Periodontal disease and its treatment by ionic medication

Front matter

Book '38

COPYRIGHT DEPOSHi

TREATMENT BY IONIC MEDICATION

Introduction

It would be difficult to name a disease associated with more controversial literature than "pyorrhoea alveolaris." Historical evidence places it in the category of one of the oldest existing maladies, for anatomical specimens in museums which date back to many centuries B.C. reveal unmistakable evidence of the disease as known to us today. Writers about the middle of the eighteenth century first began to describe it, and later on, in the early part of the nineteenth century, more frequent reference was made to this disorder. About the year 1875 Dr. Riggs first accurately described the disease; he regarded it as purely local, and treated it from that aspect in a highly satisfactory manner. Since then the etiology, pathology and treatment of periodontal disease has attracted ever-increasing interest and been debated on such controversial lines that it has become well-nigh impossible to determine, without vast personal experience, which are the correct deductions to accept. The medical profession has recently discovered the disease, and are now imposing their will on the dental profession; some are treating it themselves by vaccines, others are condemning all teeth affected with the disease to the forceps, while others are content with attributing nearly every disease of the human body to the effects of oral sepsis and saddling the dentist with the responsibility of treatment.

But dentists themselves have not settled on any fixed etiology or pathology, and consequently vary in lines of treatment to a remarkable degree, and a serious feature of consequent inability to cope with the disease is a strong conviction prevalent that under no circumstances is it curable when the teeth are retained. There is usually a vague or controversial element introduced by even the most recent writers on the subject, making it difficult for the most ardent student to determine what is meant or which conclusions are the correct ones. The disease is usually studied in the advanced stages, the preliminary stages being overlooked as a gingival affection with no direct bearing.

Howe 1 in his report on pathology and etiology to the sixth International Dental Congress states: "This fully developed pathological condition presents three distinct phases. . . . I refer to bacterial activity, pathological calcifications, tissue degeneration." The last of these is a vague statement over which great division of opinion exists and refers to advanced stage.

In a recent and important work — The Science and Practice of Dental Surgery, by Norman Bennett, is recorded : " The causes of chronic suppurative periodontitis are at present very vaguely understood, some writers attribute the disease to Constitutional Disorders, while others consider it to be due to local irritants. The consensus of opinion seems to favor the belief that both play an important part."

A great deal of stress is laid on the constitutional causes by the vast majority of writers, but local causes are always

1 Sixth Inter. Dent. Congress, p. 115.

IXTRODUCTIOX 19

included and so mixed up as to make the student wonder which is really the important factor.

Talbot presented a mass of evidence to demonstrate " that the causes of interstitial gingivitis are de visible into predisposing causes (which may be subdivided into local predisposing and constitutional) and exciting causes. The exciting causes are either constitutional or local, but as a rule are local or have local action."

For many years the disease was associated with gout, and uric acid was made responsible for at least one form of pyorrhoea, 1 "in which the local necrosis of the periodontal membrane is caused by gouty disease of one of the bloodvessels in its substance."

Xewland Pedley 2 concluded that " 'pyorrhoea alveolaris is essentially of constitutional origin," and asserts that "the weight of evidence tends to place pyorrhoea alveolaris hi the category of bone disease."

Hopewell-Smith, 3 in his research on Pathohistology of the disease, considers that "pyorrhoea alveolaris does not commence as a gingivitis," but that "it is essentially dependent upon an osseous lesion."

H. P. Pickerill 4 asserts that "The direct cause in all cases is infection by pathogenic organisms."

Miller 5 says : " It is still a matter of debate whether a local irritant be at all required to the origination of the disease. As regards the participation of bacteria in pyorrhoea alveolaris, our present knowledge of suppurative inflammations compels us to consider the former as the cause of the suppura-

1 Fitzgerald: Pyorrhoea Alveolaris. 2 Dental Record, May, 1887.

3 Pvorrhoea Alveolaris: Its Pathohistologv. Dental Cosmos, April. 1911, p. 397.

4 Stomatology in General Practice, p. 11.

3 The Microorganisms of the Human Mouth, p. 332.

tions incident to the disease. Microorganisms which possess pyogenic properties, temporarily or permanently, inhabit every mouth. If, therefore, the power of resistance of the periodontal membrane be impaired by any one of the abovementioned local or constitutional causes in such a manner as to furnish a suitable culture medium for the bacteria, they will, of course, begin their ravages and the usual symptoms will follow."

