibi-ane. W, Epithelial Debris. 
 
X 15. 75M.M. obj. Spencer. Micro-photograph, refluced one-third. 
 
 Fig. 42. — Longitudinal Section of Tooth, Alveolae Process, Peridental Membrane, 
 Showing Interstitial Gingivitis and Pyoerhcea Alveolaris, with Tooth Aboft to be 
 Exfoliated. Dog. 
 
 C, Cementum. 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. CC, Cementosis. DD, Calcific Deposits Destroj^ed bj' Acids. 
 
X 40. 35 M.M. obj. Zeiss. Micro-pliotogi'aph, reduced one-third. 
 
 Fig. 43. — Longitudinal Section of Tooth, Alveolae Process, Peridental Membrane and 
 Gum Tissue, Enlarged from Fig. 42, Showing Active Inflajimation, with Pus Pocket. 
 Dog. 
 
 C, Cementum. E, Epithelial Tissue. G, Submucous Membrane. I', Inflamed Peridental 
 Membrane. J, Alveolar Process. L', Inflammation Extending throush Enlarged Haversian 
 Canals. M', Inflamed Fibrous Tissue. R, Pus Pocket. V, Viorent Inflammation. AA, Point 
 of Union of Epithelial Tissue and Peridental Membrane. FF, Food Containing Micro- 
 organisms. 
 
 113 
 
X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 
 
 Fig. 44. — Longitudinal Section of Tooth, Alveolar Process, Peridental Membrane anD' 
 GoM Tissue, Enlarged from Fig. 42, Showing Active Inflammation with Pus Pocket.. 
 Dog. 
 
 C, Cementum. E, Epithelial Tissue. J, Alveolar Process. M', Inflamed FitooiLS Tissue. 
 R, Pus Pocket. V, Violent Inflammation. 
 
INTERSTITIAL GINGIVITIS IN DOGS. 115 
 
 fat globules nui}^ be seen, while in the larger space at the upper 
 right-hand corner is evident entire destruction of the fibrous 
 tissue. 
 
 Fig. 39 illustrates a cross section of alveolar process and 
 cuspid root, showing absorption of the root. Inflammation 
 extends throughout the peridental membrane (I). The cajDil- 
 laries (K) are quite numerous. These are cut both crosswise and 
 lengthwise. Absorption (S) of the root may be seen progressing 
 at these localities. 
 
 Fig. 40 shows a longitudinal section of the end of the root. 
 Active destruction has been going on both in the pulj) 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 place. Below the constricted j)ul2) may be 
 seen three divisions of the pulp (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 
 (O). Thus results a building up and tearing down of the same 
 tissue from the same cause, interstitial gingivitis.. 
 
 Fig. 41 shows inflammation of the peridental membrane (I') 
 "with epithelial debris (W) scattered throughout the field. 
 
 Fig. 42 is a section through the jaw and incisor tooth, showing 
 the relation of the structures to each other in a severe case of 
 interstitial gingivitis and pyorrhoea alveolaris. The tooth is 
 attached at only a very small portion of the apical end of the 
 root. The disease has been of long standing. Absorption of the 
 alveolar 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 boi'der and extended through 
 the periosteum (H), peridental membrane (I) and alveolar 
 process (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 fistulous tract is the epithelium layer next to the tooth. It is 
 evident that the pus burrowed to the snrfice 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 bv 
 
116 INTERSTITIAL GIXGIVITIS. 
 
 the movement of the tooth has caused the cementoblasts to 
 deposit large quantities of material upon the sides and the end of 
 the root. The main nei've trunks (U) may be seen at and below 
 the end of the root. 
 
 Fig. 43 illustrates the alveolar border on the right side of 
 Fig. 40, greatly amplified. This shows the progress of intersti- 
 tial gingivitis extending through the alveolar process producing 
 absorption with intense inflammation of the peridental membrane 
 and abscess with fistulous tract. 
 
 Fig. 44 shows a similar process amplified from the left side of 
 Fig. 42. 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 023j)Osite 
 direction from those in the other side of the tooth, and in other 
 illustrations. The fibers from the mucous 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 o'ingival border. 
 
CHAPTER XI. 
 
 MERCURIAL INTERSTITIAL GINC4IVITIS IN DOGS. 
 
 To secure a chain of evidence that interstitial gingivitis (due 
 to the metals, drugs, uric, lactic and other acids) commenced in 
 the papillary layer of the sub-ej^ithelial, mucous membrane, I 
 instituted a series of experiments in mercurialization of dogs. 
 
 Proj. 14 inch, ocular lii inch. Spencer. 
 
 Fig. 4.5. — Longitudinal Section op Gingival Boedke, Showing Eound-Cell 
 Inflajimation Due to Mercurial Poisoning. 
 
 Dogs for the purpose were picked up in the streets. Some 
 of these were operated upon by myself, but most of them were 
 under treatment at the Post-Graduate Medical School. Care 
 Avas taken to secure those in health and with healthy gums. 
 Mercury was introduced l)y the mouth, skin and liypodermic 
 
118 
 
 INTERSTITIAL GINGIVITIS. 
 
 injection. It was no easy matter to get them under influence 
 of the drug, since the power of the glands to elimina,te the poison 
 was enormous. In no case was salivation produced. The first 
 symptom noticed was exhilaration, which would last from three 
 days to a week. 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 poison. There was a 
 
 Pantachr. oil imm. iV inch ocular. No. 3. Leitz. 
 
 Fig. 46. — Longitudinal Section of Gingival Border. Higher Magnification, 
 Showing Connective Tissue Infiltration with Plasma Cells and Polynu- 
 
 CLEAR LeUCOSYTES. 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 
 diseased. The time required to obtain results was from three to 
 eight weeks. The age and physical condition of the dog caused 
 
MERCURIAL INTERSTITIAL GINGIVITIS IN DOGS. 
 
 119 
 
 this variation in time. After death the gum tissue was dissected 
 from different parts of the jaws and phxced in either fifty per 
 cent alcohol, Miiller's fluid, or two per cent formalin. 
 
 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 
 methods : Delafield's hsematoxylin, eosin (Unna's), alkalin 
 methylblue, carmin, Gramm's stain, etc. 
 
 Fantaclir. oil imm. i\ inch ocular. No. :i. Leitz. 
 
 Fig. 47. — Longitudinal Section of Gingivat, Boedek. Higher Magnification, 
 Showing Round-Cell Inflammation Extending to the Inner Coat of the 
 Blood Vessel and also Plasma-mast Cells. 
 
 Microscopic examination showed that the epithelial lining of 
 the gums did not present pathologic changes, but appeared 
 normal in every respect. Connective tissue below the gum 
 epithelium (the tissue analogous to the papillary layer of the 
 derma and the derma proper) presented unmistakable evidences 
 of a mild inflammatory process. There occurred in this con- 
 nective tissue round-cell infiltration, oenerallv moderate l)ut in 
 
120 
 
 INTERSTITIAL GINGIVITIS. 
 
 some places quite dense. This cellular infiltration extended 
 from below (where it was densest) upward into the papillary 
 layer (Figs. 45 and 46). The densest cellular infiltration 
 usually occurred around the vessels (Fig. 46). 
 
 Under high magnification, the cellular infiltration was found 
 to consist of polymorphonuclear leucocytes, plasma cells and 
 
 Projection % inch, ocular 1'/^ incli. Spencer. 
 
 Fig. 48. — Longitudinal Section or Gingival Boeder, Showing Round-Cell Infil- 
 tration IN the Connective Tissue and Extending into the Papill.e. Dog. 
 
 plasma-mast cells, the latter with coarse basophilic granulations 
 (Figs. 47 and 48). 
 
 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. 49). No 
 bacteria were found either in the areas of cellular infiltration 
 (inflammatory areas) or elsewhere. In these cases it is obvious 
 that there had occurred a mild inflammation of the gums (gingi- 
 
MERCURIAL INTERSTITIAL GINGIVITIS IN DOGS. 
 
 121 
 
 vitis). While this couhl not be seen with the naked eye, 
 microscopic examination demonstrated histologic features of an 
 inflammatoiy process. The absence of bacteria justified the 
 belief that this inflammation was not of microbic origin, but due 
 to mercury, which by its well-known chemotactic influence pro- 
 duced the histolos'ic changes of an inflammation. 
 
 Pantachr. oil imm. 
 
 iich ocular. No. 
 
 Fig. 49. — LoxtiiTUDiNAL Section of Gingival Border, Showinu Round-Cell. 
 Inflam.mation Due to Mercurial Poi.soninci. Higher MAcisiFicATiON. 
 
CHAPTER XII. 
 
 BACTERIOLOGY OF INTERSTITIAL GINGIVITIS. 
 
 The bacteric etiology of interstitial gingivitis has been inci- 
 dentally discnssed by many wi'iters. 
 
 Gali2325e' was probably among the first to make analytic 
 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 j)ig, 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- 
 ments as suggestions for further research, but not demonstra- 
 tive. Miller," after explaining his 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. Staj)hylococcus 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 con- 
 nective tissue Among the nine species found in 
 
 dogs, staj)hylococcus pyogenes albus occurred once. Of the 
 -other eight, two subcutaneously injected caused no reaction, and 
 five but slight. One caused very profuse sujjpuration, by which 
 
 large portions of skin exfoliated Microscopic exami- 
 
 jnation 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 jjyogenic properties, but was not able to 
 
 ' Die Infectiose Arthro-Dentiiire Gingivitis, 1888. 
 ^ Micro-Organisms of the Human Mouth. 
 
BACTERIOLOGY OF INTERSTITIAL GINGIVITIS. VIS- 
 
 determine the constant occurrence of any one which might be 
 regarded as the si^ecific micro-organism of pyorrhcea alveolaris. 
 jNIiller remarks that it is not evident from Galippe's communica- 
 tion whether he found the N or ,3 bacterium in all cases exam- 
 ined, or but once. 
 
 Sudduth, after repeated examinations, arrived at the same 
 conclusion as INIiller. 
 
 The results obtained in the Columbus INIemorial Laboratory 
 of Chicago, by W. A. Evans, Avere as follows : 
 
 In order to determine wdiether 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 fifty 
 cases was examined. In all, the pus was obtained from the gums 
 by a platinum needle under proper methods of sterilization. The 
 pus from some cases was smeared on a slide. This was stained 
 and such determination made as was possible with this proce- 
 dure. With the pus from fifteen cases, agar was inoculated 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 were found. In two there was 
 no growth. 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 excep- 
 tionally 23athogenic to man, and those never pathogenic to man. 
 The first class was found thirty times, the second twelve, and the 
 tliird thirteen. Class third is, no doubt, seemingly smaller than 
 it sh(juld 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 diplococcus, growing like 
 pneumonococcus, was found six times. Streptococcus pj^ogenes 
 was found twice. Bacillus coli commune w^as found twice. A 
 bacillus growing like the diphtheria bacillus occurred twice. 
 This last bacillus had the appearance of the Kleb-Loeffler bacil- 
 lus. It lay on the slide like it and it stained irregularly. Of 
 the less important organisms, bacillus jjyocyaneus was found thi-ee 
 times, micrococcus tetragenus seven times, leptothrix seven times. 
 
124 INTERSTITIAL GINGIVITIS. 
 
 bacillus meseutericus twice, bacillus subtilis three times. There 
 was also j)i'esent 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, Galipj^e 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. 
 
 M. Herzog, of the Chicago Polyclinic, on examination of 
 cases of iutei'stitial gingivitis, which had not reached the i^yor- 
 rhoeic stage, had the following results : Pieces from the gum mar- 
 gin which had been fixed and hardened in a formalin solution, 
 were partly imbedded in celloidin, jmrtly in paraffin. The sec- 
 tions 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 23eriosteum, 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 lym2:)hocytes, 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 sup- 
 ply of the connective tissue apj^ears to be considerably increased 
 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 tyjje 
 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 
 
 ' Some Points on the Etiology, Pathology and Treatment of Pereistent Pyorrhoea 
 Alveolaris. 
 
BACTERIOLOGY OF INTERSTITIAL GINGIVITIS. 125 
 
 American IMedical 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 ^his 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- 
 rhrea and pus from a chronic ulcer ; j)us infection resulted. 
 
 Like experiments were made in the human mouth on gums 
 which had been neglected as well as on healthy gums, and with 
 similar results. His experiments tend to show that, when animals 
 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 ])yo- 
 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 exjjerimental inoculation. 
 The jsrevalence 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. 81ight inflammation, and, in one case, a little supjjuratiou 
 alone resulted. He afterward isolated twenty different bacteria 
 from the human mouth and nine from dogs. Some of the 
 uncommon varieties were infective, but without marked results. 
 Isolated varieties would probably not produce results that could 
 be attained by inoculating animals with the fresh secretion (j^us 
 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 were of 
 all breeds and conditions. Some were well fed, others very thin. 
 Many had sound, healthy gums ; others had slight inflammation 
 
 ' Micro-Orijanisms of the Human Mouth, page 329 
 
126 INTERSTITIAL GINGIVITIS. 
 
 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 jarocess and ^^eridental 
 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 second pre-molar was 
 selected because it is the least prominent. The secretions about 
 the teeth and gums 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. Su]3pura- 
 tion was slight in four and considerable in three. The j^atho- 
 logic findings in these cases were not unlike inflammation and 
 infection in other tissues. Similar results would, no doubt, have 
 taken place if inoculation had been performed with j)us from an 
 abscess. The last three dogs were allowed to dej)art at the end 
 of four weeks with slight pus infection. 
 
