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Infectious Factors in Gingivitis and Their Relation to the Dentist*
IN FEC TIO U S FACTORS IN G IN G IV ITIS AND T H E IR RELA TIO N TO T H E DENTIST* By ROBERT A. KEILTY, M.D., Washington, D. C. H E purpose of this paper is to pre sent to the dental profession a med ical point of view on the infectious conditions operative about the necks of the teeth. In a previous paper,1 before a mixed medical and dental group, I re viewed my concepts of this subject, and in a series of papers,2 some of which have been published, I present the details and facts of the study. T h e problem of gingivitis belongs to the dentist, since it concerns the preserva tion of the structures upon the care of which th at profession is founded. I t is
T
*Frora the Pathological L ab o rato ries of the D iagnostic C enter, U. S. V eterans B ureau, W ashington, D. C. *R ead before the Section on P e riodontia at the Seventy-F irst A nnual Session of the A m erican D ental A ssociation, W ashington, D . C., Oct. 10, 1929. 1. K eilty, R. A .: G in g iv itis: A n Infectious E ntity, from M edical and D en tal Aspects, J. A. D. A., 17:271 (F eb.) 1930. 2. K eilty, R. A .: P resen t State of O ur K now ledge of G ingivitis, J. L ab. & Clin. M ed., 13:451-468 (M ay ) 1928; G ing iv itis I I : C linical A p p e ara n c e of G in g iv ae in D ifferent Form s and Stages, J. Lab. & C lin. M ed., 14: 48 (Ja n .) 1928; G in g iv itis: L ab o ra to ry M eth ods fo r Study, J. Lab. & C lin. M ed., 14:165 (Feb.) 1928; G in g iv itis: C h a rac te r of E x u date in G ingivitis, J. Lab. & Clin. M ed., to be p u b lish e d ; Specificity of B a cteria to the B acteriolytic A ction of Chem icals, w ith a Note on T h is A pplication to Chem otherapy, J. Lab. & Clin. M ed., 14:539 (Ju n e ) 1929; p. 539; Specific C hem otherapeusis w ith R e la tionship to the B acteria Involved, J. Chem o therapy, 6, J a n u a ry , 1929.
Jour. A . D . A ., Ju ly , 1930
certainly complex and takes into account facts well known to dentists but not even familiar in terminology to medical men. I t is difficult, therefore, for the medically trained mind to evaluate the problem in complete ignorance of dental facts and terms. O n the other hand, even welltrained dentists, as a class, must admit some ignorance of the dental pathology and bacteriology involved. These two positions are not meant as an indictment, but are merely statements of fact. I t is not advisable for the medical profession to become familiar w ith dental practice, but it is advisable for the den tists as a whole to know more about pathology and bacteriology. I t is hoped that the researches in dental bacteriology which are now so popular will be even more strenuously pursued. I am making a plea that the maze of entangled facts, now known as the bacteriology of the mouth, be attacked by a mass of workers and the importance of each individual finding be thoroughly checked and evalu ated. T h e subject w ill then be on a firm footing and not, as now, often merely held in erroneous opinion. M y own experience goes back to 1914, when B arrett first made smears from pyorrhea pockets at Allen J. Smith’s sug gestion and endamebae were recognized and reported in forty-nine consecutive cases. I saw the first smear and examined many mouths myself at that time. You are all fam iliar w ith the rise and fall of
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Endameba gingivalis and the false prem planations and details of controversial ises regarding emetin as a specific in pyor points to other papers. Inflammatory proc rhea. T h is is an instance of erroneous esses about the structures of the teeth are evaluation of facts in the light of com described under a m ultitude of names, of plete knowledge. O n the other hand, the which the term “pyorrhea” is most com endameba is n(it a simple resident present monly used. T h is has almost had its in a large percentage of mouths but is a centennial and can be discarded. In view definite im portant pathogen. In this light, of the fact th at most, if not all, of the in it m ust be rediscovered and again reck flammatory changes begin in the soft oned w ith for its proper value. I t is not structures, I have included all cases un in any sense specific; a fact which D r. der the short simple term “gingivitis.” Smith never did believe; but th at does T h ere are many other terms, possibly just not mean that it is not pathogenic. as good, such as periodontitis and perio D uring the intervening years, I have dontoclasia, but they are not so expressive pursued the subject more or less con and do not lend themselves to qualifying stantly, and I now have records of nearly adjectives as does gingivitis. A ll forms 7,000 cases. T his has given me an experi of inflammatory change in the gingivae, ence resulting in a varied contact with from the slightest marginal gingivitis dental men which has been most enlight through V incent’s infection to the most ening for me, and which has caused me severe “pyorrhea” can be classed under to change my evaluations as the facts gingivitis, acute, subacute or chronic, become more and more definitely estab with expressive modifications, such as lished. T here is still much to be done, traum atic, exudative, ulcerative, sup and I feel that I have hardly entered on purative, gangrenous, fibrous or recessive. the problem, owing to its complexity. In T his immediately simplifies a classifica a series of papers, through the American tion and gives a common ground for the Society of Clinical Pathologists, I am etiology. T he pathology of all these attem pting to present the technical bac changes in the gums, the subgingival teriology of this experience, and it would tissues, the peridental membranes and the seem to be the proper time to present the bone is that of inflammation, in one or practical side to the dental profession. another of its manifestations, and to a In the whole work, there will be noth degree comparable to the advance which ing startling, but certain well-devised the gross morbid changes indicate. procedures and facts gleaned from rou In the etiology of this inflammatory tine observations on a large number of complex, bacteria play the most important cases along w ith experimental w ork will role, since they invade not only the gin eventually satisfactorily solve the whole gival sulcus, which is used as a medium problem. T h e laboratory and the dentist of growth, but also the tissues themselves, must w ork together, for the present at which is more im portant in producing least. T his relationship may be perma the actual inflammatory reactions in nent, or, when completely understood, these structures. O f all the conditions may be so simplified that the dentist can which have been advanced as causative handle the work alone. of these changes, the presence of bacteria In order to present as much as possible per se is the most im portant. T his is true in the time allotted, I am going to sum not only from the standpoint of the marize w ithout comment, leaving ex pathologic changes present but also from
K eilty— Infectious Factors in Gingivitis the fact that the inflammatory changes subside, and repair prom ptly takes place when the bacteria are eliminated. A ll other conditions, some of which are now accepted as prim ary causes, are in reality secondary, in spite of the fact that they may be actual initiating factors in the disease. F o r example, there is no question that traum atic occlusion, by sud denly placing an abnormal stress on one or more teeth, allows an easy invasion of bacteria which otherwise would not take place. T h ere is no question that the cor rection of traum atic occlusion will many times obviate an inflammatory reaction, removing the possibility of further in vasion by bacteria, w ith a reparative effort on the part of the cell structures when the traum atism ha? been removed. W hile most mouths show a certain amount of traum atic occlusion, bacterial invasion will take place w ith or w ithout traum atic occlusion, and w ill often involve teeth which show no evidence of such traum a. In this sense, I feel no hesitancy whatso ever in placing bacterial invasion ahead of traum atic occlusion as an etiologic factor, but I do give traum atic occlusion its proper importance as one of the initiat ing factors and one which may often con tinue as an im portant factor. M uch has been said and will be said concerning calculi, serumal or salivary, with sordes, ta rta r and film. C ertain mouths tend to collection of sordes, or, we may say, debris deposits, about the necks of teeth, which tend to calcify in spite of careful mouth hygiene and fre quent scaling. T h is is due, probably, to an individual chemical character of the saliva, w ith the proper hydrogen-ion con centration for calcium deposit. These cases are very decidedly in the minority. By far the greatest number of cases showing deposits of calcareous ma terial, either a§ the so-called serumal