G. V. Black was the first to classify the disease from symptoms observed into two classes, both closely allied "gingivitis" and "phagedenic pericementitis," the former dependent on the presence of two forms of calculus and the latter, of a more destructive character, he associated with a specific form of microorganism, at the time undiscovered, as well as the presence of calculus, which causes "an inflammation of a peculiar character which results in a destruction of the periodontal membrane." 1 Black's conception of the disease at that time holds good now in many respects. Knowledge has been added, but his teachings on the subject laid the foundation for much of the conservative work now done.

Recent investigations on the protozoa of the buccal cavity by A. Chiavaro, 2 of Rome, and M. T. Barrett, 3 of Philadelphia revealed the presence of Entamoeba? buccalis almost constantly in pyorrhoea pus, and Barrett leans toward the view that this protozoa causes the disease, while Chiavaro holds the opposite view.

Colyer, 4 studying the anatomy of chronic general periodontitis, draws the conclusion " (1) that the bone lesion is a progressive rarefying osteitis commencing at the margin

1 Black, G. V.: Am. System of Dentistry, i, 954. - Dental Cosmos, September, 1914, p. 1089.

4 Chronic General Periodontitis, pp. 30 and 64.

INTRODUCTION 21

of the alveolar process, and (2) that the varying density of the bone influences the rate of destruction." The cause of the disease in man he attributes "to the disease being started by injury of the gingival margin from food debris or the local action of toxins as seen on the marginal gingivitis of mouth breathers." He also points out that ''The prevalence of the disease is probably due to the character of the diet of the present day."

Znamensky, 1 studying the disease from the anatomopathological standpoint, concluded that constitutional disorders as well as local irritants are responsible for osteoporosis characteristic of the disease. He says: " The different diseases which produce an osteoporosis of the bones in the whole system, and particularly in the sockets, may be the predisposing cause of alveolar pyorrhcea. The diseases of general constitutional character which belong to this class are osteomalacia, rickets, scrofula, syphilis, acute eruptive processes, fevers and typhus. Further, there are also diseases of the blood, exchange of matter in the system, such as anemia, chlorosis, scurvy, leukaemia, hemophilia, diabetes mellitus and gout. The causes of atrophy of the tissues are scanty nourishment, repeated pregnancy, chronic catarrh of the stomach, diseases which exhaust the system, tabes dorsalis, tuberculosis and rheumatism." Referring to the local causes, on which he lays very little stress, he says: "The most frequent of these is an accumulation of tartar deposits." He also vaguely refers to local influence of irregularities of teeth and the use of soft foods.

These divergent views on etiology and pathology of periodontal disease here mentioned are but a few selected from

1 XVIIth International Congress of Medicine, Section XVII, p. 26.

some of the best known recent writers — many more might be quoted to emphasize the confusion which exists regarding the character of the disease. The great lack of some recognized system in the treatment of the disease is undoubtedly due to these divergencies of opinion as to its cause, for all treatment is based on the conception of certain etiology — those who believe in constitutional causes, or local causes or gouty diathesis, or osseous lesion or pathogenic organisms, or protozoa, base their treatment accordingly, and unfortunately the majority have little real conviction that any form of treatment is likelv to succeed.

Chapter I. Etiology Of Periodontal Disease

No useful etiology of periodontal disease can be based on the conception that pus must be visible or present in the diagnosis of the disease. When the recognition of the disease is delayed until this stage is reached, the most important stages have simply been overlooked until the disease has been in existence for a very long time, and it is on this account that the very term pyorrhoea, employed to express it, is bad and misleading. When pus is exuding or can be expressed from the sides of the teeth, the disease has already advanced considerably.

A study of the pathology of the disease should leave no doubt in our minds that it is of purely local origin; it only needs to be recognized in the incipient stages to impress us with the force of this conclusion. The vast majority of cases have some local irritant cause or series of local irritant causes directly responsible for the starting of that inflammation which lends itself to the possibility of septic infection of the adjacent tissues.