CHAPTEE XIII. 
 
 . SCORBUTIC INTERSTITIAL GINGIVITIS IN MAN. 
 
 While hundreds of slides could 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 (hsemorrhagic 
 gingivitis); chronic aortic and mitral endocarditis; fibrous 
 myocarditis ; chronic nephritis ; caseo-calcareous areas in the 
 right apex, spleen and left adrenal ; double hydrothorax ; bron- 
 chitis ; 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 j^lates 
 Avere 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. Ac/ar 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 tulndar in deeper 
 
128 INTERSTITIAL GINGIVITIS. 
 
 jDortions. Flocculent masses throughout. Glucose Agar: Gas 
 produced, white, thick growth on top. Milk : Alkaline, soft 
 coagulation. Botiillon : Cloudy. Characteristics : Rapid growth, 
 a sour, nauseating odor given oflF from all media. Morjihology : 
 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 peripheral 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 cauliflower. Gelatin Slab : Liquefied, saucer-shaped 
 at top, tubular in deeper part. Growth mostly in upjoer stratum. 
 Lit. llilk : Negative. Bouillon : Cloudy. Glucose Agar : 
 Gas i^roduced. Characteristics : Rapid growth, stinking odor 
 from all media. Morpholoyy : Small, slender bacilli ; actively 
 mobile, spores. Takes ordinary stains readily and is not decol- 
 orized by Gram's method. 
 
 Only the lower frontal teeth and corresponding j^ai't of the 
 jaw could be examined. The epithelial covering of the gums 
 appeared to be quite intact. In 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 flbrous, 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 jDlaces 
 small sub-epithelial abscesses were met with, which (in the instance 
 of a district including a lower incisor) were really subperiosteal. 
 The contents consisted of nuclear detritus and bacteria (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 (capillaries) with 
 typical bacteria masses, staining a peculiar bluish violet color 
 
X 40. 35 M.M. Zeiss. Micro-photograph, reduced one-third 
 
 Fig. 50. — Longitudinal Sechon op Tooth, Alveolar Process and Gingival Border, 
 Showing Active Inflammation in Scurvy in Man. 
 
 B, Dentine. C, Ceinentiim. E, Epithelial Tissue. G, Submucous Membrane. 
 
 H, Periosteum. J, Alveolar Process. L, Haversian Canals. M, Fibrous Tissue. V, Violent 
 
 Inflammation. AA, Point of Union of Epithelial Tissue and Peridental Membrane. 
 RR, Space Pocket from Want of Union of the Epithelial Fold. 
 
X 40. 35 M.M. Zeiss. Micro-photograph, reduced one-third. 
 
 Fig. 51.— Longitudinal Section of a Tooth, Alveolar Process and Gingival Boeder, 
 Showing Active Inflammation in Scurvy in Man. 
 
 B, Dentine. C, Cementum. E, Epithelial Tissue. G, Submucous Membrane. V, Violent 
 Inflammation. Z, Sloughjng of the Epithelial Tissue Due to Calcic Deposits. AA, Point of 
 Union of Epithelial Tissue and Peridental Membrane. 
 
X r.'i. A. A. iil)j. ZrisK. MicrO'iihotograpti, reduced one-third. 
 
 Fig. 52. — Longitudinal Section op Tooth, Alveolar Process and Peridental Membrane, 
 
 Showing Blood Pigment in Blood Ve.ssels of Peridental Membrane in Scurvy in Man. 
 
 i 
 
 C, Cementum. J, Alveolar Process. K, Capillaries. V, Inflamed Peridental Membrane. 
 
 K', Blood Pigment in Capillaries. 
 
X 75. A. A. obj. Zeiss. Micro-pliotograpli. reduced one-third. 
 
 Fig. 53. — Longitudinal Section of Tooth and Gingival Boeder, Showing Active Inflam- 
 mation Extending thkough the Mucous and Peridental Membranes. Scurvy in Man. 
 
 B, Dentine. C, Cementum. 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. 
 
SCORBUTIC INTERSTITIAL GINGIVITIS IN MAN. 133 
 
 with hematoxylin, and blue with Gram's method, so that the 
 vessels i^resented the appearance of being very successfully filled 
 by an infection mass : the small dilatations, the branches and the 
 larger vessels (judging from structure 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 process, being confined (as far as there 
 was occasion to observe) to the external aspect of the jsrocess. 
 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 
 trabeculse were generally covered by a thin layer of osteoid 
 tissue, which (from the greater number of cells it contains, as 
 compared with the other bones) must be newly formed. Rows of 
 osteoblasts were found often ujion the trabeculse. Few How- 
 ship's lacunae 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 is quite unchanged. 
 
 The "bacterial thrombosis " not unusually extended into the 
 peridental membrane, which then refused to stain as clearly as 
 normal. The upper Y)art 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 ; calcified, 
 concentrically lamellated, round or oval bodies, not unlike the 
 " corpora amylacea." In many instances, it seemed as if the 
 body had formed in the cement or at its margin — the cement 
 presenting here a nodular condition. 
 
 Fig. 50 illustrates a section through the tissues of the jaw 
 
 ' 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. 
 
134 INTERSTITIAL GINGIVITIS. 
 
 and cusjjid tooth. The epithelium 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 
 ujion itself, formiilg a j)ocket (R R). 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 j)eriosteum contrast decidedly with the finer fibers of the 
 sub-epithelium. Absorption and contraction of the alveolar pro- 
 cess (fully one-half the length of the root of the tooth), has taken 
 place, as well as lateral absorjjtion. The inflammatory process 
 extends through the Haversian canals (L). 
 
 Fig. 51 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 
 extends throughout the entire submucous membrane (G). The 
 most marked inflammation in this case is entirely upon the 
 outer border (V). 
 
 Fig. 52 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 ^ligment containing bacteria are notice- 
 able (K'). 
 
 Fig. 53 is an amplification of a section depicted in Fig. 50. 
 This gives a clearer idea of the folding of the eiiithelium (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 jjoint 
 of union of the sub-epithelial layer and the periosteum is shown 
 (AA). 
 
 Fig. 54 illustrates inflammation of the peridental membrane 
 with epithelial debris (W) scattered over the field. Endarteritis 
 
X V5. A, A. obj. Zeiss. Micro-photograph, reduced one-third. 
 
 Fig. 54. — Ckoss Section Peridental Membrane, Showing Active Round-Cell Inflamma- 
 tion. Scurvy in Man. 
 
 'C, Cementum. V, Violent Inflammation. AV, Epithelial Debris. EO, Endarteritis Obliterans. 
 10 135 
 
X 75. A. A. obj. Zeiss. Micro-photograph, reduced one-third. 
 
 Fig. 55. — Cross Section op 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, Endarteritis Obliterans 
 W, Epithelial Debris. 
 
 ISp 
 
X ;5. A. A. obj. Zeiss. Mioro-photograpli, reduced one-third. 
 
 Fig. 56.— Ckoss Section op Tooth, Alveolar Phocess and Peridental Membrane, Showing 
 Active Infl.\mm.\tion and Absorption op Bone. Scurvy in Man. 
 
 C, Cementum. I, Peridental IMembrane. J, Alveolar Process. P, Perforating Canal Absorp- 
 tion. V, Violent Inflammation. 
 
X 40, 35 M.M. obj. Zeiss. Micro-iDhotograpli, reduced one-third. 
 
 Fig. 57. — Cross Section op Peridental Membrane and Alveolar Process, Showing Active 
 Inflammation and Ab,sce.ss. Sci'kvy in Man. 
 
 J, Alveolar Process. T, Bacteria. Y, Abscess. I', Inflamed Peridental Membrane. 
 L, Inflammation Extending through Enlarged Havereian Canals. 
 
X 75. A. A. obj. Zeiss. Micro-photograph, reciuced one-third. 
 
 Fig. 58.— Ceoss Section op Peridental Membrane and Alveolar Process, Showing Active 
 Inflajimation and Another Larger Abscess. Scurvy in Man. 
 
 J, Alveolar Process. P, Perforating Canal Absorption. V, Violent Inflammation. 
 Y, Abscess. I', Inflamed Peridental Membrane. L', Inflammation Extending through Enlarged 
 Haversian Canals. 
 
140 
 
 INTERSTITIAL GINGIVITIS. 
 
 obliterans (EO) is also noticed at various j)Ositions. Marked 
 inflammation may be seen at V. 
 
 Fig. 55 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, 
 nearer the alveolar process than the root of the tooth. Epithe- 
 lial debris are evident at W. Endarteritis obliterans (EO) may 
 
 X 300. Nu. ;i piujeciion ocular. D. D. obj. Zeiss. 
 
 Fig. 59. — Cross Section of Tooth, Alveolae Proce,ss and Peridental Membrane, Showing 
 Active Inflammation with Calcospherite in Membrane. Scurvy in Man. 
 
 B, Dentine. C, Cementum. I, Peridental Membrane. J, Alveolar Process. HH, Calco- 
 spherite. J', IntiamedtPerideutal Membrane. L', Inflammation Extending through Enlarged 
 Haversian Canals. 
 
 be seen in different portions of the field. Inflammation has 
 extended into the Haversian canals (L) but absorj)tion has not 
 occurred to any great extent. The blood vessels of Von Ebner 
 (BB) are quite well shown. 
 
 Fig. 56 is a section shoAving the cementum (C), the peri- 
 dental membrane (I) and the alveolar process (J). Marked 
 
SCOKBUTIC INTERSTITIAL GINGIVITIS IN MAN. 141 
 
 inflammation extends through the 2)eridental membrane, thence 
 through the Haversian canals (which are entirely obliterated). 
 Absorption of the trabeculis (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. 57 shows a section of the peridental membrane and 
 alveolar process with a large abscess originally within the 
 alveolar wall. Inflammation spreading through the peridental 
 membrane has occurred at I', while the decalcified alveolar 
 process is also shown (J). Violent inflammation has taken 
 p)lace 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 diflferent stages 
 in the process by which this has been accomplished are beauti- 
 fully shown. 
 
 Fig. 58 illustrates a larger abscess (Y) from another loca- 
 tion. This is also situated within the alveolar wall, showing 
 that the inflammatory j^roducts extend through the blood ves- 
 sels. Marked inflammation is seen upon the side next to the 
 peridental membrane (I')> while rapid absorption — halisteresis 
 (Q) and perforating canal (P) — is proceeding at the borders 
 of the abscess and nearest the alveolar process. 
 
 Fig. 59 shows a section of a tooth (B and C), inflamed 
 jjeridental membrane (I')) with absorption of the alveolar pro- 
 cess (J). In the inflamed peridental membrane may be seen 
 a calcospherite, oblong in form. 
 
CHAPTER XIV. 
 
 INTERSTITIAL GINGIVITIS IN MAN FROM DRUG ACTION. 
 
 A fortv-eight-year-old merchaut was dysiDeptic, debilitated 
 and asthmatic, aud for the treatment of these conditions he had 
 been nndei- calomel and tonics for a little less than two weeks. 
 When he came nnder observation, the mucous membrane and gums 
 
 were then much 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 mv sugges- 
 tion, his medical attendant sto^^ped the calomel. He was then 
 ordered' six pints of spiring water daily. The gums were, on 
 alternate days, saturated with iodin. In a few days the soreness 
 and swelling were so reduced that the deposits could be removed. 
 The patient was discharged cured in a short time other than as to 
 the right inferior second molar, which was so loose as to require 
 removal. This tooth was j^laced immediately in fifty j^er cent 
 alcohol for twentv-four hours and then removed to absolute 
 
INTERSTITIAL GINGIVITIS IN MAN FROM DRUG ACTION. 143 
 
 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. 60 shows a small fragment of inflamed 
 peridental membrane. Fig. 61 exhibits violent round-cell inflam- 
 mation, degeneration and liquefaction of tissue. 
 
 A thirty-flve-year-old diabetic painter came under observation 
 for jihmibic poisoning. His gums were swollen. There was 
 decided sialorrhoea. The teeth were loose. Pus flowed from the 
 
 Fig. G1. 
 
 gums. He was placed on ozonate spring water and the gums 
 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 bicuspid gave results on micro- 
 sco^jic examination similar to those already described as occurring 
 in mercurial poisoning. Fig. 62 shows round cells of inflamma- 
 tion. Fig. 63 illustrates very marked degeneration of the peri- 
 dental membrane. In the lower right-hand corner are seen the 
 root of the tooth, dentine and cementum. The whole surface of 
 
144 INTERSTITIAL GINGIVITIS. 
 
 the peridental membrane is in an advanced phase of inllamma- 
 tion. Just at the border of the root is evident an area of mem- 
 brane 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 >Yhich 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 
 is detectable on the necks of the teeth between the croAvns and 
 the gum insertion. This is most obvious in the upper jaw. 
 After a while, as E. Hogben^ has shown, the teeth become 
 
 Fig. 62. 
 