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calculi beneath the gingival margins or as deposits in the interproximal spaces, where cleaning is not actually accom plished, are due to the natural deposition of calcareous material in necrotic exuda tion and debris which is acting as a for eign body. T his phenomenon takes place all over the body. If the original exudate is cleaned out and kept clean, or if there is no reason for its formation, this type of deposit will not take place. As such, then, all types of calcareous material can not ,be considered as etiologic factors in any sense but are the results of a condi tion present. T hey do continue as irri tants when present. T raum atic occlusion and gingival cal culus are assumed by the dental profes sion today to be the two outstanding etiologic factors in gingivitis. I consider them both secondary in importance to bacteria. T h ird and less important, although less understood, in the view of many w riters is somatic influence in relation to local resistance and secondary mouth fac tors. Some men assume that general body chemistry, such as calcium phosphorus and glandular deficiency, and such, gen eral diseases as tuberculosis, syphilis and diabetes, present the sole causative factor in the development of gingivitis. T his cannot possibly be true, else these factors would be present in 90 per cent of our population, which they are not. T h ere is no question that a certain percentage of cases showing these deficiencies w ill show marked gingival changes. These gingival changes are a general part of the reaction, and while they are aggravated by the somatic condition, that condition is in no sense the sole etiologic factor in the gingivitis. T h ere are many other secondary con ditions which have been presented as etiologic factors, and which, in individual
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cases, do play some part, but which in no sense can be considered as the important etiologic condition in all cases of gingi vitis. I refer to such things as smoking, gingival traum a in mastication, the pres ent state of our prepared foods, which are soft and rich in their preparation, the accumulation of food debris, mouth breathing and acid mouth. In a certain group of cases w ith ill-fitting dentures, partial or complete, w ith poorly made crowns or crowns which have long since served their purpose, bridgework improp erly applied, fillings of all kinds which are poorly finished, leaving, especially in the interproxim al spaces, roughened areas or shelves, and dental caries, which fortu nately is very decidedly on the decrease, one may find local reasons for a traum a which admit bacterial invasion in the same sense that traum atic occlusion plays its role. T hus, after all is said on the various etiologic factors in gingivitis, by a process of elimination and a study of the accepted data on the pathology involved, bacteria must be given first place in the etiology. W h a t of these bacteria ? H ere contro versy and lack of exact knowledge are frequent. In the “ M anual of Bacteri ology” (B ergey), forty-six different types of bacteria are described as occurring in the mouth. T h is does not include the entire number isolated by all workers. O f this number, I have records of the isolation of thirty-three different and dis tinct species, and I am sure that if time permitted, this number would be in creased. Can one pick out of this any particular species or type of bacteria and consider it a specific etiologic factor? A t the present time, in the records of my cases, certain bacteria repeat themselves constantly, but I do not consider in any sense that any are specific, unless it be the spirilliform and fusiform groups. These
two types are present in almost 100 per cent of gingival exudates, are not present in perfectly normal mouths, are greatly increased in acute conditions, are much reduced in inactive conditions and clear up w ith complete disappearance in suc cessfully treated cases. In this study, one must know w hat bacteria the perfectly normal m outh contains. T his is most difficult or almost impossible since the conception of the normal mouth is open to a great deal of discussion, and w hat one considers normal, another may consider highly pathologic, and vice versa. I con sider normal only the mouth which is absolutely perfect in its construction and absolutely free from gross morbid signs of inflammation. T his makes up, in my series of cases, not much over 1 per cent. Bacteria seen in fresh or stained smears and by culture vary w ithin wide limits in a group of cases but are more or less constant in a given case. I t will be seen from this that the gingival flora must be worked out for every case. I t is here that the cooperation of the laboratory is essen tial. C ertain groups are best seen by smear and others by culture. T he fresh smear offers the best means of rapidly determining the m ajor types of bacteria as well as any protozoa present. I have described methods in a previous paper. T h e spirilliform organisms under the general group of Borrelia vincenti are seen in their active form by fresh smear. T hey cannot be easily cultured, and until a method of culture is described, they had all best be grouped together as far as gingivitis is concerned. T hey are pres ent in all forms of gingivitis and are probably the most important of all the groups. T h e fusiform organisms are also con stantly present and are best grouped under the heading of Fusiformis dentiumHoelling. T hey are difficult to isolate in
K eïlty— Infectious Factors in Gingivitis culture and also require much further study. T h e cocci may next be taken, as to both importance and frequency. These can be seen in smear but are best studied by culture, and routinely the blood agar plate picks out as many as any other single medium. A large moist mucoid colony of staphy lococci is a constant finding. T h is colony offers a symbiotic relation for several forms of staphylococcus, white and yel low, and for bacillary forms associated w ith the higher mycelia. T h e streptococci are quite constant, pigmented, nonhemo lytic, plain hemolytic or w ith green hem olysis. T h e pneumococcus goes in waves. Several other types of easily recognizable bacteria appear on culture, but are not constant in every mouth. These are B. catarrhalis, B . coli, B. diphtheria, B. hofmannii and B . influenzae. B . aci dophilus is recognizable in smears quite constantly, but is not brought out on blood agar plates easily. M any other forms, such as rosettes or actinomycetes, short vibrios and long mycelia, singly and in multiple branches, are more or less common. T h e yeasts, saccharomycetes and monilia are only very occasionally seen but may be frequently obtained on culture. T h e protozoa Endameba ging'walis, Trichomonas buccalis, bodo and occasion ally giardia and cercomonas are the types that I have so far encountered. These organisms, as already stated, are not mere benign residents in dirty mouths, but are part and parcel of the gingivosulcal exu date. I f they do not invade the tissue and if they do not produce a toxin, both of which are highly probable, they at least act as distinct local irritants. I can say definitely th at as long as they are present, a gingival reaction w ill not en tirely clear up.