The incipient stage of the disease is to be found about the gingival margin in what is usually termed gingivitis and not generally associated with pyorrhoea. At this stage if the gingival trough (Fig. 1) or space be examined, it will be found to contain some local irritant in the form of salivary calculus or stagnant food or coating of translucent mucous

ETIOLOGY OF PERIODONTAL DISEASE extending from the necks of the teeth into the trough, or, in the case of badly kept teeth, quantities of salivary calculus on the teeth impinging on the gingival margin. This local irritant causes a slight inflammation of the gingival margin, which may be general or may be confined to the dental papilla?, but wherever there is foreign matter in contact with the delicate epithelial lining of that fold of gum which constitutes one boundary of the gingival trough, inflammation occurs. This inflammation may not be visible on the outer surface of the gum (as it often is not in well kept

Fig. 1. — A, gingival trough; B, alveolus; C, periodontal membrane.

teeth which are constantly massaged by the brush) but may be confined to the gingival trough, extending chiefly in the direction of the upper fibers of the periodontal membrane. Mouth bacteria are ever present, and when a stagnation area is produced it is impossible to designate the precise stage at which proliferation of pathogenic bacteria first takes place; it is probably at a much earlier stage than usually estimated.

This local inflammation, if left unchecked for any considerable length of time, or if allowed to recur at frequent intervals,

SUBGINGIVAL CALCULUS 25

leads to the next stage in the disease, in which the local irritant is augmented by one of the products of inflammation, which is subgingival or serumal calculus. Considerable doubt has been expressed by some authors on the existence of this form of calculus, and many writers ignore it altogether, but there is nothing so certain as the production of this form of deposit, when inflammation of the gingival fold occurs.

Subgingival Calculus. — Subgingival calculus is formed at a very early stage in the gingival inflammation, which precedes chronic periodontal disease, and is one of the primary causes of the severing of the fibers of the periodontal membrane, and the rarefying osteitis associated with pyorrhoea alveolaris.

This form of calculus is derived from "an exudation of mucus rich in colloidal material," 1 which exudes from the inflamed surface of the gingival fold in direct contact with the necks of the teeth; it is a product of the blood, consisting of inorganic salts, principally magnesium phosphate, calcium phosphate and calcium carbonate; the predominating salt being dependent upon the amount of surcharge of that particular salt present in the blood of the individual. The amount of subgingival calculus derived from so small an area of inflammation is no doubt exceedingly small at first, and in the early stages of its formation on the roots of the teeth only amounts to a delicate granular layer, which is difficult to detect, but gradually the deposit increases, and itself becomes a source of further irritation to the inflamed area immediately covering it. It further increases, until it is readily discernible in the form of granular nodules or a hard, smooth, brownish crust, which adheres firmly to the necks of the teeth.

Subgingival calculus having once been deposited, inflamma-

1 Kirk: Operative Dentistry, p. 484.

ETIOLOGY OF PERIODONTAL DISEASE tion seems to take on a more acute form, the gums become turgid and heaped up in the interdental spaces (increasing the depth of the gingival trough), and become loosened from the necks of the teeth, forming a suitable receptacle for particles of food. The inflammation extends to the periodontal membrane and the alveolar bone, the former becomes detached and recedes, forming a small pocket, the latter is absorbed gradually from its free margin toward the body of the bone, and a process of rarefying osteitis starts (Fig. 2). At this stage bacteria undoubtedly exercise a great

Fig. 2. — Starting rarefying osteitis.

influence — hastening the progress of the disease. The contents of the gingival trough now consist of desquamation of the epithelial lining of the gingival trough, dead tissue cells, leucocytes and serum exuding from the inflamed surface, mixed with mucus and particles of decomposing food, altogether providing a most admirable culture medium which is kept at the right temperature for the development and maintenance of pathogenic organisms.

Up to this stage no pus is visible and pressure on the gums only produces bleeding, but the soft tissues are in a diseased state and bacteria contained in the gingival trough find

SUBGINGIVAL CALCULUS 27

ready access into the intercellular spaces and capillaries, and probably penetrate into the alveolar bone.

In many well kept mouths some of these symptoms are entirely absent — there is no swelling or turgidity of the gums, no discomfort, the gingival trough, instead of being widened for the reception of foreign matter, appears to be shrinking gradually. The gingival margin is thinned and taut about the necks of the teeth, the alveolar border has obviously absorbed away, and the dental papillae have disappeared leaving the necks of the teeth well denned, revealing wide interspaces. The teeth may be beautifully kept as far as the free margin of the gums, but if the gingival trough be examined by passing a delicate probe into it, a finely granular layer of subgingival calculus can be detected adhering to the necks of the teeth. Sometimes it takes the form of sharp nodules. Sometimes this local irritant is readily detected in larger quantities on the approximating surfaces of the roots of the teeth. Subgingival calculus is the active exciting cause of the trouble in these cases, and the process, although slower than the acute form already described, is just as sure in its destruction of the periodontal membrane and alveolus.