 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 gingivitis. 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, produc- 
 ing irritation of the mucous membranes of the mouth and else- 
 where, may act as predisposing and exciting factors of interstitial 
 gingivitis.^ 
 
 ' Birmingham Medical Review, 1887. 
 ^ Lewin : Untoward Effects of Drugs. 
 
INTERSTITIAL GINGIVITIS IN MAN FROM DRUG ACTION. 
 
 145 
 
 Among the drugs which shouhl be taken into account in the 
 •etiology of interstitial gingivitis is potassium bromide. Tliis 
 produces in certain indivichials, or when given to excess, marked 
 increase of the saliva with ii-ritation 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 tendency to irritate all the mucous membranes of 
 the body as well as the skin. Therefore, in dealing with cases 
 •of interstitial gingivitis in which the bromides are being taken, 
 this factor should not be neglected. In these cases the symptoms 
 
 ■tine to the bromides are apt to be charged to the nervous state for 
 which the bromides have been given. The irritation of the 
 nuicous membrane by the liromides may occur quite early among 
 the untoward effects produced by them. In all probability the 
 bromine 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. 
 
 ' Alienist and Neurologist, July, 1S9(!. 
 
CHAPTER XV. 
 
 CONCLUSIONS. 
 
 "While, as ali'eady shown, the teeth originated in the epider- 
 mis, still, even as early as the sharks, the teeth of the mouth 
 departed from this primitive method of development, since they 
 did not arise on the surface, but deep down, as Minot' has 
 pointed out. As Hertwig has shown, this occurs because the 
 dentiferous epithelium grows down into the dermis, forming an 
 oblicjue shelf, which may be regarded as a sj)ecial tooth-forming 
 organ. On the under side of the shelf the teeth are developed 
 in the same way as over the skin, although they are much larger. 
 The teeth are, however, in various stages of develojjment, and 
 only one is fully exposed ; when, as happens in time, it is lost, 
 the next tooth behind rej^laces it. Since the production of new 
 tooth germs goes on in adult life, replacement of the tooth in the 
 shark's jaw continues indefinitely ; hence sharks are termed 
 polyjihyodont. Mammals, having two sets of teeth only, are 
 called diphyodout. There is, therefore, even in mammals where 
 the change is limited, a tendency to change. Since the human 
 being and the higher mammals (noticeably the omnivora, like 
 dogs, whose food is as varied as that of man) are born jjractically 
 toothless, this struggle begins between the teeth at a later time 
 than in the lower vertebrates. 
 
 The teeth are temporary structures, intended to be shed at 
 certain times ; the temporary set ere the onset of puberty, the 
 permanent with the onset of senile involution at the jDremonitory 
 jieriod of old age. This last period depends on the individual 
 rather than the number of years lived. At the senile j^eriod, 
 which may occur at any time after the eruption of the perma- 
 nent set, osteomalacia (which is the normal absorption of the 
 alveolar process) may take place. The period at which this 
 commences de^^ends upon the constitution of the patient. 
 Through congenital defect or disease, senility may begin earlier 
 
 ' Human Embryology. 
 
coNCLusioisrs. 147 
 
 in life. In certain types of degeneracy (precocity, for example), 
 senility with absorption of the alveolar process may begin even 
 at twenty. Absorption of the alveolar process and loss of the 
 permanent teeth, is, therefore, certain at a period dependent 
 upon the constitution of the patient. Between these two periods, 
 birth and senility, two sets of teeth have been furnished man. 
 In the meantime, the alveolar process, the gums, periosteum, 
 peridental membrane, blood vessels, nerves, have come and gone 
 to suit the convenience of these two sets of teeth. Tissues like 
 these are called adventitious or transitory. Adventitious tissues 
 are much more apt to be affected by disease than permanent in 
 type and persistent in function. 
 
 As transitory structures, destined to fulfill temporary jjur- 
 poses, the teeth of necessity tend to decrease in number with 
 advance in development for the benefit of the organism as a 
 whole, thereby preventing waste of nutriment on useless struc- 
 tures. The shapes of teeth hence vary in order to adapt them- 
 selves to the work and surroundings produced by evolution. 
 The teeth and its setting being of different structures and com- 
 position, each proceeds to destruction along lines imposed by the 
 laws of its structure. The tooth is destroyed by decay, the 
 alveolar process by inflammation. Decay of the tooth and inter- 
 stitial gingivitis are expressions of that natural line of involution 
 which is foreshadowed from the outset in both by laws of their 
 development. The laws governing transitory structures natu- 
 rally place these at the mercy of both under and over stimulation. 
 From its jjosition, location and functions the mouth is of neces- 
 sity exposed to invasion of microbes. These tend directly and 
 indirectly, from infection and through their toxins, to aggravate 
 the effects of both under and over stimulation. Not only do the 
 very structure and embryogeny of the teeth and alveolar process 
 expose them to the too early onset of the processes of removal, 
 initiated by under and over stimulation, but these last increase 
 and are increased by the local results of constitutional defects, 
 like idiocy, and diseases, like tabes dorsalis, paretic dementia, 
 and allied disorders, as well as the results of injuries to the jaw. 
 
 When more work is required of one tooth (as when the 
 dental arch is broken by the loss of one or more teeth, and the 
 others have moved out of their normal jiosition, or when a seam- 
 
148 lyXEESTITIAL GINGIVITIS. 
 
 stress bites her thread with one or more teeth, or when plates are- 
 attached or come in contact with natural teeth, or when a piece 
 of bridgework is adjusted) and the roots of one or two teeth 
 must supjjort and do the work of a greater number, this charac- 
 ter of adventitious structure j^redisjDOses to inflammation about 
 the root or roots of the teeth. 
 
 When due to irregularities of the teeth, or when antagonizing 
 teeth have been extracted, or in the mouths of idiots, paretic 
 dements, etc., who do not use their teeth, understimulation also 
 predisposes to inflammation. 
 
 The mass of evidence previously jjresented demonstrates that 
 the causes of interstitial gingivitis are divisible into predisposing 
 causes (which may be subdivided into local predisposing and con- 
 stitutional) and exciting causes. The exciting causes are either 
 constitutional or local, but as a rule are local or have local action. 
 
 The predisposing factors of this disease, as already men- 
 tioned, are : conditions of jaw evolution, transitory nature of cer- 
 tain structures, degeneracy and conditions of previous irritation 
 and inflammation. 
 
 Moreover, in accordance with a general law of j^athology 
 whereby tissues (for example the lungs in pneumonia once 
 attacked by toxic agencies or even by the toxins of germs) 
 acquire a local predisposition to future attacks of disease, the 
 gums and alveolar process often become thus susceptible to con- 
 stitutional and local influences. 
 
 It is obvious from the data given in the chaj^ter upon " His- 
 tory " that interstitial gingivitis is as old as man and that it was 
 observed and discussed by the earliest writers on medicine^ 
 While it is l)y no means improbable that constitutional factors 
 assisted in its early progress in man, still the exciting cause of 
 this disease was tartar. Many skulls from prehistoric jjeriods. 
 exhibit gingivitis wpon the teeth exposed to the influence of tar- 
 tar. This gingivitis extends along the roots nearly or quite to 
 the apices, resulting in absorjDtion of the alveolar process. Upon 
 the surface of the teeth where tartar is absent, interstitial gingi- 
 vitis and absorption rarely occur. The same is true of the 
 teeth of wild animals at large and confined in zoological gardens. 
 In them gingivitis from local conditions, other than tartar, very 
 seldom occurs. The jaws of the skulls of prehistoric periods are 
 
CONCLUSIONS. 149 
 
 always broad, measuring 2.25 to 2.50 inches in diameter. Third 
 molars are always present. The' vaults are very low, the alveolar 
 j)rocess short and thick, and the teeth short. As already shown 
 in the chapiter on the "Alveolar Process," the jaws have been 
 growing smaller until they range in diifereut races from 2.50 to 
 1.75 inches in diameter. Mixed Celto-Teutouic^ races, like the 
 English-speaking peoples and the Scandinavian i^eoples, have the 
 smallest jaws with the most marked deformities as a result. 
 These changes in jaw forms occur, as has been elsewhere shown, 
 in harmony^ with the -law of evolution of the race in face forms. 
 With these changes in jaw diameter there also occurs an altera- 
 tion in the antero-posterior diameter. A change in tooth forms 
 also occurs. Small crowns and long roots replace large broad 
 crowns and short roots. 
 
 These changes necessarily alter the shape and form of the 
 alveolar processes. Instead of being short and broad, they 
 become long and thin. The septum between roots is not as wide, 
 thick or heavy as formerly. The long, thin alveolar process is- 
 more subject to the influence of local irritation and trophic 
 change than the short, thick one. A long, thin alveolar process 
 will be more readily absorbed than a short, thick one. This is 
 demonstrable Avhere the roots of the teeth are situated near the 
 outer border of the process. Disease of the peridental membrane 
 and absorjDtion of the outer plate extends along the roots, expos- 
 ing them throughout their entire length. Similar conditions are 
 noticeable along the palatine roots of the molar teeth in the 
 upper jaw. 
 
 From the length and thinness of the alveolar process result- 
 ant on the evolution of the jaws, the periosteum on one side 
 and the peridental membrane on the other hold the structures 
 together and afford nourishment for the tooth and bone tissues. 
 The blood vessels pass, as elsewhere shown, in a vast plexus from 
 the periosteum to the peridental membrane through the ^^I'ocess. 
 This plexus deposits and removes calcium salts. Potent for good 
 under normal conditions, it is equally potent for evil under states- 
 of irritation and disturbed nutrition. Local irritation is greatly 
 
 ' Keane, Ethnology. 
 
 -Degeneracy : Its Causes, Signs and Results (Talbot). 
 
 Osseous Deformities of the Head, Face, Jaws and Teeth (Talbot). 
 
150 CONCLUSIONS. 
 
 assisted by a peculiar structural variation of the gum tissue (R 
 R, see any figure); accumulation of debris and resultant chemi- 
 cal decomposition producing inflammation. 
 
 Tartar is an active source of local irritation and inflammation 
 of the gum margin. This in turn extends through the capilla- 
 ries to the alveolar process. Calcic deposits are a result and not 
 a cause. 
 
 A predisposing cause for local inflammation is that of approx- 
 imal tooth decay or cutting away the apj)roximal surfaces for the 
 purpose of filling this class of cavities. If the teeth be not so 
 contoured (Bonwill) as to retain them in their proper positions, 
 absorption of the alveolar process between the roots will take 
 ]3lace, thus bringing the crowns in contact. The result of such 
 absorption will restrict bone surface for the protection and nour- 
 ishment of the gum tissue. Undernourished tissues are hence 
 more liable to irritation and inflammation. 
 
 When death of the pulp occurs, the teeth often become loose 
 without inconvenience to the patient. This results from the for- 
 mation of gases in the pulp chamber, which sufiice to produce 
 inflammation of the peridental membrane with or without pain. 
 This occurs, since slight irritation only is needed to produce 
 absorption of the alveolar process, at the apicial end of the root. 
 Chronic inflammation of the peridental membrane and the 
 flbrous tissue of the alveolar process occurs. The teeth finally 
 become loose. Irritation from movements of the tooth increase 
 the inflammation through the Haversian canals and further 
 absorption takes place, until the tooth is exfoliated. 
 
 This disease from the onset of gum inflammation may proceed 
 for years without pain. Indeed, not until the formation of 
 abscess, or until absorption has affected the nerve at the end of 
 the root does pain occur. Slight soreness may be felt after the 
 tooth begiias to loosen. Absorption of the alveolar process and 
 exfoliation of the tooth may occur without any pain whatever. 
 
 In the chapter upon " Transitory Structures," it has been 
 shown that the alveolar processes have their structures arranged 
 to accommodate the teeth. When the teeth are extracted, the 
 alveolar j^rocess becomes entirely absorbed. The periosteum, 
 peridental membrane and fibrous tissues are entirely lost. The 
 mucous membrane and gum tissue so contract that none of the 
 
CONCLUSIONS. 151 
 
 original struc'turc remains. Absorption of the alveolai' process is 
 very eomnion in advanced age. Even when the teeth remain in 
 the jaw in old age, whether of man or animal (this is es^^ecially 
 noticeable in old dogs), absorption of the alveolar process con- 
 tinues. This is due to the fact that the alveolar jirocess, esi^ecially 
 when long and thin, is composed of cancellated bone structure 
 which is easily acted upon by its abundant blood and lymph sup- 
 ply. This produces absorption upon the slightest stimulation or 
 irritation of nerve fibers. Even such slight factors as heat, brain 
 overstrain, and want of proper articulation and occlusion and 
 imjjlantation of the teeth, suffices so to stimulate the nerve fibers 
 as to jDroduce absorj^tion. There are four varieties of absorption ; 
 osteoclast or lacunar absorption, penetrating canal absorption, 
 halisteresis, and osteomalaciary absorption. These have already 
 been beautifully shown in the illustrations. It is, therefore, not 
 astonishing that the slightest local irritation or tissue nutrition 
 disturbance from constitutional causes suffices to jDroduce local 
 tissue change. This unstable condition of structures tends to 
 j)revent successful implantation of teeth. 
 
