Interstitial gingivitis : or so-called pyorrhoea alveolaris

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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 applicable to dental problems as to those of biology generally. Treatment of any disease without knowledge of its pathology is practically a failure.

While much has been written upon the pyorrhceic stage of interstitial gingivitis and its treatment, during the past two decades, no new principle has been advanced whereby the parts can be restored to a healthy condition, or whereby the disease can he prevented. The disease is admittedly on the increase. This seems at first sight to indicate that dental prophylaxis and treatment, so tar as this disease is concerned, is a failure.

Other specialists restore patients to health. Nearly every patient with this disease applies to dentists. Most dentists, however, hardly know the disease exi.--.ts and much less arc capable of ottering suggestions as to treatment. It seems strange that in America so little original work has been done upon 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, 188(5, page C>S(.)) of the clinical aspects and etiology of this disease. Even during apparently diverse and separated 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 Medical Laboratory, Professor of Pathology, Chicago College of Physicians and Surgeons and Milwaukee Medical College ; Dr. J. A. Wesener. Chemist, Columbus Medical Laboratory, Professor 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 electrotypes, etc.

THE AUTHOR. 103 State Street, Chicago.

CONTEXTS.

CHAPTER. PACK.

II. Introduction ........ 10

III. Transitory Structures —

The Jaws * . .2(1

The Alveolar Process ..... 21

Periosteum and Peridental Membrane . 33

The Gums -and Mucous Membrane ... 42

Do Glands Exist in Epithelial and Peridental Membrane? ........ 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

• XI. -Mercurial Interstitial Gingivitis in Dons . 117

XII. Bacteriology of Interstitial Gingivitis . . . 122

XIIL Scorbutic Interstitial Gingivitis in Man . . . 127

XIV. Interstitial Gingivitis in Man from Metallic and Other

Drug Action . . . . . . .142

XV. Conclusions . . . . . . . .146

Pathogenesis of Interstitial Gingivitis . . 151

Endarteritis Obliterans ..... 154

Absorption of the Alveolar Process . . . 157

Pyorrhcka Alveoi.aris from Interstitial Gingivitis . 162 Constitutional Effects of Pyorrhcea Alveolaris . 167 Calcic Deposits ....... 168

XVI. Treatment . . . ... . .172

ix

INTERSTITIAL GINGIVITIS.

Chapter I. History

Inflammation of the peridental membrane is probably coeval with man. Some of the skulls found earliest in the cave-dwelling period exhibit evidences of its presence. In some of these, careful observation lias shown deposits encroaching upon the roots of the teeth and resultant absorption of the alveolar process.

In the Swiss lake-dwellings and in the earlier Irish crannoges of like construction and situation, skulls are found, which exhibit deposits of tartar, inflammation of the peridental membrane and al (sorption of the alveolar process. These skulls were those of primitive races in whom disease of the jaws and teeth isupposed to he absent or infrequent. In the skulls of the peoples exhibiting the highest civilization at the earliest period — those of the Accadians and Egyptians — similar inflammatory conditions are to be found. This, however, was to have been expected, to judge from the dental directions left among the medical records of these peojjies. The Greeks, Syrians, Arabians, Dravidians and Aryans of India and the early Burmese all suffered from this disorder. In the museum at Constantinople 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, hut one which attacked man early

Z INTERSTITIAL GINGIVITIS.

in his evolution. Like most diseases it has been chiefly discussed 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. Jourdain2 advanced the opinion that the disease was of scorbutic origin.

In 1821 L. Kaecker3 discussed the disorder in an essay on the devastations of the gums and alveolar processes.

In 1822 M. Joirac4 (in a discussion of the disease), Avhile advancing no theory as to its origin, called it " pyorrhoea interal veolo-dentai re. ' '

In 1860 Marshall de Calve 5 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 subsequently, is not the original seat of the lesion. In his opinion systemic disorders like gout, rheumatism, albuminuria, diabetes and anaemia had an influence.

Bonwill6 during the same year expressed the opinion that the disorder was due to thinness of the alveolar process between the teeth, thus depriving the peridental membrane and gum tissue of proper support, The want of proper articulation of the teeth also exerted an influence.

In 1870 Brown ascribed the disorder to seminal calculus.

In 1875 John T. Riggs, after whom the disorder is frequently called, entitled it (in a paper read before the American Academy of Dental Surgery) suppurative inflammation of the gums and absorption of the gums and alveolar process.

