Entamoeba buccalis showing phagocyted cocci.

which we absolutely know to be responsible for many types of secondary inflammation as well as the chief etiological factor in apical abscess. I repeat,

Pyorrhea alveolaris : Ulcerated margin. of the gum showing chronic inflammation-no amoeba in the tissues altho many were present in the pus.

ries of lantern slides showing human tissue taken from the sides of human teeth which were exhibiting intense pyorrhoeal inflammation. These tissues were removed with the teeth and hardened, cut, and stained for the express purpose of studying their amoebal content. We find many bacteria on mucous membranes, and the smears from the pockets taken before these tissues were cut away showed a few amoeba and infinite numbers of what proved to be streptococci in culture. A close study of these tissues, however, does not reveal a single amoeba embedded in the tissue. It would seem if amoeba were

pathogenic that these five cases should show amoeba embedded in the granulation tissues of the bottom of the pockets, but they do not.

In the last two years, we have been encouraged to believe by Hanssen of Christiania (*1) that there was a specific micro organism responsible for pyorrhoeal infection, designated by him as bacillus pyorrhea, tho the writer has been absolutely unable to find an organism corresponding to the bacillus pyorrhea of Hanssen in pyorrhea pockets. The bacillus subtilus, a common laboratory growth, more nearly fills the morphological and cultural requirements of Hanssen's bacillus than any we have yet been able to find.

The medical and dental professions all over the world have been lead to believe that the amoeba is the responsible factor for all pyorrhoeal processes and that its destruction would be a panacea in the cure of pyorrhea, and the author earnestly hopes that this may be true. Nevertheless, his own experience does not lend color to this belief and we are thrown back upon the best teacher we have had in this matter up to the present time, experience, which indicates in no uncertain terms that the gingival margin is the point where pyorrhoeal inflammations begin and that the pyorrhoeal inflammations are wrought by and maintained by the poison proteins (*2) induced by the presence and destruction of mixed bacterial infections, by the body ferments, and experience has also taught us that clean tooth surfaces preclude gingival infection and that heavy massage of the gums also tends to harden and render more resistant the gingival margins to infection. Experience has further taught us that the logical place to begin the treatment of pyorrhea is the tooth's surface and that the first step in the treat

*1-Journal of Norweigan Dental Society, 1914. *2-Victor C. Vaughan's-"Protein Split Product in Relation to Immunity and Disease."

such demonstration, the next step should be the elimination of all rough areas on the tooth's surface which may retain bacteria on or in the tooth's surfaces, and this is accomplished by applying to them, the type of stones shown on the screen, (Fig. 8) swinging them across the enamel surfaces, thus grinding out the pits that have been induced by the acid formed by the bacteria on these surfaces, getting rid of the bacteria themselves and polishing out the inequalities which serve to retain and foster bacterial growth. After the use of the coarse stones on the tooth surfaces, disclosing stain should be again used to make sure that all pits have been beveled out. After all pits that

contain bacteria and inequalities have been beveled out, and the application of the disclosing stain reveals nothing, then the tooth surfaces should be thoroly polished with the type of Arkansas stones shown on the screen, and the brilliance increased by the use of Moosehide wheels loaded with jeweler's rouge or with any other abrasive which will give a high degree of brilliance to the enamel.

When the tooth's surface has been properly cared for in this manner, we are then ready to attack root surfaces.

Fig. 8.

Arkansas and Carborundum stones used to perfect the tooth surfaces.

Before proceeding to a discussion of the pyorrhea pocket, the author desires to discuss for a moment other forms of irritation than that of bacteria which may be responsible for gingival inflammation and will make the statement that any irritant which will induce congestion of the gingival margin favors bacterial infection; e. g. lack of contact point, permitting the bruising of the soft tissues ill fitting regulating appliances, the mechanical irritation of bands, imperfect fillings, malocclusion, thus delivering undue force in some point in certain direction, all of which induce congestion and which in time stimulates osteoclasis and destruction of the bone just as surely as will bacterial growth or the continued application of force by regulating appliances.

There is an additional reason for beginning the treatment of pyorrhoeal in fection on the tooth's surface, the introduction of polishing materials into the pockets themselves. Pumice or silex introduced into the pocket must always be an irritant to the tissue cells of the surrounding area. If all polishing and cleansing of the tooth's surface is done before the pockets are disturbed by scalers or planes, we avoid getting polishing material into them.