 The question has arisen whether there exists a specific 
 bacterium, which bears the same relation to the pyorrho?ic 
 stage that the strej^tococcus does to streptococcus diphtheria. 
 This question, raised by Galippe, must, in the light of careful 
 research, be regarded as settled in the negative. No special 
 bacterium has been found which complies Avith the laws of Koch. 
 Dogs are liable to this disease. Galippe had but to infect their 
 gums with his bacterium to demonstrate its s^jecific pathogenic 
 activity. He has not done this. As the researches (already 
 cited) also failed to find a bacterium which could comply with 
 this test required by the laws of Koch, it must be admitted that 
 there is no bacteriologic evidence of a sj^ecific bacterium. 
 Furthermore, the pathologic evidence demonstrates that bacteria 
 23lay the very subordinate role in this disease that they do in 
 ordinary wound infection. 
 
 PATHOGENESIS OF INTEKSTITIAE GINGIVITIS. 
 
 Inrianiniation of the gums and deeper structures chiefiy 
 results from mechanic and chemic (lactic and uric acid, ])Otas- 
 sium iodide, mercury, etc. ) causes, bacterial influence being an 
 
 11 
 
152 I]S'TEESTITIAL GINGIVITIS. 
 
 incidental complication. From their action, the blood stream is 
 increased and dilatation of the capillaries is produced. The 
 capillaries become crowded with blood corpuscles. These 
 accumulate along the walls of the blood vessels, to which they 
 appai'ently adhere. Accumulations of small, round cells occur, 
 in the submucous connective tissue, the spaces of which are 
 filled with inflammatory exudate. The papillte become enlarged. 
 The epithelial layer becomes hyperplastic. As a result, the gum 
 tissues swell and become intensely crimson. They bleed upon 
 the slightest touch. 
 
 Inflammation may be confined to a single point upon the 
 side of a tooth. This localization often results from predisposi- 
 tion due to a local injury, originating in a cavity in the tooth 
 ■with sharp, rough edges, from overlapping fillings or from too 
 frequent and violent use of the toothpick at one point. As a 
 result, granulation tissue forms, which (according to Sudduth) is 
 often due to the irritation of lactic acid.' In the production of 
 this, however, the influence of the lactogenic bacteria on particles 
 of food cannot be excluded. 
 
 The peculiar formation of the gum tissue on the inner border 
 of the gingivus into a pocket or cul-de-sac (RR in Figures) here 
 described for the first time, is a- fertile source of this irritation 
 and consequent inflammation, from its collection of resultant 
 decomposition of foods. This pocket varies, as has been shown, 
 in size as well as locality. Sometimes it is very large and deep, 
 or it may be almost, if not entirely, obliterated. Frequently it is 
 situated near the gum margin, again near the union of the sub- 
 nnicous and peridental membranes. The degenerate epithelium 
 cell structure (so-called glands of Serres) is also more liable 
 and more easily irritated than the normal epithelium structure. 
 As in the similar crypts of the penis," the degeneration and 
 death of the epithelial cells with which this cavity is lined 
 produce liy their accumulation a source of irritation as well 
 as culture medium for jjathogenic bacteria. Therefore, not 
 only is the anatomical arrangement of the structures a fruit- 
 ful source for the accumulation of irritative substances, but 
 
 ' I have made examinations of pockets about the necks of teeth and can cor- 
 roborate this statement. 
 2 Medicine, 1898. 
 
coxcij'sioxs. 15B 
 
 the structures tlicmsclvcs ai'c also well adapteil tnr intlainina- 
 tory action. 
 
 The gum tissue abuut one or more teeth may be iujurecl by a 
 badly fitted gohl crown, with rough edges. The gokl crown may 
 be too far down on the I'oot. Injury may result from ligatures, 
 rubber dam and bands left about the teeth after operations. 
 Accumulations of tartar or any local irritation may lead to 
 inflammation varying with the extent of the dej^osit. The extent 
 of the inflannnation will depend upon the nature and duration of 
 the irritating influence. If it l)e local in action and temporary, 
 slight gingivitis results. If it be permanent, gingivitis assumes 
 a chronic type, extends into the fibrous tissue below and becomes 
 interstitial in character. The extent of this interstitial inflam- 
 mation depends upon the nature of the irritation. If the irrita- 
 tion be located upon the side of one tooth, the inflammation will 
 extend through the filjrous tissue in the direction of the course of 
 the blood vessels. It may be in line with the peridental mem- 
 brane. It may be in line with the periosteum, or it may be 
 in direct line with the alveolar process. Interstitial inflammation 
 (if one or more teeth be iuvolved) extends not only through the 
 peridental membrane, but to the periosteum and alveolar process 
 as well, since the capillaries in surrounding structures are in- 
 volved. The inflammation extends into the alveolar jjrocess 
 through the Haversian canals and the blood vessels of Von Ebner 
 by way of the periosteum and peridental membrane. Irritation 
 thereon resultant causes absorption of the alveolar process by ( a ) 
 halisteresis, (b) Volkmann's perforating canals, (c) lacunar 
 absorption (osteoclasts). The interstitial inflammation and the 
 absorption of the alveolar process continues so long as the irrita- 
 tion remains or until the tooth or teeth are exfoliated. Previous 
 irritations often produce osteom.dacia and trophic changes, and 
 thus assist greatly the progress of the pathologic phenomena. 
 Loosening of the tooth or teeth adds a very efiicient irritation 
 which increases the extent of and intensifies the inflammation. 
 Loosening of the teeth is their death knell, no matter what the 
 original cause for the disease may have been. 
 
 The following complications may occur : Endarteritis Oblit- 
 erans, Absorption of the Alveolar Process, Pyorrhoea Alveolaris, 
 and finally Calcic Deposits. 
 
154 INTERSTITIAL GINGIVITIS. 
 
 ENDAETEEITIS OBLITEKANS. 
 
 Endarteritis is an inflammation of the internal coat of an 
 artery or ca|3illary, generally of elironic type. Its pathogeny is 
 as follows : In direct contact with the blood streams is the 
 endothelinni (a layer of flattened cells); next is the tunica 
 intima, comjjosed of elastic fibers arranged longitudinally ; next 
 comes the middle coat, composed of muscular fibers arranged 
 transversely. The outer coat consists of longitudinal connective 
 tissue, Avhich contains the vasa vasorum. In the capillaries, the 
 intima lies in immediate contact with the surrounding tissues, or 
 accomj^anied by a rudimentary adventitia. In other words, the 
 walls of the capillaries consist of almost nothing but the intima. 
 The cajoillaries 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 
 
 , / 
 
 ?-\N ..J 
 
 Fig. 64. — Endarteritis Obliterans (Kaufmann). 
 
 A, Adventilia. E, Elastic Tissue between Middle Coat and Intima. M, Muscular. 
 J, Thickened Intima. 
 
 the intima. Each coat of the arteries takes on s^Decial tyjie of 
 inflammation. The causes of endarteritis are numerous. Inflam- 
 mation of the intima of the blood vessels may be due to irritation 
 from without or within. 
 
 When it occurs from without, any local irritation will set up . 
 an inflammation which may extend to the outer coats of the cap- 
 illaries. This i^roduces a marked increase of blood. The vasa 
 vasorum becomes swollen, the white blood corpuscles crowd into 
 the terminal capillaries and migrate into the extra vascular 
 sj^ace. 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. 64). 
 
CONCLUSIONS. 155 
 
 Irritation occurring from witliin, results either from trophic 
 changes in the system from direct irritation from toxjemias, or 
 from both interdependently. Under these circumstances a germ 
 disease or other toxins may liave an affinity for a certain organ, 
 tissue or part, and produce irritation in the capilhiries in a dis- 
 tinct 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 becomes 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 esiDecially the gums, become 
 diseased. In many of these conditions, 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, neu- 
 roticism and degeneracy, and last, but not least, stomach neuras- 
 thenia. The poison in the bloody together with the diseased 
 Ijeripheral nerves, produce irritation and inflammation of the 
 inner coat of the capillaries. If this irritation does not disap- 
 pear 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, p)i'oliferation of the endothelium occurs. This 
 inflammatory growth tends to obstruct the lumen of the vessel. 
 The media may likewise become thickened by an increased con- 
 nective tissue. The capillaries become obstructed, and finally 
 obliterated. This finally impedes the circulation. Fig. 65 
 shows such a condition in the scurvy case, elsewhere illustrated. 
 
 Irritation may be of less intensity but greater duration, as in 
 case of syphilis, tuberculosis, scurvy, mercurialism, plumbism 
 (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. 
 
 The recent studies of Hektoen' on menino-eal tuberculosis 
 
 'American S3'stem of the Practice of Medicine, page 119. 
 
156 INTEESTITIAL GINGIVITIS. 
 
 demonstrate that tubercle bacilli may penetrate the unbroken 
 endothelial layers of the vessel and stimulate marked pi-oliferation 
 of the sub-endothelial connective tissue. An internal irritant, 
 such as may be 2jroduced in the course of any infectious disease 
 or from suboxidation, probably acts uj)on the endothelium of the 
 walls of the smaller blood vessels in such a way as to permit the 
 escape through the walls first of serum, then of leucocytes, the 
 
 X Ino. D. D. obj. Zeiss. 
 
 Fig. 6o. — Cross Section of Peridental Membrane, Showing Endarteritis 
 Obliterans. Scurvy in Man. 
 
 C, Cementum. D, Dentine. I, Peridental Membrane. V, Nerve Tissue. 
 EO, Endarteritis Obliterans. 
 
 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 througli the 
 blood are forced to remain, hence discoloration of tissue along the 
 gum margin. Interstitial gingivitis, resulting in a slow disturb- 
 
CONCLUSIONS. 157 
 
 ance of uutritioii, piddiices overgrowth of connective tissnc. In 
 all cases of clironir interstitial gingivitis, as shown in the illus- 
 tration, cwv the hlood vessels thus involved. 
 
 Among the pretlispt)sing influences which cause this disease 
 are syphilis, tuberculosis, mercurialism, plumbism, brass poison- 
 ing, lithagmia, nephritis, gout, rheumatism, alcoholism, scurvy, 
 nervous diseases, jjregnancy and old age. Under certain con- 
 ditions of the system any and all diseases which tend to lower the 
 vitality, producing antemia, will assist in producing this disease. 
 The direct cause may be resultant overstrain of the blood vessels. 
 
 Owing to obliteration of the arteriols in the alveolar process 
 stasis of blood nuist follow. The detritus from the alveolar pro- 
 cess, therefore, must remain in tlie tissue and collec-t upmi the 
 roots of the teeth. 
 
 ABSOKPTIOX OF THE ALVEOLAR PROCESS. 
 
 Absorption of the alveolar process is the result of irritation, 
 resultant malnutrition, and subsequent inflammation. The osteo- 
 blasts and osteoclasts are ever present to build up and tear down 
 bone structure on the slightest provocation. Hypertrophy 
 (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 susceptible to these influ- 
 ences. The causes of absorption are loss of teeth liy exti'action, 
 undue pressure upon one or more teeth from improper articulation 
 ( Bonwill ), wedging and ii'regnlarity correction, heat under arti- 
 ficial 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, l)ut 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 with," is certainly very com- 
 mon, while lacunar absorption holds third posititm. This ordei' 
 of absorption is accounted for by the fact that where struc-tures 
 
158 INTERSTITIAL GINGIVITIS. 
 
 are transitory, halisteresis, as quickest method, follows by the law 
 of the survival of the fittest. For the same reason perforating 
 canal absorption should stand second. The blood vessels of Von 
 Ebner being most numerous, although considered smaller, they 
 would naturally be the second tissue involved. As in interstitial 
 gingivitis, absoristion of the alveolar process is invariably due to 
 inflammation, halisteresis apjDarently starts at the larger Haver- 
 sian 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 Ossium («»/«? of salt, trrs/ihu? deprivation) or 
 decalcification, is that process of absorj)tion wherein solution of 
 the lime salts first takes ]3lace, 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- 
 beculse. This absorption follows, as a rule, the bone layers. Bone 
 centers are, therefore, usually the last to be absorbed. Fre- 
 quently decalcification becomes complete ; nothing remaining but 
 the organic matrix or cartilage. Finally, this is also entirely 
 destroyed. As the osteoblasts occur in the matrix or cartilage, 
 it is not difiicult to understand that absorption may extend far, 
 yet restoration of the alveolar process may occur. After destruc- 
 tion of the matrix such a restoration is imjiossible. 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 
 
 ' Special Pathological Anatomy, page 151. 
 -Pathologische Anatomie. 
 
conclusiojSts. 159 
 
 the " vertebrae and thorax ; hiter 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. 
 
 This is due to three reasons : first, to trophic changes ; sec- 
 ond, to the alveolar process? being a transitory structure ; and 
 third, to improj^er 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. At any period beyond that year, it occurs probably from 
 the prematurely senile states of which precocity is a type. The 
 lost tissue is regained often after confinement in the " preg- 
 nancy " 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 Eechlirighausen 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 Rechlinghausen, 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 disea^ie. 
 
 Premature absorption, or osteomalacia of the alveolar process, 
 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 is 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 iR'ulth, struc- 
 
160 
 
 INTEEl^TITIAL GINGIVITIS. 
 
 tural change has taken phice to such an extent that it ever 
 remains a predisiaosing factor to interstitial gingivitis. 
 