During the same year Scheff 7 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,

1 Independent Dental Journal, 1875.

2 Philadelphia Journal of Medical and Physical Science, 1821.

3 International Dental Journal, Vol. XIII.

4 Journal of the American Medical Association.

5 Journal of the American Medical Association. G Dental Cosmos, Vol. XXIV.

very often obscure. He doubted, however, the influence of rheumatism.

In 1876 Sirlctti ' ( in a discussion of the pathology of the disorder, which he called alveolo-dental periostitis) regarded it as due to constitutional conditions, like rheumatism, scrofula, syphilis, etc., with local causes as exciting factors.

In 1S77 Rehwinkle,2 in a paper on pyorrhoea alveolaris, after citing from Albright (of Berlin) the claim that the disorder was due to unclean liness, 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 influence in its causation. Salivary deposits were, in his opinion, without influence. Clowes3 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,4 in 1880, expressed the opinion that its predisposing 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. Mills5 expressed the opinion that the disorder was of systemic origin. Various mental and physical influences aided its progress, such as nervous exhaustion and bodily and mental overwork. In his opinion it frequently occurred in children and adolescents from eruptive fevers. The deposit was only a local manifestation of the disorder.

In 1881 X. S. Niles6 expressed the opinion that constitutional conditions were, as a rule, without influence, and that local irritating deposits were the cause in twenty-five per cent of the cases coming under his observation. He was of opinion also that the amount of lime salts taken into the system in drinking water exerted an influence. A calcic and phosphatic diathesis had an influence in the production of the disorder.

-Dental Cosmos, Vol. XIX. 'Ibid., Vol. XXI.

4 Dental Cosmos, Vol. X XI.

5 Ibid., Vol. XXIII.

6 Ibid., Vol. XXIV.

In 1881 (when there seemed to have been many contributions to the literature of the subject) Atkinson 1 expressed 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 secondary deposit of tartar.

In a paper read before the Dental Section of the International Medical Congress, Walker2 claimed that the starting point of the disease was subacute inflammation passing into the depths of the alveolar process adjacent to the inflamed gum. In the discussion of this paper, Archovy and Joseph Izklai, of Buda Pesth, ascribed the disorder to minute organisms. Oakley Coles thought that systemic states were the predisposing factors, while minute organisms exerted an exciting influence.

In 1882, L. C. Ingersol 3 regarded sanguinary calculus as a manifestation of the disorder, and distinguished it from salivary deposits.

Malasses and Gallippe,4 in 1884, expressed the opinion that the disorder was of microbic origin.

In 1885, A. O. Rawls5 expressed the opinion that the causes were environment with morbid factors, such as malaria, excessive sodium, etc., chloride and mercury.

In 1886, Reese6 expressed the opinion that the disorder had its source in the uric acid diathesis resultant on abuse of alcohol.

During the same year, J. D. Patterson 7 expressed the opinion that the disorder was of catarrhal origin. Later, in 1886, J. N. Farrar8 regarded the disorder as a combined result of systemic tendencies and local irritants. There was a peculiar condition of the system associated with hypersecretion laden with increased earthy deposits.

1 Dental Cosmos, Vol. XXIV.

2 Transactions of the International Medical Congress, 1881.

3 Dental Cosmos, Vol. XXV.

4 Ibid., Vol. XXVI.

5 Ibid., Vol. XXVII.

fi Independent Practitioner, Vol. VI.

7 Dental Cosmos, Vol. XXI.

8 Independent Practitioner, Vol. VII.

A. R. Starr later also expressed the same opinion. He, however, was unable to determine the local irritation factor, but regarded it as the same as that which causes exostosis of the cementum. He had found most cases in the upper jaws.

Black1 designated the disorder phagadenic pericementitis. It was a specific infection of an inflammatory character, having its origin in the gingiva, and was accompanied with destruction of the peridental membrane and alveolar walls.