In these cases there is no loosening of the teeth, and sometimes the alveolar bone is enlarged over the roots of the teeth from the pathological action of a continuous slight inflammation. There is also a slight fetor from the region of the molars.

In the more acute forms, where marked inflammation is present, the tissues break down rapidly under the influence of bacteria, deep pockets are formed, in which pus collects. This may be confined to certain localities, where the inflammation has existed the longest, or it may be general. As the disease advances in severity and the pockets deepen by the loss of periodontal membrane and bone, bacteria become

28 ETIOLOGY OF PERIODONTAL DISEASE

largely responsible for the maintenance of the inflammatory process, which now extends deep into alveolar bone: the sockets become enlarged by the absorption of bone salts and a rarefying osteitis ensues, affecting the lamella?, lacuna? and canaliculi of this transitory bony structure. The teeth become loose in their sockets, and every motion of mastication tends to increase the process of absorption set up by this new irritant which acts as a stimulant to the osteoclasts located in the proximity of the alveolar wall surrounding the roots of teeth. Pathogenic microorganisms enter the inflamed periodontal membrane and pass into the alveolar bone, where they exercise a deep-seated inflammatory action and are readily absorbed in large numbers into the general circulation. The system is able to resist this invasion of bacteria only to a certain point; beyond this immunity becomes lost and a general toxaemia often results. The toxaemic effect of microorganisms varies largely with the individual, and those previously or at the time affected by constitutional disorders, such as gastro-intestinal toxaemia, diabetes, neurasthenia, rheumatism, intestinal nephritis, anaemia or any form of toxaemia occurring in other parts of the system, would naturally lose immunity to the action of bacteria from the pyorrhoea source of infection much quicker than those who are otherwise sound. The effect of general toxaemia is undoubtedly that it aggravates the local affection and makes it more intractable. But constitutional disorders cannot be accounted the direct cause of the local infection.

As the disease advances to the last stage, when the teeth become so loose that it is a question whether they can be retained by any means (Fig. 3), when constant and copious discharge of pus indicates the severity of the affection, it will often be observed that the roots are smooth and entirely free

SUBGINGIVAL CALCULUS from calculus. This is not due to there never having been a deposit previously on them, but to the fact that the exudate of the first inflammatory process (from which subgingival calculus was first deposited on the upper portion of the roots) has been supplemented by infiltration of leucocytes and broken-down tissues mixed with microorganisms which constitute the pus, and this flowing constantly over the surface of the root gradually liquefies and dissolves those inorganic salts and carries them away, leaving the cementum smooth and clean.

Fig. 3. — Advanced pyorrhoea.

There are many other local irritant causes, besides those so far mentioned, which in some cases are the sole and only cause of the starting and maintaining of the disease, together with the bacteria, which are always a factor and fulfil the final destruction of the tissues concerned. They are often of a subtle nature and are readily overlooked in the search for the cause of the disease. They sometimes reveal no symptoms approaching the common forms of pyorrhoea, and their effect is principally on the periodontal membrane and the osseous structure of the parts. Prominent among these subtle causes is faulty contact points of the cusps of two or more teeth; this is brought about by the loss of one or more

30 ETIOLOGY OF PERIODONTAL DISEASE

teeth, and among the most obscure of these are cases of extractions in early life, which have apparently rectified irregularities of the teeth in a simple and sometimes apparently effective manner. An old practice of extracting the four first molars or the second premolars to overcome irregularities is sometimes responsible for this effect. Sometimes the effect can be traced to the loss of a single tooth, usually a first molar. This throws undue strain on certain teeth, which eventually results in a chronic irritation and inflammation of the periodontal membrane, accompanied with bacterial infection and resulting in periodontal disease, starting in the teeth affected.

Adenoids is another obscure cause by which mouth breathing induces the premonitory symptoms, at a very early stage, by impairing circulation in the gingival border.

Many other local irritant causes are to be found which produce more localized effects and provide a starting-point at the particular teeth concerned, the other parts of the mouth remaining normal. These include ill-fitting crowns or bridges, fillings with overhanging cervical margins or faulty contact points, abnormal spacing of the teeth, irregularities of the teeth, ill-fitting dentures, insufficient use of the teeth and the use of soft, pappy foods, these last two having a general influence on the whole denture. With all these local causes microorganisms are intimately concerned, and after a certain stage of advancement of the disease they may continue to maintain the progress of the disease even after the local irritant cause has been removed, giving the impression that pathogenic organisms are a direct cause of the disease.