 In Fig. 36 may be seen the bhwd vessels of Von Ebner. 
 These blood vessels are also to be observed in Fig. 55. They 
 are very common in the alveolar process and, according to Volk- 
 mann, are the source of the perforating canals which bear his 
 name. 
 
 X60. ;i-incliobj. No. Oc. 
 
 Fig. 66. — Cnoss Section of Tooth, Alveolar Process and Peridextal Mejebrane, 
 Showing Lacunar Arsorptiox. Man. 
 
 C, C'ementum. D, Dentine. I, Peridental Membrane. 
 O, Lacunar Alssorption. 
 
 J, Alveolar Process. 
 
 These canals run in all directions. After absorption has gone 
 on to form medullary spaces, these canals penetrate through the 
 trabeculse from one sj)ace to the other (Fig. 38). The position of 
 this type of absori^tion in the order of fre(piency comes from the 
 fact that, in this disease, absorption is almost entirely due to 
 
('()X('Lrsi().\> 
 
 161 
 
 inflaniination ; licncv the hlood A'eissel.s arc the iirst to liccoinc 
 involved. Those entering the Haversian canals, heing the larger, 
 are first affected, and hence halisteresis naturally precedes. 
 
 When irritation takes place in a nerve or part of bone which 
 is about to be absorbed, nuiltinuclear cells arise at the border in 
 the 2Jei"iosteuni and peridental mend)rane. They attach them- 
 selves to the surface of the bony trabeculie. According to Sud- 
 ilutli, " the absorber and the absorl)ed must be in touch with each 
 
 X 300. No. i. projection ocular. D. D. obj. Zeiss. 
 Fig. 67. — Section of Peridental Membrane, Showing Lacunar Absorption in Dog. 
 .1, Alveolar Process. O, Lacunar Absorption. I', Inflamed Peridental IMenibrane. 
 
 other." Kollikcr has named thvsv cells "Osteoclasts," which 
 tei'iu has come into general use. Very soon after these cells 
 make theii- appearance, cavities ai-e seen in the bone tissue. 
 These cavities are called Howshi])"s laciune. Lacunar al)s()rp- 
 tion, as elsewhere sliOAvn, takes place as a result of irritation and 
 overstimulation. Fio-. 6(5 shows a cross section of the end of one 
 
162 INTERSTITIAL GINGIVITIS. 
 
 of the buccal roots of Fig. 68. As will be observed, this tooth 
 was held in place by two buccal roots. As much resistance was 
 required of these two roots as was formerly required of three. 
 Irritation due to excessive force in mastication was causing 
 absorption. Round-cell inflammation is not present in the peri- 
 dental membrane. The irritation may be continued until inflam- 
 mation sets in and until the bone is entirely absorbed, as noticed 
 in Fig. 67. Small round-cell inflammation is quite noticeable in 
 the surrounding tissue. 
 
 Sometimes these lacunae may be seen extending along the 
 entire length of bone. As many as thirty-seven may be counted 
 in some fields (Fig. 37). Lacunar absorption frequently so 
 extends through the Haversian canals as to cut off pieces of the 
 alveolar process. A casual glance at Fig. 66 demonstrates this. 
 This figure could be multiplied 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 chie 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, absorption 
 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 inter- 
 stitial gingivitis and absorption of the alveolar 2:)T0cess. Absorp- 
 tion of the alveolar process takes place also in diathetic diseases 
 in which the nervous system has been involved (syj)hilis, scurvy, 
 lithsemia, etc.). 
 
 PYOKKHCEA ALVEOLARIS FROM INTERSTITIAL GINGIVITIS. 
 
 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. Absorption of 
 the alveolar process may take place, and exfoliation of the teeth 
 
CONCLUSIONS. 163 
 
 result without jius infection. The tissues may be in a favorable 
 condition for infection, yet the mouth and blood vessels be free 
 from pus germs. This is not uncommon. The tissues are often 
 invaded, however, by micro-organisms, resulting in suppuration. 
 Interstitial gingivitis, with, pus infection in and about the alveolar 
 process, resembles suppuration elsewhere in the body. It results 
 either in an abscess or ulceration. An abscess is a collection of 
 pus within the tissues. Ulceration is a collection of pus upon 
 the surface of the tissues. Both of these marked conditions, 
 being dependent upon intlammation, are associated with intersti- 
 tial gingivitis. 
 
 Suppuration (due to jiyogenic cocci) is the usual termination 
 of infective inflammation. Healthy gum tissue is intolerant of 
 bacteria, and will resist the invasion of micro-organism. When 
 inflammation takes place, the diseased part is unable to resist 
 them. Lowered vitality of tissue is a fruitful source of infection 
 and supj^uration. Since, as Miller' has shown, pus germs are 
 found in almost every mouth, infection is a very probable outcome 
 of gingivitis. 
 
 The organism 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 
 sjDread 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 
 convenient lodging place for swarms of bacteria, OAving to the 
 slowness of the blood current and the tortuous course of the 
 blood channels. When ~ the circulation has been imj^eded or 
 arrested by an extravasation of blood or congestion of a part, the 
 conditions are favorable for intravascular infection if organism 
 happen to be circulating in the blood at the time. As we 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 suppuration 
 in certain localities. 
 
 ' Micro-Orgaiiisms of the Human Mouth. 
 - American Text-Book of Surgery. 
 
164 IXTEESTITIAL GIXGIVITIS. 
 
 Ill whatever part or tissue the change may occur, the j)rocess 
 is the same. The original structures disintegrate. Their place 
 is taken hy 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 
 nutrition by pressure are exposed to the injurious action of 
 micro-organism. 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 most 
 every locality within the peridental membrane, jieriosteum and 
 alveolar ^^I'ocess. These abscesses are just as likely to j^oint 
 upon the surface of the gum as on the inner surface next to the 
 root of the tooth. When abscesses form in and about the 
 alveolar process, with fistulas oj^ening outside of the inner 
 alveolar wall, the disease cannot be entitled pyorrhoea alveolaris, 
 since, as elsewhere shown, strict definition of this title implies 
 pus flowing from the alveolus. 
 
 Abscesses which discharge their contents into the space 
 between the alveolar wall and the root of the tooth, and ulcer- 
 ation of the peridental membrane only, could literally be con- 
 sidered under the head of pyorrhoea alveolaris. 
 
 Abscesses in and about the alveolar process (other than those 
 due to dead pulps) are very common. This is due first to the 
 unstable conclition of the structures, and second to the ready 
 access of ]3us 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 inflamed surfaces of the epithelial layer, and entering 
 the circulation are carried into the deeper structures. Intense 
 inflammation results. Abscesses form, discharging their con- 
 tents upon the surface. Pus germs also enter the deeper struc- 
 tures through exposed pulps. 
 
(■()N(']j'Si()Xs. 165 
 
 Two cases of interest in tliis eoiineetion occurred recently in 
 practice. An active Inisiness man, fit'ty-tive yeai's of age, |>re- 
 seuteil himself Avith an abscess over the buccal roots of the left 
 superior second molar. There were no dead pulj^s in any of the 
 teeth u])ou that side of the jaw. Absorption of the alveolar 
 process 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 rcs-ealed 
 slight angemia. 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. 8ul)sequently 
 he returned Avith anothei- abscess over the root of the right 
 superior central incisor. Live jjulps Avere in all tlie teeth tipon 
 this side as far as the second molar. Infection, therefore, must 
 have occurred through the gnm and peridental membrane. 
 
 The teeth of a lady forty-six years of age were being j^ut in 
 order ; after filling a cavity, May 14, 1899, she called attention 
 to a space between the second and third supei'ior right molars, 
 and stated food lodged at that point, causing pain and bleeding. 
 The space Avas cleansed Avitli an excavator and the cavity 
 syringed Avith Avarm Avater and then explored. Absorption of 
 the gums and alveolar process had extended one-half the length 
 of the buccal root. Applications of iodin Avere made to reduce 
 the inflammation. The patient Avas dismissetl Avith an appoint- 
 ment for May 17. She returned at the appointed time Avith an 
 abscess over the palatine root as large as the thumb. The lady 
 had had acute i^ain from the time she left the oflice until her 
 return. The parts had been infected with i^us germs through 
 the peridental membi-ane. The pus Avas collected in a tin tea 
 spoon, from which cultures Avere obtained and glass slalts 
 smeared for microscojiic examination. The pus was examined 
 by George T. Carjienter for calcic deposits ; the usual asejitic 
 l)recautions having been taken. 
 
 Microscopic examination revealed the usual pus geiins. 
 Chemical analysis for calcic deposits in the pus Avas made as 
 folloAVS : The pus Avas placed in a test tulie with hydrochloric 
 acid (diluted Avith four times its bulk in Avater). The phosphate 
 is dissolved. It is then diluted with Avatei', boiled, and when 
 
160 INTEESTITIAL GINGIVITIS. 
 
 cold excess of solution of ammonia added. The lime salts are 
 then re-precipitated as an amorphous j)Owder. 
 
 Many dentists, ignoring the laws of pathology, insist that 
 intense inflammation in remote parts of the alveolar process is 
 not due to invasion by micro-organisms of an inflamed tissue, 
 but is the result of gouty deposits. The utter lack of foun- 
 dation for this theory must be apparent on the slightest study 
 of pathology. 
 
 Ulceration is always located ujDon the surface of a tissue. 
 When ulceration occurs from contact irritation of the gum margin 
 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 inflannnation. 
 
 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 fllled with 
 foreign material in which decomposition continually occurs. 
 The tissues are thereby constantly irritated. Necrosis occurs at 
 the surface. In the deeper tissues that have become 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 
 deposits of blood pigment (Fig. 52) occur. The surface is 
 covered with granulation tissue. The tissue may, in part, 
 resemble the tj-pe of healthy granulation. It is composed of 
 round cells closely packed together and supplied with rich capil- 
 lary network. Coagulation necrosis from breaking down of 
 granulation tissue may be present. 
 
CONCLUSIOXS. 1<>7 
 
 CONSTITUTIONAL EFFECTS OF J'YOHIUKEA A I.VKOl-AKI.S. 
 
 The influence of" the staine of interstitial iiiiigivitis known as 
 pyorrhoea alveolaris on the system has been (Hsenssed hy .lolni 
 Fitzgerald.' He points out that pj^orrlnjea alveolaris may act in 
 three different ways in the causation of systemic disease. The 
 pus, with its multitude of putrefactive organisms and decayed 
 food remnants from the pus pockets, may be swallowed and either 
 act locally upon tlic stomach Avail or set up fermentation of the 
 stomach contents. The toxins generated in the mouth may be 
 absorbed by the nnicous membrane of the mouth or stomach and 
 thus pass into the general circulation. The local conditions of 
 the mouth may favor the growth of pathogenic organisms, and 
 thus render the patient more liable to certain infectious disorders, 
 noticeably influenza. The power of pyorrhoea alveolaris to pro- 
 duce aggravation of existing gastric trouble reaches its maxinuim 
 in cases where there is retention of food residues. 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 produced, with the result that the stomach 
 is never completely emptied. The first condition is a very fre- 
 quent concomitant of neurasthenia and allied .states. It is easy 
 to see how pyorrhoea can at once be 23redisposed to by neuras- 
 thenic states and at the same time increase the neurasthenia by 
 causing gastric trouble through its interference with gastro-intes- 
 tinal digestion under the conditions mentioned. 
 
 Herschell~is of opinion that nuniy of the chronic indigestions 
 are due to continual absorjition of pus into the system from a 
 pyorrhoea alveolaris. In these cases he remarks there should be 
 other evidences of the absorption of toxins, such as pigment sjiots, 
 urticaria, etc. Fitzgerald points out that the bacterium coli com- 
 mune is a constant inhabitant of the oral cavity, and. as a I'ule, 
 seemingly harmless. Under the influences of a culture medium 
 such as would be furnished by a pyorrhoea or an inHammatory 
 state of the gum, this bacterium might, as elsewhere in the 
 mucous membrane, acquire sufficient virulence to produce serious 
 disturbances of the system, such as colitis, dysentery and cholera 
 nostras. 
 
 ' Clinical Journal, March (i, 1899. '-' Indigentinn, 1.S9-") 
 
 12 
 
168 
 
 IXTEESTITIAL GINGIVITIS. 
 
 CALCIC DEPOSITS. 
 
 There are many instances in which interstitial gingivitis takes 
 place, with absorption of the alveolar process and exfoliation of 
 the teeth, Avithont 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, this waste mate- 
 rial is carried into the circulation. In this way, calcic material 
 
 
 
 
 
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 Rife- ' 
 
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 1 
 
 1 
 
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 ■ 
 
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 4P- 
 
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 1 
 
 1 
 
 1 
 
 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 place. The percentage 
 of teeth so found, however, is not so large as those with deposits. 
 Examination, by a magnifying glass, of a recently extracted 
 tooth (whose root is covered with serumal 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. 68). This condition is due to deposits from the blood, 
 resultant on biochemic chauaes in the inflamed tissues. Blood 
 
COXCLUSTONS. 
 