E. S. Talbot J 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 1887, the following analytic picture was drawn by W. X. Sudduth3 : Pyorrhoea alveolaris is a term applied to the secondary stage- 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," wTere it not for the general catarrhal tendency shown by the entire mucous membrane of the mouth and nasal passages. The intimate relation between a general catarrhal idiosyncrasy and pyorrhoea alveolaris is more than mere coincidence. Its common occurrence in persons who have irregular teeth has also been often noted by Dr. Sudduth. who considers that this fact has, besides the matter of uncleanline>s, a direct bearing upon its pathogeny. It is well known that the irregularities of the teeth present an indication of a degenerative taint, and that persons in whom irregularities occur are very prone to catarrhal affections of the respiratory organs, including the nasal passage. Their skin is usually very susceptible to inflammatory affections. Another feature is offensive odor of the saliva of individuals who show this particular tendency to catarrhal affections even in persons who take most scrupulous care of the teeth. In the majority of cases, pyorrhoea is a stomatitis in which the local and constitutional factors in the production of the disease are largely dependent upon hereditary catarrhal dyscrasia for their ability to engraft themselves upon

1 American System of Dentistry.

-' Dental Cosmos, Vol. XXVIII. ; Sajous' Annual, 18S8, Vol. Ill, page 365.

b INTERSTITIAL GINGIVITIS.

the tissues. This position is borne out by the clinical experience of Patterson, of Kansas City, Missouri, who reports thirty-eight cases of well marked pyorrhoea observed by him, thirty-three of which presented undoubted evidence of nasal catarrhal conditions ; two were the result of direct irritation of misfitting partial plates, and the remaining three were apparently caused by calcific 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 classing 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 rugse 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 of 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 passes into hypertrophy ; at other times there is an indurated appearance that may last for some time. Granulation tissue may be produced as the result of overstimulation. The gums become detached from the necks of the teeth ; and pockets are formed from which a fetid discharge may be pressed, giving a peculiarly disagreeable odor. Bulla 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, "hypertrophy of the muco-periosteal fold around the teeth, accompanied by dilatation of capillary loops, enlargement of the papillae and rapid proliferation of epithelial cells. Later the gums become firm and contracted and display increase of fibrous tissue. The changes which go on in the socket have not been as yet satisfactorily worked out. The examination of the jaws of earnivora, apparently affected with pyorrhoea alveolaris, leads to the supposition that osteitis of the alveolar process spreading toward the apex of the socket is present. 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-brown 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 explained in several ways. The general causes are local or symptomatic, or both combined. The most common cause of catarrhal gingivitis is found in local irritation, combined with some hereditary disposition to catarrhal affections. The next greatest etiologic factor is symptomatic — the local manifestation of a constitutional vice. The most common 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 pyorrhoea alveolaris. As a complication of the disease in its secondary stages there can be no doubt of the action of micro-organisms, but Sudduth does not feel justified in conceding to them a position of specificity.

His position above quoted is sustained by Pedley, who finds that in most instances it is due to some constitutional condition. The fact that it is often symmetrical and frequently hereditary gives support as to this view. It occurs in mouths of patients whose health has been undermined by debilitating influences and injudicious habits of living. It is a common sequel of malarial fever. Young persons recovering from eruptive fevers are sometimes 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 rheumatoid arthritis in animals. He has also met with it in mollities ossium and other wasting diseases. Magitot (who views the

8 IXTEKSTITIAL GINGIVITIS.

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 phenomenon is absolutely constant.

Patterson holds that " mouth-breathing has, in his experience, 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 up 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 condition was evidently aggravated by constitutional derangement and cure was thereby retarded. The great majority of cases, however, have shown no indication of constitutional predisposition, but have pointed 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 inflammatory 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 Miller1 expressed the opinion that the disorder was of a parasitic nature.

In 1892 C. N. Pierce2 charged the disorder chiefly to systemic predisposition and enthusiastically advocated the theory of Reese as to the influence of the uric acid diathesis. In 1894 W. X. Sudduth 3 strongly urged the influence of lactic acid as a local factor in the disorder.

Micro-Organisms of the Human Mouth.

International Dental Journal, Vol. XIII. 'Ibid., Vol. XIV

John Fitzgerald,1 in 1899, claimed that "The production of pyorrhoea depends upon two factors, a predisposing cause and a local irritation. The predisposing cause may be tubercle, syphilis, scurvy, the exhaustion of acute infectious di>e;i>r> 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 substance."

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 study of either the predisposing or the exciting causes of the condition. Even the impetus given the study of etiology by bacteriology and embryology has as yet failed to make itself felt to any considerable degree in this department of dental pathology.

'Clinical Journal, March 1, 1899.