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I have tried to present a concept that all forms of inflammatory changes in the structures about the teeth are to be con sidered as one entity and spoken of under the general term of gingivitis. T h is in cludes everything from simple marginal gingivitis to the most advanced “pyor rhea,” along with acute exudative and gangrenous changes now known as V in cent’s infection. Such a concept will sim plify the whole situation, and the bac terial flora becomes the most im portant study in every case. I t is necessary to enumerate all bacteria and protozoa present in quantitative terms in every case. These findings are not only impor tan t from the point of view of knowledge to be gained, but also must be known if intelligent treatm ent is to be carried out. By intelligent treatm ent, I mean a plan of treatm ent mapped out beforehand and based on the conditions present in a given mouth, correcting each and every condi tion by a specific line of attack as nearly as the present state of our knowledge will allow. T his attack implies that every case must be individually studied from the dental, roentgen ray and pathologic aspects and every possible angle corrected. T h e laboratory must aid in the pathologic and bacteriologic study and the dentist must carry out the procedure based on this study. In the correction of dental mechanics, the dentist, of course, is guided entirely by his training and experience. In the correction of deep-seated dental disease as developed by the roentgen ray, the oral surgeon must be guided by his train ing and experience. In the same way, the correction of bacteriologic factors, now so universally neglected, must be guided by the training and experience of the bac teriologist. W hen all three of these trained groups are utilized, the end-re-
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suits for correction and maintenance of a perfect mouth are such as cannot be ob tained by any other line of attack. Tim e does not perm it my attem pting anything on treatm ent in this presenta tion. I t has been necessary to devote con siderable study to this phase of the sub ject, in order to obtain facts on bacterial reactions. Fortunately, we have a num ber of quite specific drugs which can be directed against predominance of bac terial factors present in a given case. It is the combined use of the proper drugs in a given case which constitutes the bac terial side of intelligent treatm ent. One of the most im portant phases of the whole subject is the use of a pretreatm ent stage in all operative work in the mouth. I have not seen a postoperative infectious reaction in a single successfully pretreated case in years. I have seen many post operative infections during the same time, in which the preparation of the patient did not take into account the actual bacteriologic factors in th at m outh by a specific preoperative chemotherapeusis.
CONCLUSION Gingivitis represents an inflammatory entity now known under a variety of names, from acute V incent’s infection to pyorrhea, which is subjectLta.a precise and accurate terminology based, on the pathologic process which is present. Considered as such an entity, bacteria play the most important part in the actual etiologic role. I t is possible to m aintain a study of these bacteria, but owing to their tech nical complexity, it is necessary to have the aid of a bacteriologist until methods of procedure can be furth er simplified. Such a complete bacteriologic study allows a plan of intelligent and quite specific treatm ent mapped out on the find ings in a given case, which can and should
be carried out by the dentist in addition to the correction of purely dental me chanics.
DISCUSSION
Israel S. Miller, Jersey City, N. J.:
D r. K eilty has m ade a contribution to o u r clearer u n d e rstan d in g of periodontal disease w ith the re p o rt on thousands of sm ears pro v in g th a t the fu sifo rm bacillus and the spirillum of Vincent a re the pred o m in atin g bacterial destructive agents a n d not the streptococcus and staphylococcus, as h a s g en erally been claim ed, but w ithout sufficient proof. I have th erefo re found it helpful to employ F o w ler’s solution ( solution of potassium arsen ite) com bined w ith liquor antisepticus alkalinus in the p ro po rtion of 3 to I (one tablespoon in o ne-half glass of w arm w a te r), as a sw ab of the teeth and m outh before operating, and as a m outh w ash. T h e arsenic in F o w ler’s solution is considered a specific fo r the sp iril lum ; and the other ingredient, destructive of the fusiform bacillus. T in c tu re of green soap in solution m ay be em ployed also. I employ this in addition to the re g u la r clinical p ro cedure in the trea tm e n t of periodontal disease, w hich I call the sta n d ard ize d periodontal procedure. T h is consists of six steps: (1) d iagnosis; (2) b a la n cin g occlusion; (3) in stru m en ta tio n ; (4) tissue stim u latin g ; (S) p lan n in g re sto ratio n s; (6) re tu rn fo r re g u la r prophylactic treatm en ts. T h e re is another point th a t has been illum inating to m e: D r. K eilty finds th a t a norm al m outh does not contain the V incent organism s. T h is fact w hen clinically applied m eans th a t the o perator m ust take sm ears d u rin g and a fte r treatm ent of a ll types of periodontal disease in ord er to m ake certain th a t he has elim inated these organism s. Unless tw o o r th ree negative sm ears in succession a re obtained, the m outh cannot be called norm al, reg ard less of how beautiful the tissues look clinically. I endorse D r. K eilty’s advice to dentists to cooperate w ith the pathologist in th e ir trea tm e n t of periodontal disease.
Wilhelmina Yeretsky, Mich.: I agree w ith D r.