Chapter II. Bacteria And Mouth Protozoa

BACTERIA.

One of the most important factors which has to be taken into consideration in every case of periodontal disease is the bacteria which are associated with the suppurative inflammation characteristic of the disease. Microorganisms, which possess pathogenic properties, are always present in the oral cavity of healthy as well as impaired subjects. Whether pathogenic bacteria are capable of starting the irritation, which would lead to the establishing of the disease without the cooperation of any mechanical local irritant, is a question which does not seem to have been decided by authorities on the subject. Miller, 1 referring to this, says: "I am not able to form any decision regarding this matter, but so much is unquestionably certain, that the symptoms are greatly aggravated by local irritants, and that a removal of all irritations and extreme cleanliness are imperatively necessary in contending against this disease." It may be taken as an established fact, however, that whenever a slight irritant exists and has caused the appearance of the disease in a localized area of the mouth the pathogenic bacteria are capable of spreading the inflammation to adjacent parts and establishing the disease practically all over the mouth.

This fact is of great significance, because it points to the

1 Microorganisms of the Human Mouth, p. 332.

32 BACTERIA AND MOUTH PROTOZOA

important change which takes place in these microorganisms, which in healthy mouths are perfectly harmless, but in the changed environment resulting from existing disease are capable of becoming pathogenic organisms, exercising influence on neighboring healthy tissues and conveying disease to them. The establishing of disease from this source would be infinitely more marked in every case if it were not for the power of resistance with which healthy tissue is endowed, by which antibodies are produced to combat the bacteria; the toxic effect of the bacteria is overcome to a point of immunity, to which the tissues are capable of resisting, beyond this point it exercises an irritant effect on the tissues, resulting in inflammation, and organisms are able to multiply and dominate the tissue area affected by their presence in large numbers.

The degree of immunity varies considerably according to the power of resistance endowed in the tissues; thus it may be observed that some individuals retain a considerable amount of local irritant in very uncleanly mouths without developing pyorrhoea, while others develop the disease readily from the slightest amount of foreign matter about the teeth. In this respect environment, mode of living, occupation, heredity and constitutional disorders undoubtedly exercise great influence.

In the presence of the smallest amount of irritant in the gingival trough, which produces even a slight inflammation of the gingivus, it is possible that pathogenic bacteria are capable of entering the tissues and increasing in numbers, and although combated by the tissue-resistance to a point, local infection is inevitable, except there is an unusual immunity. It is therefore impossible to designate the stage at which pathogenic infection first takes place. -It is erro-

BACTERIA 33

neous to diagnose the disease as only starting when the gingival trough is deepened or pockets have been formed or pus is present. The early infection doubtless starts with the first slight inflammation and microorganisms begin then to adapt themselves to the tissues and to multiply in their effort to overcome immunity of the local area and to inflict their toxins on the tissues; from this stage onward, until immunity is lost and the tissues have broken down into deep pockets with pus, they are always present in ever-increasing numbers.

If this view of the early influence of microorganisms on the gingival margin were more universally accepted and acted upon the development of the disease in its advanced forms would be much rarer than it is at the present time, at least in individuals who visit their dentists at regular intervals.

A large number of different bacteria have been cultivated from pyorrhoea pus. Miller isolated twenty different bacteria from twelve cases of pyorrhoea, among which he mentions Staphylococcus pyogenes aureus, Staphylococcus pyogenes albus and Streptococcus pyogenes, "but was not able to determine the constant occurrence of any particular one which might be defined as the specific microorganism of pyorrhoea alveolaris." Miller's investigations appear to have been made from specimens taken from advanced cases, and in most instances he found but one kind of organism or one kind so predominated that the others could be left out of account. Later investigators describe the presence of many different kinds of bacteria very constantly present in the pus. Dr. C. P. Brown 1 found the almost constant presence