Introduction

The attempt has been made in the present work to reduce to order the chaotic notions as to etiology, pathology and treatment which, during the present century, have gathered around the morbid condition erroneously entitled Pyorrhoea Alveolaris. While even erroneous titles may have their meaning so fixed by usage that any danger from the error involved in the title may be practically nil, still this is not the case with the title just cited. It suggests erroneous etiology, since pyorrhoea implies that there must always be a flow of pus, and hence that the disease 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 designation for the condition hitherto known as pyorrhoea alveolaris, the term "Interstitial Gingivitis." To this designation (as to all other attempts to express within a small space an extended pathology, etiology, prognosis, and clinical aspects) there are some objections. The term interstitial is used by some pathologists in a limited obscure sense. By the mass of dental pathologists, surgeons, physicians, and by medical lexicographers, the term is employed in precisely the sense in which it is used in the present work. The English surgeon and lexicographer Quain defines interstitial as follows : " 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 connective 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 implication of the interstitial tissues in morbid processes or their infiltration with morbid products, as interstitial pneumonia, interstitial hepatitis."

The Encyclopaedic 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 affecting the connective tissue of an organ ; second, it is also applied 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 applied to pathologic processes occupying the space between the essential parts of an organ which constitute its proper tissue, and is then employed in a sense opposed to that of parenchymatous.

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 pyorrhoea alveolaris.

I have adopted the term gingivitis for reasons which will be obvious at the first glance. The philologic objection may be made that in it Greek and Latin are yoked together. Practically this is no objection, since German, French, as well as English, medical authorities employ such terms of mixed origin. Indeed the French (Mailhol1 for example) apply the term gingivitis to the very condition to which I have applied it. In addition, they add to it the specific term " expulsive," to designate " a form of recession of the gums, accompanied by alveolar osteoperiostitis, and the gradual expulsion of the tooth from its socket." Foster2 suggests the substitution of the term ulitis as more philologically 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 employed convey a fairly correct idea of the pathologic process involved, and do not imply erroneous views as to etiology, pathology, prognosis and treatment.

The pathologic conception adopted in the present work anent interstitial gingivitis is that the disorder is a local inflammatory

1 Odontalgie.

- Foster, op. cit.

condition of the gums, tending to accelerate their normal tendency to disappearance at certain periods of stress, or involution, of which involution the changes jDroduced by old age are a type. 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 predisposing causes. The exciting causes may be purely local, or may be local expressions of constitutional states. Thus it will be shown that the influence of uric acid when present is exerted as a local irritant, and not as a constitutional factor — the theory urged so strongly by Pierce, whose views have been of late so advocated by Kirk.1 The uric acid hypothesis, once very dominant in medicine, is now losing its force. The trend of medical opinion is to consider it one of the danger signals of auto-intoxication 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 jn-esent work it will be shown by all laws of bacteriology (under which investigations must be conducted) that there is no specific germ which is caj)able of producing the disease itself, and furthermore, that the pyorrhoea stage of the disease is merely a complication due to pyogenic germ infection of the already diseased gums. The views of Galippe as to a specific organism will be shown to have failed of support by numerous control experiments described in the present work. As these have been conducted by different experimenters they are free from the personal elements of error which vitiate the researches of Galippe, who violated that canon of the laws of Koch which compels production of the disease by the alleged specific germ. One predisposing factor will be shown in the present work to be the nature of the structures affected. This in pathology is called local predisposition. The gums, etc., will be shown to be transitory structures in themselves predestined (as already stated) to certain changes at certain 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

1 International Dental Journal, May, 1899.

INTRODUCTION. 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 ease 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 governing local blood supply and tissne 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 nut to lie great. The influence, however, of degeneracy expressing itself along the lines of least resistance will appear as an ominously important factor. Heredity here, as elsewhere, is a warning rather than a destiny.

The influence of the nervous system on the processes of growth and repair, which is called its trophic function, has been shown to play a part in both the etiology of the disease and in its progress. This function has received but little attention from dentists, albeit its influence has been recognized in dental pathology in connection with great neuroses like paretic dementia .and locomotor ataxia, in which gum disorders occur, followed by loosening of the teeth. The pathology of the disease has been discussed in the light of established facts of general pathology which have been accepted by the leading dental investigators, and not merely from a hypothetic standpoint. The disease has been regarded as a local exaggeration of certain physiologic processes, accompanied by diminution of the intensity of others. In the study of this phase of the question, the latest researches of dental pathologists as well as original observation and experiment have been employed.