 160 
 
 stasis occurs in the gum tissue, fibrous tissue of the periosteum, 
 peridental membrane and alveohir process, througli whirl) last 
 nuwh 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 
 deposit 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 
 destroyed. It may encircle the root. The inflammatory process 
 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 not improbaljly 
 soon deposited upon the root or roots because of the impeded cir- 
 culation.' " Ossification, 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 intersti- 
 tial 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 Avere foi-mcd 
 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 exam^^le, to disease or senile change. In 
 composition the blood may be so altered as to contain an abnormal 
 amount of calcareous matter. This effect is most commonly pro- 
 duced by absorption of lime salts from osseous tissues which are 
 the seat of extensive caries, osseous cancer, osteo-sarcoma or osteo- 
 malacia. The calcareous matter thus taken up is conveyed to 
 other and often remote parts and there deposited, constituting the 
 "metastatic calcification" of Virchow. Kuttner, of St. Peters- 
 burg, has observeil a rapid calcification of nearly all of the smnll 
 arteries as a result of cai'ies involving the dorsal and luiubar 
 
 ' Wood's Handbook of Medical Sciences, Vol. I, page 743. 
 
170 INTERSTITIAL GINGIVITIS. 
 
 vertebrae in a niueteen-year-old boy. Virehow has observed & 
 case in which, as a result of bone cancer (aifecting 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. 
 
 Calcification rarely, if ever, depends upon general causes 
 alone. There is, as a rule, a local influence. Very often this is 
 due to preexisting 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 calcification. 
 Such is the case in and about the tissue of the alveolar process. 
 The decalcified material from the alveolar process collects in the 
 soft tissues as well as upon the roots. In his pajjer George T. 
 Carpenter ' asks the question : Can a tissue be absorbed and still 
 remain as debris in the pocket? Such is the condition 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 j^recipitate the phosphate 
 and the calcium. The same results may be obtained 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 precipi- 
 tated. 
 
 Roots of teeth that have become entirely denuded of peri- 
 dental membrane and bathed in pus accumulate large quantities 
 of calcic dejiosits direct from the absorption of the alveolar 
 process. 
 
 Difference of opinion exists as to the nature of the process 
 immediately involved in j)recipitation of lime salts. The simplest 
 and seemingly most logical exjjlanation is that the process is 
 similar to that involved in the formation of stalactites. A certain 
 
 ' Some Points on the Etiology, Patiiology and Treatment of Persistent Pyorrhoja 
 Alveolaris, 
 
CONCLUSIONS. 171 
 
 amount of ealearcoiis matter is a normal constituent of the blood. 
 Herein it is held in solution l)y t'arl)onic acid, always present in 
 sufficient quantity for this jjurpose. When the circulation is 
 impeded the free carbonic acid (because of its great diflf'usil)ility) 
 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 undergoing fatty degenera- 
 tion and absorption. In a fil)rous 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 primarily within the cells. The 
 process may advance slowly or rapidly. AVhen local causes exert 
 the chief influence it is more limited in area of invasion than 
 when there is a general factor in its jiroduction, as in the meta- 
 static forms. 
 
CHAPTER XVI. 
 
 TREATMENT. 
 
 The clinical history of interstitial gingivitis is essentially that 
 of any other disease of the mneons membranes. The disorder 
 responds qnickly to treatment at its outset. Later, its complica- 
 tions and the extent of structure involved render treatment very 
 ineffiacious, 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 possible, so the dental surgeon's 
 duty is to remove the teeth, if need be, for the benefit of the 
 general health, but to save them, when possible, for the same 
 reason. The patient, therefore, should be told 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 practi- 
 tioner of a surgical specialty, not a mere tooth-puller. The sur- 
 gical side of dentistry has received too much attention, however ; 
 the medical or prophylactic too little. Patients are beginning to 
 jiay more attention to the prophylaxis of the teeth and jaws, and 
 need but little encouragement and instruction to see the absolute 
 necessity of early prophylaxis and treatment of interstitial gin- 
 givitis. The trend in general medicine is to j^rophylaxis, and 
 this has undoubtedly so imj^ressed patients as to open the way 
 for dental prophylactic suggestions. Viewing the question from 
 the narroAvest standpoint of remuneration, the dentist could not 
 fail to profit by instructions to his patients on j^ro^ihylaxis. He 
 certainly fails in his duty as the member of a learned profession 
 by not doing this. Furthermore, with the known necessity for 
 proj)hylaxis, 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 ajjpear 
 simple and easy. 
 
TREATMENT. 173 
 
 Early diagnosis is not difficult, since the sini])le infliunniation 
 of the gums is easily recognized by the patient. Bk'cding when 
 the toothbrush or tootlipick is used can never be mistaken. 
 The dentist with liis 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. Redness, puffiuess 
 and bleeding are pathognomonic of this disease in its incip- 
 iency. 
 
 Few dentists have, however, 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 inflannnaticjn 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 
 an uncommon occurrence. The excuse usually made by the 
 dentist is that he cannot get paid for his time. Gingivitis is 
 a disease 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 profession is overcrowded. Were this disease treated 
 until the gums were placed in a healthy condition, there would 
 be practice enough for as many more dentists as there are today. 
 The busy dentist of today could attend only to one-half the 
 patients w4iom he now serves. 
 
 The treatment, then, should be proi^hylactic 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 with 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 to be kept 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 accom- 
 plished by properly made brushes. The ordinary toothbrush is 
 not adapted to the work under discussion. It will brush the 
 teeth but not reach the gums. What is needed is a massage 
 bi'usli tliat will miss tiic tcclli to a certain extent, but will reach 
 
174 INTERSTITIAL GINGIVITIS. 
 
 the gums and contract them tight around the teeth, thus pre- 
 venting the accumulation of foreign substances. The jjatient 
 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. 69), will do sufficient work upon the teeth with 
 the aid of the floss silk and toothpick. It should have printed 
 upon the handle, in large letters, "gum massage brush." The 
 handle should be bent a little more than the " prophylactic," so 
 that the end containing the bristles can be brought in contact 
 with the gum, posterior to the central incisors, 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 sj)aces 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 de]Dend, 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." Beodecker " remarks 
 that too frequent application of the toothljrush is sufl!icient to 
 
 1 Dental Cosmos, 188.3, page 5.32. 
 
 -Anatomy and Patholog)' of the Teetli, page l!()5. 
 
TnRAT:\rENT. 175 
 
 prdiliu'c |):i])illiiry liy]i('i'|)lasi!i. Tomes' Hays, " in my (iwii cxpt'- 
 riciu'c 1 havr tuiiiid tliat frequent and vigorous rubbing of the 
 gums with tlie finger, sluuupooiug them in fact, has often been 
 productive of great advantage, the patient of course lieing cau- 
 tioned not to rub the actual edge ; but even on this point there 
 is difference of opinion, for in a recent 2)aper on the subject, rest 
 and the avoidance of all friction is advocated." Dr. Meyer L. 
 Rhein- in introducing the "Prophylactic Toothbrush" to the 
 profession, says, in his article on " Oral Hygiene," each brush 
 comes inclosed in ;ui envelope, upon which are printed directions 
 for the intelligent use thereof, and the following caution : " Never 
 pass the brush aci'oss the teeth, as this movement destroys the 
 delicate membrane wliicli 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, showing the gen- 
 eral impression is that the gums should not be stimulated to any 
 great extent ; that the finger, a soft cloth, or a very soft tooth- 
 brush alone should be employed. The use of the finger is a 
 superstition which is handed down from generation to generation 
 without the slightest critical analysis. If the advocate of this 
 use would try the exj^eriment, he would see how impossible it 
 would be to bring it in contact Avith all the tissues of the mouth 
 that are involved in this disease ; were it i^ossible, the fingers, 
 cloth and soft toothbrush would not accomplish the desired 
 result. 
 
 Xo In-usli should l)e used whose l)ristles 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 u^ion the gums 
 was detrimental on account of the resultant tendency to absorj;)- 
 tion of the gums. While this may exceiJtionally 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 jn'ocess be 
 very thin over tlie roots (if the tcetli, especially the cuspids, the 
 
 ' Dental Surgery, imge, 704. 
 
 -New England Journal of Dentistry, October, 1884. 
 
176 INTERSTITIAL GINGIVITIS. 
 
 patient must be instructed so to use the brush as not to over- 
 stimulate these particular parts. In such cases the inner alveolar 
 process and gum tissue may be stimulated with impunity and 
 with the hardest brush. Again, if the chronic interstitial gingi- 
 vitis be of long standing, or even if chronic gingivitis has 
 been jsresent for some time, stimulation of the brush will 
 cause the gums and mucous membrane to recede until hard, 
 sound, healthy structure has been secured. Then absorption 
 will 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 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 fifteen years and have failed to see any ill results. For the 
 past four 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 stimulated, but 
 the bristles should be so jiassed in between the gum margin and 
 the tooth as to remove the debris and exfoliated epithelial scales 
 which have accumulated therein. These are often the cause of 
 the irritation. Unless this be done the gum or epithelial tissue 
 cannot perform its functions or be restored to health. Stimulat- 
 ing astringents and germicidal mouth washes should be employed 
 whenever the gums are massaged. The massage should be done 
 three times a day. The j)atient 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 ^^atience 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 for further instruction. If on inspection the 
 gums be found diseased at any point, the dentist can direct the 
 attention of the ^^atient to the particular locality and the disease 
 
TREATMENT. 177 
 
 l)e ei-adicatecl. By this inetliod and this alone can tlie gnms be 
 kejit in a healthy condition. Each jiatient must be given si^ecific 
 directions as to the treatment of his or Iier case. 
 
 If the gums have become swollen and engorged with blood 
 a different method must be employed. Here the absolute law of 
 medicine obtains — " reiuove the cause," no matter whether of 
 local or constitutional origin. If due to improper articulation 
 this must be corrected. If constitutional, and due to any of the 
 mineral poisons or scurvy, the system should be flooded with large 
 quantities of pure water. There is nothing better to rid the sys- 
 tem of poisons and imj^urities than flushing the blood with from 
 threeto five quarts of pure water a day. Cathartics should be 
 employed. A Turkish bath should be used to open the pores of 
 the skin, at which time the masseur should be instructed to stim- 
 ulate the liver, kidneys, skin and peripheral nerves. If the 
 patient suffer from disease like syi^hilis, tuberculosis, diabetes, 
 Bright's disease, colds, including catarrh, nervous prostration, 
 antiemia, etc., special treatment is indicated. Kemove all deposits 
 and other irritants from around the teeth. 
 
 Two decades ago, I advocated the use of the following set of 
 scalers ; nothing better has been produced since. -They consist 
 of handles, shanks bent at different angles, and blades three- 
 cornered, so that they can be used in three directions without 
 removing the fingers from the tooth (Fig. 70). These are all 
 delicately made, and tempered very hard. Sharp edges are 
 there retained. They will reach every point where tartar can 
 collect. After the dejsosits have been fairly well removed, the 
 gums may be syringed with hot water (Cravens) to remove all 
 debris. The gums should be saturated with tincture of iodin 
 (U. S. P.) or iodin and aconite, in the following manner : Have a 
 nund)er of wooden toothpicks (Portuguese preferable) wound with 
 cotton, and kept in a little box. Saturate the cotton and paint 
 the gum as far as it will go. Throw this into the waste l)asket 
 and take another, and so on until the gums are well saturated. 
 From three to five picks will be required. The assistant can 
 keep these in order between patients. In such cases a ditt'erent 
 massage brush is to be used. One is here required that will so 
 lacerate and stimulate the gums as to relieve the congestions. 
 This brush, made of coarser andstifter bristles, should be used like 
 
178 
 
 INTERSTITIAL GINGIVITIS. 
 
 the otlier. After two or three days the gums will contract, and 
 healthy circulation follow. Pain will now be experienced in the 
 gums. The massage must still be kept up. An astringent, 
 stimulating and general mouth wash, should be used in connec- 
 tion with the massage. The patient should return every other 
 day for further treatment with the iodin, or iodin and aconite 
 used as before. To reach an inflammation, chronic and deep- 
 seated, extending into the peridental membrane, periosteum and 
 alveolar jDrocess, there is nothing in medicine better than iodin, 
 or iodin and aconite. This, and this alone, will reach the deeper 
 inflammation. After a few treatments and constant use of the 
 massage brush, the gums will contract, and other deposits which 
 
 Fig. 70. 
 
 were overlooked at the first sitting will now be presented to 
 view. If the gums be very painful at the first sitting, no effort 
 should be made to remove the deposits until the inflammation 
 has, in a measure, subsided. The iodin treatment and massage 
 should be conducted as suggested until the gums have been 
 reduced and the pain ceases. After they have been restored to 
 health, constant massage with the medium brush must be 
 employed two or three times a day . The patient should return 
 to the dentist as often as necessary (every month or two) to 
 have the gums examined, and for further direction. 
 
TREATMENT. 179 
 
 As has been already shown, chronic interstitial gingivitis may 
 extend only to the peridental membrane, to the periostenm, or it 
 may extend throughont the alveolar process with the absorjition 
 of the bone the entire length of the root of the tooth. Pns 
 infection and serumal deposit may or may not take place. In 
 the early stages of this progressive inflammation, the first is prob- 
 able. If pus and deposits are present they can be treated with 
 signal success according to the symptoms and as hereinafter 
 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 suggested. 
 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 mastication inten- 
 sifies the irritation, which in time only increases the absorption. 
 Liberal use of iodin or iodin and aconite and the gum massage 
 brush is all that can be done to reduce the inflammation and 
 absorption as nuich as possi1:)le. The exfoliation is only a matter 
 of time. If the tootli or teeth cannot be retained perfectly tight, 
 no matter how healthy the surrounding tissues may be restored, 
 the irritation produced by 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 
 restored, if the matrix or cartilage be destroyed, since in this tlie 
 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. 
 