Grand Rapids,
K eilty th a t a p e r fectly norm al m outh does not h a rb o r Vincent’s organism s, the spirochete o r fusiform . I h ave not run through the series of sm ears th a t D r. K eilty has, but in a series of p e rh ap s a hundred, w e have n e v er found those o rg a n isms in perfectly norm al m ouths. T h e difficulty w as in finding norm al m ouths, b u t the men,
K eilty— Infectious Factors in Gingivitis p a rtic u la rly the physicians a n d the lab o rato ry m an, w ere not fa m ilia r w ith the a p p earan ce of pathologic g in g iv a l conditions, and m ade the b ro a d statem ent th a t there w ere alw ays fu sifo rm bacilli a n d spirochetes in the m outh, because they did not recognize the pathologic conditions. I alw ays take my ow n m outh sm ears from the superficial and buccal m em b ra n e a n d also from the pockets before send in g them to the lab o ra to ry fo r diagnosis. D r. M ille r says th a t he also finds V incent’s o rg a n ism in the p e riodontal lesions. I h a v e h a d the in te restin g experience of finding, in young people, 22 or 23 y e ars old, the pocket extend ing the entire length of the root, tw o -th ird s of the w ay o r com pletely aro u n d it. T h e ro e ntgenogram show ed a trem endous am ount of bone gone, w hen we consider the age of the p a tie n t in these cases. In these pockets, I found a p u re sm ear of V incent’s organism s. I feel th a t th a t destruction of bone is due to infection from V incent’s organism s, in yo u n g er people. I do not think th a t w e find them in o ld er people. T h e y h a v e the m ore u sual form s of organism s in the p e riodontal pockets. R. A . Adams, Denver, Colo.: A s a p ra c titio n er w ho lim its his w ork entirely to periodontoclasia, a n d speaking to g en eral p ractitioners, let me say th is : Do not become p erturbed a t w h a t you have h e ard . G o back to y our office rem em bering the o th er things th a t you h e ard yesterday and to d a y ; follow them out, and you w ill get results. Do not be discouraged. M ost of the p a p er is true, as f a r as th a t is concerned, but th ere a re other truths. G o back to yo u r offices w ith th e d e term ination to recognize p e riodontal lesions in th eir incipiency, and tre a t them as you have been in structed to tre a t them , this m orning and yesterday, and you w ill get results, w ith out cooperation w ith the bacteriologist and the pathologist. I am telling you this because fo r m ore th an tw elve y ears I h av e not h a d a drop of m edicine on the bracket in tre a tin g chronic cases of these diseases. W e get re sults in chronic cases especially, a n d the only case in w hich I use m edicine is in acute in volvem ents. T o g et results, cooperation w ith a bacteriologist is not especially necessary. T r e a t these lesions as you h a v e been ta u g h t in o u r textbooks. T h e bacteriologist is not im perative to y our success in tre a tin g these cases. I f it is convenient, and you w a n t this service, I have no objection. B ut if you p ra c tice the things you h e a rd y e sterd a y a n d this
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m orning, and th a t a re constantly a p p e a rin g in our periodicals and textbooks, you w ill get results. H. JV. Krogh, Washington, D. C.: I speak from the point of view of the practitio n er and not the bacteriologist. T h e bacteriologic ex am ination of my patients is m ade by D r. Keilty, and he is the biggest single aid in my practice. M uch harm w as done in the tr e a t m ent of periclasia by subgingival m edication because the thought w as given out th a t it w as only necessary to m edicate these cases and they w ould p rom ptly cle ar up and rem ain so; th a t scaling or attention to restorations, o r any of the things th a t we w ere accustom ed to doing, w as unn ecessary ; ju st pum p in the d ru g and all w ould be w ell. T h a t w as not all by any m eans. If one does all th a t D r. A dam s ju st spoke of, using D r. K eilty ’s technic, one w ill re ally g et results. I did not agree w ith D r. K eilty w hen he said th a t if these cases a re cleared up bacteriologically, they w ill alw ays cle ar up clinically. T h a t is not alw ays tru e in my experience. In those cases in which the result is not good, I usually dissect the pocket according to W a r d ’s technic. N or do my p atients all g e t re lief fro m cal culus. T h e relief fro m calculus is astounding in the cases th a t a re kept clear, a n d also freedom from decay and all other u n p lea sa n t things found in the m outh, but, in c ertain cases, the calculus w ill reform , not so rapidly, but it w ill come back. E ven in those cases, the g in g iv a l inflam m ation w hich accom panies larg e am ounts of calculus w ill not be so m arked. I f one h a s no convenient lab o ra to ry and cannot h ave a chem otherapeusis w orked out, the use of a com bination of m etaphen and acriflavin, in com bination w ith arsp h en am in, w ill give excellent results. T h e re w ill be probably 5 per cent of cases w hich w ill not c le ar up. I do not m ean to say th a t it is pos sible to c le ar up bacteriologically 100 p e r cent of the cases, and I think some of the fa ilu re s m ay be due to the m echanical difficulty of g etting the d ru g into the pocket. N o r should the im possible be attem pted. E x tra c t about the sam e teeth th a t you w ould otherw ise— the m ultirooted teeth w ith bifu rcatio n involve m ent, a n d single-rooted teeth w hich a re r e tain e d by less th a n one-third of th e ir roots. It is often possible to clean up these teeth, but I doubt th a t they can be kept clean, a n d to my m ind th a t is the big problem . A rsp h en am in in glycerin is the biggest single a djunct th a t I have. No m istake w ill be m ade by
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using it routinely. A nother th in g about a rsp h en a m in : it does not d is in te g ra te over night. A rsphenam in and glycerin w ill rem ain effective a long tim e if chem ically pure glycerin is used. In advanced cases, the surgical trea tm e n t m ay be best from a bacteriologic point of view because then the g in g iv a l crevice is elim inated and th ere is less possibility of reinfection. In re g a rd to postoperative infection: I h av e seen some a reas break dow n a fte rw a rd s but the cases of d ry socket w ill be reduced approxim ately onehalf. O p erativ e a rea s heal prom ptly even a fte r rem oval of bad ly im pacted lo w er th ird m olars. I still re ta in m uch of m y u n d e r g ra d u a te p rejudice a g ain st em etin, a n d I have not fu lly accepted D r. K eilty’s ideas re g a rd in g the endam eba. Dr. Keilty (closing) : I am try in g to present a concept w ithout controversy. T h is is diffi cult, giving, as it does, the b acteria a very im p o rta n t place, and re aliz in g th a t other things m ay also h ave a v e ry im p o rta n t place in any given condition. In m y first p a p e r on gingivitis, there are some controversial things th a t I am not entirely in agreem ent w ith at the presen t tim e. T h is is due to progress. One m ust h ave an open m ind on this subject as w e go along, a n d ev aluate fa cts as to re sults received. D r. M iller m entioned the organism s of V incent as of first im portance, and the streptococcus second. T h e b o rre lia is very im p o rta n t from the standpoint th a t they a re active bacteria, they a re irrita n ts locally and not v e ry pathogenic w h en it comes to the in v asio n of tissue. On the other hand, the streptococcus is not v e ry active in the m otile sense, but if it ever gets into the tissue,
it becomes responsible fo r the secondary m anifestations. D r. Y eretsky spoke of tak in g sm ears. I h ave been try in g to in te rest the bacteriologists in studying this subject more exhaustively. A s she h a s said, a slide stained for Vincent’s o rganism s in m ost cases is re ported as positive. T h e problem is not so sim ple because little is known about these organism s. T h e sp irillifo rm types h ave never been successfully cultiv ated , w hile the fu si fo rm gro u p are still in a foggy state. T h e re is a g re a t deal to clear up. You m ay m ake y our ow n sm ears, but the results w ill depend on your in itiativ e a n d tra in in g . If you can g et y our bacteriologist interested, there is a w onderful chance fo r cooperation. As re g ard s D r. A d am s’ rem arks, I do not w ish to dis courage anyone. I am not a n alarm ist. T h e re is not anything to be a la rm e d about. I did not h ave anything sta rtlin g . I w ish I did have. I w ish I could come to you and say, “T h is is a specific thing, this is the cause.” Please do everything, D r. A dam s, th a t you have ev er done. P lease do one m ore th in g ; take into consideration the b a cteria. If you w ill add that, instead of getting 75 p e r cent results, you a re likely to get 100 p e r cent. D r. K ro g h bro u g h t up some points on tr e a t ment. I could not go into this phase because of its length. I w ould like to leave a thought on the use of arsphenam in. Use this d ru g locally, and rem em ber th a t intravenously a rsphenam in has absolutely no action on the sp irilliform organism s in the m outh. No m at te r how acute or w h a t type of case, you can not influence it by the use of a rsphenam in intrav en o u sly ; it m ust be used locally.