1 New York Med. Jour., December 20, 1913.

34 BACTERIA AND MOUTH PROTOZOA

of six kinds of bacteria in pyorrhoea pus, namely, Bacillus influenzae, the streptococcus, staphylococcus, pneumococcus, Micrococcus catarrhalis and diphtheroid bacilli. Goadby 1 investigated a large number of cases of the early stages of the disease and noted some difference in the microorganisms present at this stage to those found at more advanced stages; cultures made from them showed that the most commonly occurring were those corresponding to organisms of inflammatory catarrh: namely, Micrococcus catarrhalis, Bacillus coryza segmentosa or Bacillus septus, Micrococcus pneumonia? and in addition he found Bacillus necrodentalis (Goadby) and Micrococcus citreus granulatus (Freund). In later stages of the disease, when immunity of the general system was lowered and constitutional disturbances evident from absorption of toxins, the predominating organisms were usually staphylococci and streptococci or the pneumococci. Microscopic examination of films of pus which are properly stained reveal a large variety of microorganisms (many of which do not grow on culture media), pus cells, hyaline cells, and epithelial debris. The bacteria include the numerous groups of cocci, bacilli, spirochetes and streptothrix.

MOUTH PROTOZOA.

Entamoeba buccalis has been found in the mouth from time to time and described by various authors. Gross, in 1849, described Entamoeba gingivalis, Sternberg, in 1862, Entamoeba buccalis, Grasse,in 1879, Amoeba dentalis, Flexner, in 1892, Amoeba Prowazek in 1905 Entamoeba buccalis; but it was not until 1914 that the researches of Chiavaro of Rome, and Barrett, of Philadelphia (simultaneously and

! Proc. Royal Soc. Med. (Odontological Section) iii,. 55.

MOUTH PROTOZOA 35

independently conducted), established the fact that Entamoeba buccalis is always present in pyorrhoea pus. The organism is described as measuring 6 to 30/z, with a single vesicular nucleus of 1.5 to 4.5/* in diameter, poor in chromatin, with a thick membrane. It is very mobile, constantly changing its form by thrusting out one, two or more lobular pseudopods in its activity and showing a clear distinction between the endosarc and extosarc. Chiavaro

Fig. 4. — Large oblong and medium round type entamoeba with black masses ingested and surrounded by nourishing vacuoles. Fixed and stained with ferric haematoxylin of Heidenhain. (After Chiavaro.)

draws attention to the ingestion of bacteria by entamoeba? which could be seen in the protoplasm in fixed and stained specimens (Fig. 4).

Chiavaro came to the conclusion that "the entamoeba has not a pathogenic action; on the contrary, as it feeds on bacteria, it is most probably an aid to the autodisinfection of the mouth." This view the writer is inclined to accept after investigating 50 cases of pyorrhoea in which amoebae

36 BACTERIA AND MOUTH PROTOZOA

were found in 78 per cent., and in a paper read at the Royal Society of Medicine, June, 1915, expressed doubts, from a clinical standpoint, of the pathogenic action of Entamoeba buccalis in pyorrhoea. Barrett and Bass and Johns, however, pressed the claim, on clinical grounds, that Entamoeba buccalis being present "in a large proportion of pyorrhoea pockets and the disappearance of suppuration under appropriate treatment by a known amcebicide, such as emetin, have served to justify the claim that they are the immediate important factor in an overwhelming number of pyorrhoea cases." 1 This theory has been amply disproved and the presence of Entamoeba buccalis in the mouth is looked upon as having no pathogenic influence on the disease.

1 Barrett, M. T.: Dental Cosmos, December, 1914.

Chapter III. Pathology Of Periodontal Disease

The pathological lesion exhibited in periodontal disease should be studied from its very initial stage when the physiological structure and function of the component cells are injured by some irritant cause and stimulated to excessive bioplastic activity which is always hyperplastic. The component parts of the structure under consideration must be recalled — the alveolar bone, the periodontal membrane and overlying fibrous or mucous tissue — all richly supplied with bloodvessels and containing terminal cells of singularly degenerative and transitory nature.

The initial pathological lesion is always instituted by an irritant in the gingival trough or injury to gingival tissue, resulting in inflammation, i. e., dilation of bloodvessels, acceleration of blood flow followed by retardation, exudation and migration of leucocytes, stasis and degenerative changes, with accompanying proliferative and reparative changes. At the very earliest stage evidence of irritation to the gingival trough is hardly perceptible and can only be determined by clinical examination of the condition and contents of this space; but gradually this initial inflammation leads to marked congestion of the gingival fold and swelling of interdental papillae accompanied by inflammatory exudates. A stagnation area is established in which mouth organisms are present; they begin to adapt themselves to favorable as conditions and produce an irritant influence on the tissues. The process of deposition of subgingival calculus now begins;