 13 
 
180 
 
 INTERSTITIAL GINGIVITIS. 
 
 If inflammation have extended into the j^eriosteum, peri- 
 dental membrane and alveohir ^^rocess, serumal calculi are fre- 
 quently dejDosited upon the roots of the teeth. When this has 
 taken jilace, the calculus must be removed. This should be 
 done with the utmost care, in order that adjacent tissues may not 
 be injured, or inflamed parts infected with pus germs. Since 
 dead bone is not present, the ojjerator should confine his instru- 
 mentation entirely to the root or roots of the teeth, with as little 
 injury as possible to the adjacent tissues. The alveolar process 
 must under no consideration be touched. Riggs believed that 
 the edge of the alveolar process was always in a state of dis- 
 integration, and that it should be so scraped as to get a fresh 
 surface, on the principle of caries of bone. Many dentists are 
 oj^erating in this manner at the present time. I have elsewhere 
 shown simj)le absorption and not caries is present. Such treat- 
 
 FiG. 71. 
 
 ment is wholly unnecessary and contraindicated. The object of 
 the removal 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. 
 Pushing instruments must never be used, but only such instru- 
 ments as have smooth and round backs, temjDered very hard so as 
 to retain sharp edges. These instruments should be small, with 
 small points to reach depressions, and to be as universal as jjos- 
 sible. Such an instrument is to be- found in the spoon excavator 
 (Fig. 71). The shank can be bent to suit the oiDcrator. This is 
 to be carried gently along the length of the root and passed 
 oyer the deposit with a firm liand, resting the finger upon some 
 other teeth. The drawing motion is invariably to be from the 
 membrane, and toward the crown. The deposits are scaled off" 
 
TREATMENT. 181 
 
 painleSusly. The round blade being larger than the shank, and 
 cutting upon three edges, lialf of the root in both directions can 
 be circled without removing the instrument. A similar instru- 
 ment bent at the shank in tlie opposite 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 liot 
 water (Cravens). 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 indicate its pres- 
 ence) further use of the scalers is indicated. The delicate instru- 
 ments and the accustomed sense of touch will reveal the hidden 
 calculus. 
 
 With the precautions already noted, local anaesthesia is 
 unnecessary. The smooth, round surfece 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 tincture iodin may be used, 
 together with massage, for a few days before scaling is resorted 
 to. The sensitiveness will soon disapjDear, when the instrument 
 may be inserted without difficulty. 
 
 A feAv years hence, the profession will regard a dentist whose 
 patients have pus oozing from the gums as a i^rehistoric relic and 
 the patient as an individual wliose 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 
 of the gum margin and pus infection cannot follow, no matter 
 how many germs be in the mouth. This is an absolute law of 
 general pathology. It has been proven by the experiments made 
 by Miller, G. T. Carpenter and myself on dogs, rabbits and man. 
 
 Tbe illustrations of the progress of interstitial gingivitis teach 
 that only the mildest treatment is indicated. Harsh treatment 
 on the inflamed bone or fibrous tissue, either with instruments or 
 ilrugs, nuist not be employed. Heroic treatment, such as the 
 
182 INTEE8TITIAL GINGIVITIS. 
 
 indiscriminate application of suli3hnric and lactic acid and sim- 
 ilar drugs in nearly or quite full strength, is not justified by the 
 surgical princij)les of today. No surgeon would think of making 
 such an application to inflamed bone in other parts of the body 
 without he wished necrosis with a desired sequestrum. INIuch 
 less would the intelligent operator use such treatment in a transi- 
 tory structure which predisposed to destruction. In a number of 
 instances exfoliation of the anterior plate of the alveolar process 
 has resulted from this treatment, to say nothing of the intense 
 pain produced. J. M. Whitney' has had four cases in his prac- 
 tice in which serious results followed. The first indication is to 
 remove the cause. Instrumentation should be resorted to only 
 to remove tartar and calcic deposits. This must be done in such 
 a manner as not to infect the deeper inflamed tissue 6r 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 per- 
 mitted to remain in the tissue, lest necrosis of the alveolar process 
 occur. They must be diluted or removed altogether after they 
 Irave accomplished their purpose. Very serious results have 
 occurred from careless use of drugs. When abscesses have 
 formed they should be opened and hydrogen peroxid — or, which 
 has answered my purpose equally well, hot water (Cravens) — 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 inflammation along the 
 course of the vessels quite a distance into the interstitial tissue. 
 In such cases they are difiicult to reach. A small syringe 
 (George T. Carpenter's) 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 located 
 
 ' International Dental Journal, April, 1899. 
 
TREATMENT. 183 
 
 in front of the infected surface and the drug does not i-eacli the 
 part. In such cases the deposit must be removed. If the pus do 
 not cease at the first, second or even third application, this is not 
 because tlie drug is not sufficiently strong, but because it does not 
 reach the infected part. Continued applications of iodin exter- 
 nally and internally, carried well up between the roots of the 
 tooth and the alveolar jjrocess will, in time, produce the desired 
 result. When pus ceases to flow, antiseptic treatment must stop. 
 The iodin and massage treatment nnist then be pushed until the 
 interstitial inflammation has been reduced and the gums con- 
 tracted tightly about the necks of the teeth. 
 
 After the tissues have been placed in a healthy condition, 
 they Avill require the constant attention of the operator, since, 
 like other tissues of the body when once diseased, favorable con- 
 ditions will cause a recurrence. The patient must return to the 
 operator frequently so that he can advise as to the use of massage. 
 
 I have elsewhere shown that uric acid (like lactic and other 
 acids, mercury, lead and brass poisoning) may produce local 
 irritation in a small number of cases, resulting in interstitial 
 gingivitis. Uric acid is absorbed into the blood and is thus car- 
 ried to all parts of the body. As mercury, lead, brass and potas- 
 sium iodide collect in the tissues of the alveolar process, on 
 account of the sluggish blood supply, so does uric acid, setting- 
 up inflammation. These cases are easily diagnosed, since, unlike 
 the ninety-four per cent of cases that begin at the gum margin 
 without pain and are of long standing, these set up a spontaneous 
 inflammation in an otherwise healthy alveolar process. This 
 may occur about one tooth, or more may be involved ; usually it 
 involves the tooth or teeth standing alone or having improper or 
 no articulation. The inflammation is followed liy acute pain. 
 If this be not reduced an abscess may, as elsewhere shown, form 
 at some locality about the alveolar process. Inflammation will 
 extend throughout the alveolar process and rapitl al>sorption 
 result. The tootji will loosen in the socket. If systemic treat- 
 ment be not at once instituted, exfoliation of the tooth or teeth 
 shortly ensues. The first thing indicated in sui-li cases is an 
 a]iplication of iodin to reduce inflannnation and pain. The urine 
 for twenty-four hours should be secured for chemical analysis. 
 
 The materials and appliances necessary for the ])urpose of 
 
184 INTERSTITIAL GINGIVITIS. 
 
 making an examination of the urine for uric acid are many and 
 the method requires considerable time. The dentist can do the 
 work, but it will be much more satisfactory (if he must know the 
 quantity eliminated each day) to send it to a competent chemist. 
 Should he desire to make the urine analysis, I should recom- 
 mend the method suggested by Bartley ^ in which he says, " The 
 estimation of uric acid is usually attended with much difficulty 
 and consumption of time. The author has devised the following 
 volumetric method, which is fairly rapid, reasonably accurate 
 and requires little skill. It can therefore claim a ])\nce as a 
 clinical method. The process is based upon the well-known 
 fact that uric acid is completely precij)itated from its solutions 
 containing an excess of ammonium-magnesium mixture and 
 ammonium hydroxide, by silver nitrate. When the precipita- 
 tion is complete, the slightest trace of silver in solution is shown 
 by the dark color produced in a droj) of the clear solution by a 
 soluble sulphide." The method of procedure is thus explained, 
 should the uric acid excreted in twenty-four hours be less than .8 
 grams or 10.8 grains it is safe to say that it is retained in the 
 system. 
 
 Imperfect tissue metabolism, as V. A. Gudex," of Milwaukee, 
 has shown, results in the formation of the following acids and 
 substances : uric, hippuric, oxaluric, carbonic, lactic and lac- 
 tates, caprylic, caproic, valerianic, butyric, propionic, acetic, 
 stearic, oleic, palmitic, formic, cholalic, tuarilic, damaluric, 
 damalic, and suceimic acids. Of these, the uric acid seems to act 
 least as an irritant. The urine, therefore, should be examined 
 for general acidity, the general treatment of which will accom- 
 plish all that is to be desired. A safe and delicate test can be 
 accomplished by determining the alkalinity of the urine, saliva, 
 perspiration, expectoration and dejection. The dentist is fortu- 
 nate in this because he has every convenience at hand. Lieb- 
 reich's methods of the use of plaster of paris plates as elaborated 
 by A. H. Hoy,^ of Chicago, is most admirably adapted for this 
 purpose, since the test can be readily ap^jlied. To make the 
 plates, mix a very thin quantity of dental plaster to the con- 
 
 ' Medical Chemistry, page 641 ; fifth edition. 
 2 Items of Interest, May, 1899. 
 ^Eating and Drinking. 
 
TEEATMENT. ] 85 
 
 sistency of cream, care being taken to thoroughly incorjiorate 
 the plaster. Take two panes of window glass, cut four j^ieces of 
 wood three-sixteenths of an inch in thickness and j^lfice one at 
 each corner of the glass ; now pour the plaster into the center, 
 place the other plate of glass above and press it down upon the 
 blocks of wood. By this method a very smooth surface can be 
 obtained. Make a round cutter out of tin, the size of a twenty- 
 five cent piece. Remove the upper piece by sliding it off, cut 
 out round disks just before the plaster hardens. These are pre- 
 pared in the following manner: A solution of litmus in 12 
 parts of water is rendered alkaline or bright blue by adding a 
 few drops of aqua ammonia. After the disks have become per- 
 fectly hard, the smooth polished surface is to be painted with 
 the solution, using a camel's-hair brush. Two or three apj^lica- 
 tions are to be made, until an even blue stain is obtained. Have 
 a solution of chemically pure sulphuric acid, two j)arts in five 
 hundred of distilled water, ready in a bottle, and a bottle of dis- 
 tilled water. To prepare the disk for the test, scrape one-half 
 of the dark blue surface of the plate until a slight blue sur- 
 face is obtained. This requires the removal of only a slight 
 amount, since the blue stain only j)enetrates a short dis- 
 tance. With a small brush, dipped into the acid, draw it quickly 
 over the surface exposed, giving a red appearance to the field 
 adjoining the blue.^ A bit of cotton, wound around the end 
 of a toothpick wet with distilled water and applied to the 
 two colors, will produce no change, thus proving everything to 
 be in working order. The fluid to be tested — urine, saliva or 
 perspiration — may noAV be applied. When possible, the exudate 
 must be applied to the test as soon as it leaves the body, care 
 being taken to apply a fixed amount each time. Apj^ly the 
 fluid to be examined to both the blue and red fields. When 
 saliva is used, the mouth must be rinsed two or three times and 
 the quantity first sucked out of the ducts must not be used. 
 Fresh saliva direct from the glands should only be used. The 
 plates, after they have been used, may be re-stained and used 
 indefinitely. The dentist should make repeated tests of the 
 secretions of healthy individuals under different conditions 
 
 'It is almost impossible to obtain a satisfactory permanent red litmus. By this 
 method the red and blue fields stand out in bold contrast. 
 
186 IXTEE8TITIAL GINGIVITIS. 
 
 before studying tliose of diseased conditions. This method is 
 a more delicate test than it is j)0ssible to make even with 
 litmus paper. Litmus paper often fails to reveal reaction, 
 which will be most obvious by this method. 
 
 The secretions of the body, if found to be acid, must be 
 placed in an amphoteric condition as soon as possible. An 
 amphoteric condition is a reaction of the urine, by which 
 both the blue and the red litmus are affected. If the red 
 becomes blue and the blue red it indicates that there is an 
 amphoteric reaction. The salt giving the alkaline reaction is 
 the trisodic phosjjhate ; that giving the acid reaction is the mon- 
 asodic j^hosphate. When a uniform color is produced it shows 
 that tlie alkaline iand acid salts are being properly excreted in 
 proi^er amounts with no excess of free acid. 
 
 The normal urine sjjecific gravity is 1018 to 1025. To 
 determine the specific gravity the morning urine should be used. 
 If about 1018 or lower and acid, it is due to fermentation in 
 small intestines. In such cases avoid yeast bread, acid fruits, 
 wines, vinegar and all acids. If specific gravity is 1025 or 
 more and acid, avoid meats. From five to seven pints of pure 
 water should be taken each day, to flush the blood and kidneys 
 and thus cleanse the system. Certain patients, especially neu- 
 rasthenics, nervous dyspeptics and many lithasmics, have a 
 repulsion to pure water. The water can be adjusted to these 
 idiosyncrasies by the employment of lithia or other effervescent 
 tablets. The main object is to preserve in such cases the promi- 
 nent idea of the water being medicated. Local treatment, as 
 elsewhere described, should here be resorted to. Besides the use 
 of water, dietetics in dentistry involve chiefly a conservative 
 question. 
 