T
*Frora the Pathological L ab o rato ries of the D iagnostic C enter, U. S. V eterans B ureau, W ashington, D. C. *R ead before the Section on P e riodontia at the Seventy-F irst A nnual Session of the A m erican D ental A ssociation, W ashington, D . C., Oct. 10, 1929. 1. K eilty, R. A .: G in g iv itis: A n Infectious E ntity, from M edical and D en tal Aspects, J. A. D. A., 17:271 (F eb.) 1930. 2. K eilty, R. A .: P resen t State of O ur K now ledge of G ingivitis, J. L ab. & Clin. M ed., 13:451-468 (M ay ) 1928; G ing iv itis I I : C linical A p p e ara n c e of G in g iv ae in D ifferent Form s and Stages, J. Lab. & C lin. M ed., 14: 48 (Ja n .) 1928; G in g iv itis: L ab o ra to ry M eth ods fo r Study, J. Lab. & C lin. M ed., 14:165 (Feb.) 1928; G in g iv itis: C h a rac te r of E x u date in G ingivitis, J. Lab. & Clin. M ed., to be p u b lish e d ; Specificity of B a cteria to the B acteriolytic A ction of Chem icals, w ith a Note on T h is A pplication to Chem otherapy, J. Lab. & Clin. M ed., 14:539 (Ju n e ) 1929; p. 539; Specific C hem otherapeusis w ith R e la tionship to the B acteria Involved, J. Chem o therapy, 6, J a n u a ry , 1929.
Jour. A . D . A ., Ju ly , 1930
certainly complex and takes into account facts well known to dentists but not even familiar in terminology to medical men. I t is difficult, therefore, for the medically trained mind to evaluate the problem in complete ignorance of dental facts and terms. O n the other hand, even welltrained dentists, as a class, must admit some ignorance of the dental pathology and bacteriology involved. These two positions are not meant as an indictment, but are merely statements of fact. I t is not advisable for the medical profession to become familiar w ith dental practice, but it is advisable for the den tists as a whole to know more about pathology and bacteriology. I t is hoped that the researches in dental bacteriology which are now so popular will be even more strenuously pursued. I am making a plea that the maze of entangled facts, now known as the bacteriology of the mouth, be attacked by a mass of workers and the importance of each individual finding be thoroughly checked and evalu ated. T h e subject w ill then be on a firm footing and not, as now, often merely held in erroneous opinion. M y own experience goes back to 1914, when B arrett first made smears from pyorrhea pockets at Allen J. Smith’s sug gestion and endamebae were recognized and reported in forty-nine consecutive cases. I saw the first smear and examined many mouths myself at that time. You are all fam iliar w ith the rise and fall of
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Endameba gingivalis and the false prem planations and details of controversial ises regarding emetin as a specific in pyor points to other papers. Inflammatory proc rhea. T h is is an instance of erroneous esses about the structures of the teeth are evaluation of facts in the light of com described under a m ultitude of names, of plete knowledge. O n the other hand, the which the term “pyorrhea” is most com endameba is n(it a simple resident present monly used. T h is has almost had its in a large percentage of mouths but is a centennial and can be discarded. In view definite im portant pathogen. In this light, of the fact th at most, if not all, of the in it m ust be rediscovered and again reck flammatory changes begin in the soft oned w ith for its proper value. I t is not structures, I have included all cases un in any sense specific; a fact which D r. der the short simple term “gingivitis.” Smith never did believe; but th at does T h ere are many other terms, possibly just not mean that it is not pathogenic. as good, such as periodontitis and perio D uring the intervening years, I have dontoclasia, but they are not so expressive pursued the subject more or less con and do not lend themselves to qualifying stantly, and I now have records of nearly adjectives as does gingivitis. A ll forms 7,000 cases. T his has given me an experi of inflammatory change in the gingivae, ence resulting in a varied contact with from the slightest marginal gingivitis dental men which has been most enlight through V incent’s infection to the most ening for me, and which has caused me severe “pyorrhea” can be classed under to change my evaluations as the facts gingivitis, acute, subacute or chronic, become more and more definitely estab with expressive modifications, such as lished. T here is still much to be done, traum atic, exudative, ulcerative, sup and I feel that I have hardly entered on purative, gangrenous, fibrous or recessive. the problem, owing to its complexity. In T his immediately simplifies a classifica a series of papers, through the American tion and gives a common ground for the Society of Clinical Pathologists, I am etiology. T he pathology of all these attem pting to present the technical bac changes in the gums, the subgingival teriology of this experience, and it would tissues, the peridental membranes and the seem to be the proper time to present the bone is that of inflammation, in one or practical side to the dental profession. another of its manifestations, and to a In the whole work, there will be noth degree comparable to the advance which ing startling, but certain well-devised the gross morbid changes indicate. procedures and facts gleaned from rou In the etiology of this inflammatory tine observations on a large number of complex, bacteria play the most important cases along w ith experimental w ork will role, since they invade not only the gin eventually satisfactorily solve the whole gival sulcus, which is used as a medium problem. T h e laboratory and the dentist of growth, but also the tissues themselves, must w ork together, for the present at which is more im portant in producing least. T his relationship may be perma the actual inflammatory reactions in nent, or, when completely understood, these structures. O f all the conditions may be so simplified that the dentist can which have been advanced as causative handle the work alone. of these changes, the presence of bacteria In order to present as much as possible per se is the most im portant. T his is true in the time allotted, I am going to sum not only from the standpoint of the marize w ithout comment, leaving ex pathologic changes present but also from
K eilty— Infectious Factors in Gingivitis the fact that the inflammatory changes subside, and repair prom ptly takes place when the bacteria are eliminated. A ll other conditions, some of which are now accepted as prim ary causes, are in reality secondary, in spite of the fact that they may be actual initiating factors in the disease. F o r example, there is no question that traum atic occlusion, by sud denly placing an abnormal stress on one or more teeth, allows an easy invasion of bacteria which otherwise would not take place. T h ere is no question that the cor rection of traum atic occlusion will many times obviate an inflammatory reaction, removing the possibility of further in vasion by bacteria, w ith a reparative effort on the part of the cell structures when the traum atism ha? been removed. W hile most mouths show a certain amount of traum atic occlusion, bacterial invasion will take place w ith or w ithout traum atic occlusion, and w ill often involve teeth which show no evidence of such traum a. In this sense, I feel no hesitancy whatso ever in placing bacterial invasion ahead of traum atic occlusion as an etiologic factor, but I do give traum atic occlusion its proper importance as one of the initiat ing factors and one which may often con tinue as an im portant factor. M uch has been said and will be said concerning calculi, serumal or salivary, with sordes, ta rta r and film. C ertain mouths tend to collection of sordes, or, we may say, debris deposits, about the necks of teeth, which tend to calcify in spite of careful mouth hygiene and fre quent scaling. T h is is due, probably, to an individual chemical character of the saliva, w ith the proper hydrogen-ion con centration for calcium deposit. These cases are very decidedly in the minority. By far the greatest number of cases showing deposits of calcareous ma terial, either a§ the so-called serumal