There may be a specific micro organism which is responsible for pyorrhoeal infection. While we have not proven the streptococcus viridans to be the specific organism, we are thoroly of the opinion and belief that this family of viridans is the chief offender, because of its universal presence in the pockets and in the tissues and because of its definitely proven relationship to dental abscesses and secondary lesions. It is not proven, however, that it is certainly the etiological factor, tho the evidence is slowly accumulating which in the end may be accepted as proof, sufficient to justify our believing it to be the specific factor, for wherever this organism locates in the tissues the result is death of tissue and the question naturally arises, where and how does it enter the tissues? Some authors (*1) would have us believe that it is blood borne and introduced thru the tonsil or from some other area of the body. The author does not believe this to be true, however, for the reason that most observers unite in the belief borne out by experience that the streptococcus found in tonsils is haemolytic. Davis (*2) reports ninety per cent out of 115 cases to be haemolytic. Rosenow's observations confirm the belief that the streptococcus found in tonsils is haemolytic. Dwyer and Gignoux also confirm this

*1-Ulrich Dental Review 1914.

*2-Davis Journal Infectious Diseases, Vol. 10,

1912.

fact. (*1) In the author's experience with two hundred and fifty cases, only one root tip abscess was proven to be haemolytic, which streptoccocus was found and isolated from a dental abscess in the mouth of a young Hollander by Mr. Gaskill in the early part of the winter of 1914. (*2) With this one exception, no other example of haemolysis was found by Mr. Gaskill and in some two hundred cases in which the streptococcus viridans has been isolated in pure culture by Doctor Henrici, no single example of haemolysis has been observed of a family of streptococci isolated from root tip abscesses or pyorrhea pockets. Gilmore and Moody (*3) reported a short series of cases in which they found haemolysis but the haemolysis was not definitely proven to be due to streptococci as they cultured directly from the infected field to blood agar, and there are other bacteria save haemolytic streptococci which will haemolyse blood, and the haemolyses reported by them may be and is probably due to the admixture of other bacteria in their cultures. In our own work, our cultures (*4) have invariably been plated out until the bacteria were obtained pure, and I repeat, none of these cultures have been haemolytic. I, therefore, do not believe that the infecting streptococcus in either the dental abscess or the pyorrhea pocket is introduced from the tonsil or the general blood stream, because if it came thru the tonsil path and was deep in the tissues, it certainly should haemolyse. (*5) We are, therefore, thrown back on the belief that these bacteria are introduced into the tissues by direct continuity of

*1-Dwyer & Gignoux Bacterial Exam. of Tonsil crypts, from Manhattan eye, ear, and throat reports, Feb. 1912-1913.

*2-Hartzell Dental Bulletin 1914.

*3-A study alveolar abscess and infected root canals. Journal A. M. A. December 5.

*4-National Dental Bulletin-Report on Infections of Mouth-Hartzell, Henrici, Leonard. *5-Barn's -The tonsils, pages 68-69.

tissue following down from the tooth neck into the pocket and also that apical abscesses may be planted from bacteria introduced in the same manner or thru the root canals themselves. That it is easily possible for bacteria to enter the peridental structures from the gingival culdesac is a fact. The writer of this paper has repeatedly demonstrated openings in the bottom of the gingival crevice of seemingly healthy teeth and these openings may readily be shown to exist by the use of oxygen under compression which may be allowed to flow from a blunt nosed needle into the gingival crevice. The needle is not to be thrust into the tissues but simply introduced into the gingival crevice, without pressure of the point into the tissues. A stream of oxygen thus directed into the gingival crevice will usually find its way from two or three points at least into the tissues and its movement in the tissues may be noticed for distances of as much as a half an inch more away from the point of entrance.

or

The author has repeatedly demonstrated this possibility in the case of his own teeth, the gums of which are healthy, firm, and pink, and has also noted it in a large number of other individuals and he believes that it is thru these openings leading into the deeper structures around the teeth that the bacterial infection of these structures occur. Without doubt, the most valuable work that has yet been done in the gross pathology of inflammation of the tissues contiguous to the teeth is that of Doctor Talbot, (*1) and the author now invites your attention for a few moments to pictures from the work of Talbot. Doubtless, these are familiar to most of you and the writer desires these pictures here in order to illustrate a phase of the treatment of this disease which has always

seemed exceedingly important.

*1-Talbot-Interstitial Gingivitis.