 - Under most conditions of suboxidation and imperfect elimi- 
 nation, as elsewhere shown, the gums are forced to assume an 
 excretory energy to which they are unequal. As a consequence 
 a foundation is laid for interstitial gingivitis, which, in all of its 
 types, may seriously threaten tlie integrity of the teeth. Nay, 
 more, by furnishing a culture medium for pus microbes it may 
 threaten the general health, not only through systemic infec- 
 tion, but also through its interference with proper gastro-intestinal 
 dio'estion. Amono; the restrictions in diet which dental hv2;iene 
 
TREATMENT. 187 
 
 demands is, first, a restriction in foods and water containing an 
 excess of lime salts, which produce tartar. As excess of foods 
 containing nitrogen, when aided by an imperfect assimilation of 
 the carbohydrates, tend to produce constitutional conditions like 
 lithsemia, gout, etc., which affect tissue nutrition of the gums, these 
 foods require restriction and adaptation to the particular ease. 
 While the constitutional condition underlying lithaemia markedly 
 predisposes to gum irritations and inflammations, its value as an 
 exciting cause is but slight. Lactic acid, as has been elsewhere 
 ]iointed out, is a more marked local excitant. In the constitutional 
 production of lactic acid, ingestion of the carbohydrates without 
 assimilation plays a part. Scurvy, which may seriously threaten 
 the integrity of the gums, requires the usual dietetic treatment. 
 While there are indications of the untoward effects of infantile 
 scurv}^ on the gums, the pathology and consequences of it are 
 not as well known as those of scurvy in the adult. The 
 researches on scurvy in the infant tend to show that it results 
 from a monotony of diet rather than the absence of any article of 
 diet. The dietetics of dentistry, therefore, involve precisely the 
 same princi2)les as do the treatment of the constitutional con- 
 ditions which are the predisposing factors of the gum disorders. 
 During the entire process of treatment (indeed before the 
 treatment begins) a suitable mouth wash should be used two or 
 three times a day. This should be composed of a germit'ide, 
 antiseptic disinfectant and deodorant, and should be used at the 
 time of the massage. 
 
INDEX OF AUTHORS. 
 
 PAGE 
 
 Alexander, H. C. B 145 
 
 Allbright 3 
 
 Andrews, R. R 89 
 
 Arcovy 4 
 
 Barlow, Thomas 95 
 
 Barrett 174 
 
 Bartley 184 
 
 Black . 5, 34, 41, 47, 48, 51, 53, 56, 98 
 
 Beodecker 174 
 
 Bondurant 91 
 
 Bonwill 2, 157 
 
 Brown 2 
 
 Brubaker, A. B 68 
 
 Buzzard 97 
 
 Calve, Marshall de 2 
 
 Carpenter, G. T. 125, 165, 170, 
 
 181, 182 
 
 Cartright, Hamilton 4 
 
 Clowes 3 
 
 Coles, Oakley 4 
 
 Collins, J 66 
 
 Congdon 68 
 
 Cravens 181, 182 
 
 Cruveilier, C 92 
 
 Dana, C. L 97 
 
 Dickinson, Howship 78 
 
 Ebner, Von .... 5ri, 153, 158, 160 
 
 Eisenhart 159 
 
 Enderlin . 76 
 
 Essig, C. J 3 
 
 Evans, W. A. 123 
 
 Farrar, F. N 4 
 
 Fitzgerald 9, 68, 167 
 
 Flower, Alsop 14 
 
 Foster 11 
 
 Fuchard, H. A 2 
 
 Galippe . . 4,12,122,123,124,151 
 
 Geddings, H. D 75 
 
 Gray .37 
 
 Gudex, V. A 184 
 
 Hektoen, L 127, 155 
 
 Hertwig, 56, 146 
 
 Herzog, M 124 
 
 PAGE 
 
 Hirt 97 
 
 Hogben 94 
 
 Howell 77 
 
 Hoy, A. H. ........ 184 
 
 Ingersol, L. C 4 
 
 Izklai, Joseph 4 
 
 Jacobi 95 
 
 Jacobson 75 
 
 Joirac 2 
 
 Jourdain 2 
 
 Kaecker 2 
 
 Ivaufmann 61, 154, 157, 158 
 
 Kirk 12, 68 
 
 Koch 12, 151 
 
 Kolliker .... 30,33,56,62,161 
 
 Kuttner 169 
 
 Magitot . . . 2, 7, 53, 55, 57, 58, 91 
 
 Mailhol 11 
 
 Malasses 4 
 
 Malenfant 79 
 
 Miller . . 8, cS2, 89, 122, 123, 125, 181 
 
 Mills 3 
 
 Minot 42, 53, 56, 146 
 
 Morgan, de 31 
 
 Niles, N. S 3 
 
 Noyes, Frederick 48 
 
 Patterson 4, 6, 8, 89 
 
 Pedley 6, 7 
 
 Pierce, C.N. . . . 8, 12, .37,. 08, 96 
 
 Quain 10, 11 
 
 Rawls, A. 4, 95 
 
 Rechlinghausen, Von 159 
 
 Reese 4 
 
 Reeves 68 
 
 Rehwinkle 3 
 
 Rhein OS, 175 
 
 Riggs, J.T. . 2, 180 
 
 Robin 53, 55, 57, 58, 91 
 
 Rokitansky 169 
 
 Rose 54 
 
 Salisbury, J. H. . . . 69,71, 79 
 
 Sayre, Charles E 14 
 
 Scheff 2 
 
190 
 
 INDEX OF AUTHORS. 
 
 PAGE 
 
 Scheheoetskey 78 
 
 Schmidt, C 73, 74, 7G, 78 
 
 Serres 47 
 
 Sirletti 3 
 
 Starr, A. R 5 
 
 Stevenson 78 
 
 Sudduth, W. X. ... 5, 6, 7, 8, 161 
 
 Sutton, Bland 7 
 
 Talbot, E. S 5, 47 
 
 PAGE 
 
 Tomes 27, 31, 175 
 
 Yolkmann ... 31, 62, 63, 153, 160 
 
 Virchow 169, 170 
 
 Waldeyer 56 
 
 Walker 4 
 
 Wesener, J. A 69, 70 
 
 Whitney, J. M 182- 
 
 Zawadsky 7& 
 
 Ziegler 28, 158- 
 
INDEX OF SUBJECTS. 
 
 PAGE 
 
 Acadians, Teeth of 1 
 
 Alveolar Process 21 
 
 Absorption of 147 
 
 Absorption 157 
 
 Absorption and Trophic 
 
 Change 162 
 
 Changes 149 
 
 Dermal Bones 96 
 
 Germ Infection . . . . 96 
 
 Hypertrophy of 29 
 
 Antimony 144 
 
 Arsenic 144 
 
 Bone Absorption 59 
 
 Bone Building 59 
 
 Brass 144 
 
 Interstitial Gingivitis . . . 94 
 
 Bromides 145 
 
 Calcic Deposits 168 
 
 Calcospherites 41, 133 
 
 Calculi, Salivary 78 
 
 Carnivora, Interstitial Gingivitis in . 14 
 Catarrhal Idiosyncrasy .... 5 
 Cave Dwellers, Teeth of ... . 1 
 
 Cementoblasts 42 
 
 Cementoolasts 61 
 
 Children, Degenerate 89 
 
 Diathetic 89 
 
 Interstitial Gingivitis in . . 81 
 
 Neurotic 89 
 
 Pyorrhcea in 89 
 
 Debris, Epithelial 55 
 
 Dental Operations and Alveolar Pro- 
 cess 150 
 
 and Bone Absorption . . . 150 
 
 Dental Shelf 55, 56 
 
 Degeneracy and Degenerate Tissues . 87 
 
 Dentitions, The Three 84 
 
 Dogs, Interstitial Gingivitis in . 14, 98 
 Mercuric Interstitial Gingi- 
 vitis in 117 
 
 Pyorrhcea Alveolaris in . . 98 
 Ebner, Von, Vessels of .... 31 
 Egyptians, Teeth of 1 
 
 PAGE 
 
 Embryology of the Tooth .... 46 
 Endarteritis Obliterans .... 154 
 and Tuberculosis .... 155 
 Exanthemata and Catarrhal Gingi- 
 vitis 7 
 
 Follicle, The Dental 55 
 
 Gingivitis 5 
 
 Expulsive 11 
 
 Interstitial 9 
 
 and Pyorrhcea 9 
 
 Glands of Mucous and Peridental 
 
 Membranes 47 
 
 Greeks, Teeth of 1 
 
 Gums 42 
 
 Halisteresis .... 61, 62, 153, 158 
 
 Haversian Canals 30 
 
 Heredity 13 
 
 Interstitial Gingivitis . . . .10, 12 
 
 Antimony 144 
 
 Arsenic 144 
 
 Atavism and 83 
 
 Auto-Intoxication and ... 66 
 
 Bacteriology of 122 
 
 Brass 144 
 
 Bromide 145 
 
 Carnivora in 14 
 
 Causes 12 
 
 Degeneracy and 86 
 
 Dogs 98 
 
 Environment and .... 84 
 
 Heredity and 83 
 
 Heredity in 13 
 
 Inorganic Salts and ... 73 
 
 Iodide 145 
 
 Lactic Acid and 152 
 
 Mercuric 142 
 
 In Dogs 117 
 
 Nerve Phases of .... 13 
 
 Pathogeny of 151 
 
 Plumbic 143 
 
 Pyorrhcea Alveolaris and . . 162 
 Scorbutic in IMan .... 127 
 Scurvy and . . . 13, 65, 94 
 
192 
 
 INDEX OF SUBJECTS. 
 
 PAGE 
 
 Intel stitial Gingivitis — 
 
 Tartar and 148 
 
 Theories of 65 
 
 Toxic Causes of . . . . 13, 92 
 
 Treatment 172 
 
 Troplio-Neuroses and . . 66, 92 
 
 Uric Acid and 68 
 
 Iodides 145 
 
 Jaw, Evolution of . . . . . .149 
 
 Evolutionary Changes in . .20 
 Racial Changes in .... 20 
 
 Lake Dwellers, Teeth of ... . 1 
 
 Lactic Acid and Interstitial Gingi- 
 vitis 152 
 
 Lacunar Absorption . . . . 62, 153 
 
 Lead 143 
 
 Interstitial Gingivitis and . . 94 
 Locomotor Ataxia and Gum Dis- 
 order 13 
 
 Mercury 142 
 
 Interstitial Gingivitis and . 93 
 Mouth Breathing and Catarrhal Gin- 
 givitis 7 
 
 Mucous Membrane, Glands of . . 47 
 
 Histology of 42 
 
 Mucus, Bactericidal Function of . .88 
 
 Odontoblasts 42 
 
 Osteoblasts 42 
 
 Osteoclasts 61 
 
 Osteomalacia .... 62, 146, 159 
 Papillary Layer, Comparative Anat- 
 omy 47 
 
 Paretic Dementia and Gum Dis- 
 order ... 13 
 
 Perforating Canal Absorption . 62, 153 
 Pericementitis Phagadenica ... 5 
 
 Peridental Membrane 33 
 
 Glands of 47 
 
 Inflammation 1 
 
 Periosteum 33 
 
 Periostitis Alveo-Dentalis ... 2 
 
 Dentalis 2 
 
 Pockets and Interstitial Gingivitis . 152 
 
 PAGE 
 
 Potassium lodid and Interstitial 
 
 Gingivitis 94 
 
 Pregnancy and Osteomalacia . . . 159 
 
 Primitive Races, Teeth of ... . 1 
 
 Pyorrhosa Alveolaris, Bacteriology of 162 
 
 Catarrhal Idiosyncrasy . . 5 
 
 Causes of 2 
 
 Constitutional Causes . 3, 4, 5 
 Constitutional Effects of . . 167 
 
 Degeneracy and 5 
 
 Dogs 98 
 
 Eruptive Fevers .... 7 
 
 History 2 
 
 Intestinal Disorders from . . 167 
 
 Lactic Acid 8 
 
 Nervous Causes 3 
 
 Parasites and "8 
 
 Pathology of 6, 7 
 
 Syphilis and 8 
 
 Systemic Disease and ... 8 
 
 Uric Acid and 8 
 
 Scurvy 96, 127 
 
 Sodium Chloride and Interstitial 
 
 Gingivitis 95 
 
 Stomatitis Catarrhalis 6 
 
 Teeth, Changes in ..... . 146 
 
 Changes in Position of . . .28 
 Decay of ...... . 147 
 
 Embryology of 146 
 
 Irregularities of 148 
 
 Periods of Evolution . . . 146 
 Periods of Involution . . . 146 
 Trophic Disorders of ... 96 
 
 Third Molar 149 
 
 Disappearance of .... 21 
 
 Tootli Embryology 42, 53 
 
 Form Changes 149 
 
 Transitory Structures . . . .20, 147 
 
 Tropho-Neuroses 13, 96 
 
 Ulitis U 
 
 Uric Acid and PyoiThosa Alveolaris 3, 8 
 Volkmann's Canals 31 
 
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