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calculi beneath the gingival margins or as deposits in the interproximal spaces, where cleaning is not actually accom plished, are due to the natural deposition of calcareous material in necrotic exuda tion and debris which is acting as a for eign body. T his phenomenon takes place all over the body. If the original exudate is cleaned out and kept clean, or if there is no reason for its formation, this type of deposit will not take place. As such, then, all types of calcareous material can not ,be considered as etiologic factors in any sense but are the results of a condi tion present. T hey do continue as irri tants when present. T raum atic occlusion and gingival cal culus are assumed by the dental profes sion today to be the two outstanding etiologic factors in gingivitis. I consider them both secondary in importance to bacteria. T h ird and less important, although less understood, in the view of many w riters is somatic influence in relation to local resistance and secondary mouth fac tors. Some men assume that general body chemistry, such as calcium phosphorus and glandular deficiency, and such, gen eral diseases as tuberculosis, syphilis and diabetes, present the sole causative factor in the development of gingivitis. T his cannot possibly be true, else these factors would be present in 90 per cent of our population, which they are not. T h ere is no question that a certain percentage of cases showing these deficiencies w ill show marked gingival changes. These gingival changes are a general part of the reaction, and while they are aggravated by the somatic condition, that condition is in no sense the sole etiologic factor in the gingivitis. T h ere are many other secondary con ditions which have been presented as etiologic factors, and which, in individual
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cases, do play some part, but which in no sense can be considered as the important etiologic condition in all cases of gingi vitis. I refer to such things as smoking, gingival traum a in mastication, the pres ent state of our prepared foods, which are soft and rich in their preparation, the accumulation of food debris, mouth breathing and acid mouth. In a certain group of cases w ith ill-fitting dentures, partial or complete, w ith poorly made crowns or crowns which have long since served their purpose, bridgework improp erly applied, fillings of all kinds which are poorly finished, leaving, especially in the interproxim al spaces, roughened areas or shelves, and dental caries, which fortu nately is very decidedly on the decrease, one may find local reasons for a traum a which admit bacterial invasion in the same sense that traum atic occlusion plays its role. T hus, after all is said on the various etiologic factors in gingivitis, by a process of elimination and a study of the accepted data on the pathology involved, bacteria must be given first place in the etiology. W h a t of these bacteria ? H ere contro versy and lack of exact knowledge are frequent. In the “ M anual of Bacteri ology” (B ergey), forty-six different types of bacteria are described as occurring in the mouth. T h is does not include the entire number isolated by all workers. O f this number, I have records of the isolation of thirty-three different and dis tinct species, and I am sure that if time permitted, this number would be in creased. Can one pick out of this any particular species or type of bacteria and consider it a specific etiologic factor? A t the present time, in the records of my cases, certain bacteria repeat themselves constantly, but I do not consider in any sense that any are specific, unless it be the spirilliform and fusiform groups. These
two types are present in almost 100 per cent of gingival exudates, are not present in perfectly normal mouths, are greatly increased in acute conditions, are much reduced in inactive conditions and clear up w ith complete disappearance in suc cessfully treated cases. In this study, one must know w hat bacteria the perfectly normal m outh contains. T his is most difficult or almost impossible since the conception of the normal mouth is open to a great deal of discussion, and w hat one considers normal, another may consider highly pathologic, and vice versa. I con sider normal only the mouth which is absolutely perfect in its construction and absolutely free from gross morbid signs of inflammation. T his makes up, in my series of cases, not much over 1 per cent. Bacteria seen in fresh or stained smears and by culture vary w ithin wide limits in a group of cases but are more or less constant in a given case. I t will be seen from this that the gingival flora must be worked out for every case. I t is here that the cooperation of the laboratory is essen tial. C ertain groups are best seen by smear and others by culture. T he fresh smear offers the best means of rapidly determining the m ajor types of bacteria as well as any protozoa present. I have described methods in a previous paper. T h e spirilliform organisms under the general group of Borrelia vincenti are seen in their active form by fresh smear. T hey cannot be easily cultured, and until a method of culture is described, they had all best be grouped together as far as gingivitis is concerned. T hey are pres ent in all forms of gingivitis and are probably the most important of all the groups. T h e fusiform organisms are also con stantly present and are best grouped under the heading of Fusiformis dentiumHoelling. T hey are difficult to isolate in
K eïlty— Infectious Factors in Gingivitis culture and also require much further study. T h e cocci may next be taken, as to both importance and frequency. These can be seen in smear but are best studied by culture, and routinely the blood agar plate picks out as many as any other single medium. A large moist mucoid colony of staphy lococci is a constant finding. T h is colony offers a symbiotic relation for several forms of staphylococcus, white and yel low, and for bacillary forms associated w ith the higher mycelia. T h e streptococci are quite constant, pigmented, nonhemo lytic, plain hemolytic or w ith green hem olysis. T h e pneumococcus goes in waves. Several other types of easily recognizable bacteria appear on culture, but are not constant in every mouth. These are B. catarrhalis, B . coli, B. diphtheria, B. hofmannii and B . influenzae. B . aci dophilus is recognizable in smears quite constantly, but is not brought out on blood agar plates easily. M any other forms, such as rosettes or actinomycetes, short vibrios and long mycelia, singly and in multiple branches, are more or less common. T h e yeasts, saccharomycetes and monilia are only very occasionally seen but may be frequently obtained on culture. T h e protozoa Endameba ging'walis, Trichomonas buccalis, bodo and occasion ally giardia and cercomonas are the types that I have so far encountered. These organisms, as already stated, are not mere benign residents in dirty mouths, but are part and parcel of the gingivosulcal exu date. I f they do not invade the tissue and if they do not produce a toxin, both of which are highly probable, they at least act as distinct local irritants. I can say definitely th at as long as they are present, a gingival reaction w ill not en tirely clear up.
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I have tried to present a concept that all forms of inflammatory changes in the structures about the teeth are to be con sidered as one entity and spoken of under the general term of gingivitis. T h is in cludes everything from simple marginal gingivitis to the most advanced “pyor rhea,” along with acute exudative and gangrenous changes now known as V in cent’s infection. Such a concept will sim plify the whole situation, and the bac terial flora becomes the most im portant study in every case. I t is necessary to enumerate all bacteria and protozoa present in quantitative terms in every case. These findings are not only impor tan t from the point of view of knowledge to be gained, but also must be known if intelligent treatm ent is to be carried out. By intelligent treatm ent, I mean a plan of treatm ent mapped out beforehand and based on the conditions present in a given mouth, correcting each and every condi tion by a specific line of attack as nearly as the present state of our knowledge will allow. T his attack implies that every case must be individually studied from the dental, roentgen ray and pathologic aspects and every possible angle corrected. T h e laboratory must aid in the pathologic and bacteriologic study and the dentist must carry out the procedure based on this study. In the correction of dental mechanics, the dentist, of course, is guided entirely by his training and experience. In the correction of deep-seated dental disease as developed by the roentgen ray, the oral surgeon must be guided by his train ing and experience. In the same way, the correction of bacteriologic factors, now so universally neglected, must be guided by the training and experience of the bac teriologist. W hen all three of these trained groups are utilized, the end-re-
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suits for correction and maintenance of a perfect mouth are such as cannot be ob tained by any other line of attack. Tim e does not perm it my attem pting anything on treatm ent in this presenta tion. I t has been necessary to devote con siderable study to this phase of the sub ject, in order to obtain facts on bacterial reactions. Fortunately, we have a num ber of quite specific drugs which can be directed against predominance of bac terial factors present in a given case. It is the combined use of the proper drugs in a given case which constitutes the bac terial side of intelligent treatm ent. One of the most im portant phases of the whole subject is the use of a pretreatm ent stage in all operative work in the mouth. I have not seen a postoperative infectious reaction in a single successfully pretreated case in years. I have seen many post operative infections during the same time, in which the preparation of the patient did not take into account the actual bacteriologic factors in th at m outh by a specific preoperative chemotherapeusis.
CONCLUSION Gingivitis represents an inflammatory entity now known under a variety of names, from acute V incent’s infection to pyorrhea, which is subjectLta.a precise and accurate terminology based, on the pathologic process which is present. Considered as such an entity, bacteria play the most important part in the actual etiologic role. I t is possible to m aintain a study of these bacteria, but owing to their tech nical complexity, it is necessary to have the aid of a bacteriologist until methods of procedure can be furth er simplified. Such a complete bacteriologic study allows a plan of intelligent and quite specific treatm ent mapped out on the find ings in a given case, which can and should
be carried out by the dentist in addition to the correction of purely dental me chanics.
DISCUSSION
Israel S. Miller, Jersey City, N. J.:
D r. K eilty has m ade a contribution to o u r clearer u n d e rstan d in g of periodontal disease w ith the re p o rt on thousands of sm ears pro v in g th a t the fu sifo rm bacillus and the spirillum of Vincent a re the pred o m in atin g bacterial destructive agents a n d not the streptococcus and staphylococcus, as h a s g en erally been claim ed, but w ithout sufficient proof. I have th erefo re found it helpful to employ F o w ler’s solution ( solution of potassium arsen ite) com bined w ith liquor antisepticus alkalinus in the p ro po rtion of 3 to I (one tablespoon in o ne-half glass of w arm w a te r), as a sw ab of the teeth and m outh before operating, and as a m outh w ash. T h e arsenic in F o w ler’s solution is considered a specific fo r the sp iril lum ; and the other ingredient, destructive of the fusiform bacillus. T in c tu re of green soap in solution m ay be em ployed also. I employ this in addition to the re g u la r clinical p ro cedure in the trea tm e n t of periodontal disease, w hich I call the sta n d ard ize d periodontal procedure. T h is consists of six steps: (1) d iagnosis; (2) b a la n cin g occlusion; (3) in stru m en ta tio n ; (4) tissue stim u latin g ; (S) p lan n in g re sto ratio n s; (6) re tu rn fo r re g u la r prophylactic treatm en ts. T h e re is another point th a t has been illum inating to m e: D r. K eilty finds th a t a norm al m outh does not contain the V incent organism s. T h is fact w hen clinically applied m eans th a t the o perator m ust take sm ears d u rin g and a fte r treatm ent of a ll types of periodontal disease in ord er to m ake certain th a t he has elim inated these organism s. Unless tw o o r th ree negative sm ears in succession a re obtained, the m outh cannot be called norm al, reg ard less of how beautiful the tissues look clinically. I endorse D r. K eilty’s advice to dentists to cooperate w ith the pathologist in th e ir trea tm e n t of periodontal disease.
Wilhelmina Yeretsky, Mich.: I agree w ith D r.
Grand Rapids,
K eilty th a t a p e r fectly norm al m outh does not h a rb o r Vincent’s organism s, the spirochete o r fusiform . I h ave not run through the series of sm ears th a t D r. K eilty has, but in a series of p e rh ap s a hundred, w e have n e v er found those o rg a n isms in perfectly norm al m ouths. T h e difficulty w as in finding norm al m ouths, b u t the men,
K eilty— Infectious Factors in Gingivitis p a rtic u la rly the physicians a n d the lab o rato ry m an, w ere not fa m ilia r w ith the a p p earan ce of pathologic g in g iv a l conditions, and m ade the b ro a d statem ent th a t there w ere alw ays fu sifo rm bacilli a n d spirochetes in the m outh, because they did not recognize the pathologic conditions. I alw ays take my ow n m outh sm ears from the superficial and buccal m em b ra n e a n d also from the pockets before send in g them to the lab o ra to ry fo r diagnosis. D r. M ille r says th a t he also finds V incent’s o rg a n ism in the p e riodontal lesions. I h a v e h a d the in te restin g experience of finding, in young people, 22 or 23 y e ars old, the pocket extend ing the entire length of the root, tw o -th ird s of the w ay o r com pletely aro u n d it. T h e ro e ntgenogram show ed a trem endous am ount of bone gone, w hen we consider the age of the p a tie n t in these cases. In these pockets, I found a p u re sm ear of V incent’s organism s. I feel th a t th a t destruction of bone is due to infection from V incent’s organism s, in yo u n g er people. I do not think th a t w e find them in o ld er people. T h e y h a v e the m ore u sual form s of organism s in the p e riodontal pockets. R. A . Adams, Denver, Colo.: A s a p ra c titio n er w ho lim its his w ork entirely to periodontoclasia, a n d speaking to g en eral p ractitioners, let me say th is : Do not become p erturbed a t w h a t you have h e ard . G o back to y our office rem em bering the o th er things th a t you h e ard yesterday and to d a y ; follow them out, and you w ill get results. Do not be discouraged. M ost of the p a p er is true, as f a r as th a t is concerned, but th ere a re other truths. G o back to yo u r offices w ith th e d e term ination to recognize p e riodontal lesions in th eir incipiency, and tre a t them as you have been in structed to tre a t them , this m orning and yesterday, and you w ill get results, w ith out cooperation w ith the bacteriologist and the pathologist. I am telling you this because fo r m ore th an tw elve y ears I h av e not h a d a drop of m edicine on the bracket in tre a tin g chronic cases of these diseases. W e get re sults in chronic cases especially, a n d the only case in w hich I use m edicine is in acute in volvem ents. T o g et results, cooperation w ith a bacteriologist is not especially necessary. T r e a t these lesions as you h a v e been ta u g h t in o u r textbooks. T h e bacteriologist is not im perative to y our success in tre a tin g these cases. I f it is convenient, and you w a n t this service, I have no objection. B ut if you p ra c tice the things you h e a rd y e sterd a y a n d this
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m orning, and th a t a re constantly a p p e a rin g in our periodicals and textbooks, you w ill get results. H. JV. Krogh, Washington, D. C.: I speak from the point of view of the practitio n er and not the bacteriologist. T h e bacteriologic ex am ination of my patients is m ade by D r. Keilty, and he is the biggest single aid in my practice. M uch harm w as done in the tr e a t m ent of periclasia by subgingival m edication because the thought w as given out th a t it w as only necessary to m edicate these cases and they w ould p rom ptly cle ar up and rem ain so; th a t scaling or attention to restorations, o r any of the things th a t we w ere accustom ed to doing, w as unn ecessary ; ju st pum p in the d ru g and all w ould be w ell. T h a t w as not all by any m eans. If one does all th a t D r. A dam s ju st spoke of, using D r. K eilty ’s technic, one w ill re ally g et results. I did not agree w ith D r. K eilty w hen he said th a t if these cases a re cleared up bacteriologically, they w ill alw ays cle ar up clinically. T h a t is not alw ays tru e in my experience. In those cases in which the result is not good, I usually dissect the pocket according to W a r d ’s technic. N or do my p atients all g e t re lief fro m cal culus. T h e relief fro m calculus is astounding in the cases th a t a re kept clear, a n d also freedom from decay and all other u n p lea sa n t things found in the m outh, but, in c ertain cases, the calculus w ill reform , not so rapidly, but it w ill come back. E ven in those cases, the g in g iv a l inflam m ation w hich accom panies larg e am ounts of calculus w ill not be so m arked. I f one h a s no convenient lab o ra to ry and cannot h ave a chem otherapeusis w orked out, the use of a com bination of m etaphen and acriflavin, in com bination w ith arsp h en am in, w ill give excellent results. T h e re w ill be probably 5 per cent of cases w hich w ill not c le ar up. I do not m ean to say th a t it is pos sible to c le ar up bacteriologically 100 p e r cent of the cases, and I think some of the fa ilu re s m ay be due to the m echanical difficulty of g etting the d ru g into the pocket. N o r should the im possible be attem pted. E x tra c t about the sam e teeth th a t you w ould otherw ise— the m ultirooted teeth w ith bifu rcatio n involve m ent, a n d single-rooted teeth w hich a re r e tain e d by less th a n one-third of th e ir roots. It is often possible to clean up these teeth, but I doubt th a t they can be kept clean, a n d to my m ind th a t is the big problem . A rsp h en am in in glycerin is the biggest single a djunct th a t I have. No m istake w ill be m ade by
1258
T he Journal of the American D ental Association
using it routinely. A nother th in g about a rsp h en a m in : it does not d is in te g ra te over night. A rsphenam in and glycerin w ill rem ain effective a long tim e if chem ically pure glycerin is used. In advanced cases, the surgical trea tm e n t m ay be best from a bacteriologic point of view because then the g in g iv a l crevice is elim inated and th ere is less possibility of reinfection. In re g a rd to postoperative infection: I h av e seen some a reas break dow n a fte rw a rd s but the cases of d ry socket w ill be reduced approxim ately onehalf. O p erativ e a rea s heal prom ptly even a fte r rem oval of bad ly im pacted lo w er th ird m olars. I still re ta in m uch of m y u n d e r g ra d u a te p rejudice a g ain st em etin, a n d I have not fu lly accepted D r. K eilty’s ideas re g a rd in g the endam eba. Dr. Keilty (closing) : I am try in g to present a concept w ithout controversy. T h is is diffi cult, giving, as it does, the b acteria a very im p o rta n t place, and re aliz in g th a t other things m ay also h ave a v e ry im p o rta n t place in any given condition. In m y first p a p e r on gingivitis, there are some controversial things th a t I am not entirely in agreem ent w ith at the presen t tim e. T h is is due to progress. One m ust h ave an open m ind on this subject as w e go along, a n d ev aluate fa cts as to re sults received. D r. M iller m entioned the organism s of V incent as of first im portance, and the streptococcus second. T h e b o rre lia is very im p o rta n t from the standpoint th a t they a re active bacteria, they a re irrita n ts locally and not v e ry pathogenic w h en it comes to the in v asio n of tissue. On the other hand, the streptococcus is not v e ry active in the m otile sense, but if it ever gets into the tissue,
it becomes responsible fo r the secondary m anifestations. D r. Y eretsky spoke of tak in g sm ears. I h ave been try in g to in te rest the bacteriologists in studying this subject more exhaustively. A s she h a s said, a slide stained for Vincent’s o rganism s in m ost cases is re ported as positive. T h e problem is not so sim ple because little is known about these organism s. T h e sp irillifo rm types h ave never been successfully cultiv ated , w hile the fu si fo rm gro u p are still in a foggy state. T h e re is a g re a t deal to clear up. You m ay m ake y our ow n sm ears, but the results w ill depend on your in itiativ e a n d tra in in g . If you can g et y our bacteriologist interested, there is a w onderful chance fo r cooperation. As re g ard s D r. A d am s’ rem arks, I do not w ish to dis courage anyone. I am not a n alarm ist. T h e re is not anything to be a la rm e d about. I did not h ave anything sta rtlin g . I w ish I did have. I w ish I could come to you and say, “T h is is a specific thing, this is the cause.” Please do everything, D r. A dam s, th a t you have ev er done. P lease do one m ore th in g ; take into consideration the b a cteria. If you w ill add that, instead of getting 75 p e r cent results, you a re likely to get 100 p e r cent. D r. K ro g h bro u g h t up some points on tr e a t ment. I could not go into this phase because of its length. I w ould like to leave a thought on the use of arsphenam in. Use this d ru g locally, and rem em ber th a t intravenously a rsphenam in has absolutely no action on the sp irilliform organism s in the m outh. No m at te r how acute or w h a t type of case, you can not influence it by the use of a rsphenam in intrav en o u sly ; it m ust be used locally.