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Mouth Lesions of Local and Systemic Origin
MOUTH LESIONS OF LOCAL AND SYSTEMIC ORIGIN B y L e s te r R. C a h n ,* D .D .S ., N ew Y o rk , N . Y .
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D O n ot believe th at there are such specific disease entities as, fo r e x am ple, diab etic gingivitis or pyor rhea, an d pregn an cy gingivitis. T h ere are thousands o f diabetics w h o n ever d e velop pyorrhea, and a vastly greater num ber o f w om en w ho becom e pregnant w ithout ever h a vin g gingivitis. L o ca l irritants and system ic deran ge m ent and disease m a y so underm ine the oral tissue im m unity and tone that the ever-present bacteria o f the m outh can set u p the clinical picture. M a n y o f these lesions look alike, y et their etiology is en tirely different, and in order to m ake our therapeutic measures effective, w e m ust k n ow the cause o f the trouble and the course that it w ill follow . B efore discussing oral lesions proper, I should like to m ention tw o com m only seen affections th at are due to norm al histologic conditions o f the oral mucosa. T hese are m elanin pigm entation and F o rd yce’s disease. T h e latter is a fine exam ple o f an eponym beclou d in g a sim ple anatom ic fact. In the region o f the basal layer o f the epithelium , there are den dritic cells th at in non-pigm ented areas can on ly be shown histologically b y m eans o f special stains. (Fig. i.) These cells are m elanoblasts. W hen active, th ey form m elanin, a pigm en t that is responsible fo r the brownish discoloration found n orm ally in R ead before the section on Periodontia at the Eighty-Second Annual M eeting of the American Dental Asociation, Cleveland, Ohio, September i s , 1940. •Chairm an of the Division of O ral Pathol ogy, Colum bia University Dental School.
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the m ouths o f the darker races.1 T h e y m ay, how ever, be abnorm ally stim ulated into p rod u ctivity b y traum a and in A d d i son’s disease. Sebaceous glands (F ig. 2) are fre q u en tly fou n d in the corium o f the m ucous m em brane o f the inside o f the cheeks and lips, and in that o f the bu ccal gu m near the m ucobu ccal fo ld above the m axillary bicuspids. W h en in exagger ated num bers and close to the epithelium , th ey give rise to a condition erroneously th ou ght to be pathologic and w hich has been called F ord yce’s disease.2 (F ig. 3.) e t io l o g y
T h ere are exogenous and endogenous causes fo r m ost oral lesions. E x o g e n o u s Cau ses. — T r a u m a : T h e oral m ucous m em brane is subjected to constant traum a, w h ich usually is m ild and, du rin g the ord inary course o f events, can be w ithstood w ith ou t any pathologic disturbance. T h e shape o f our teeth and their contacts prevent food from in ju rin g the gin giva. T h e epithe lium o f the m ucosa w ill also, under norm al circum stances, w ithstand the a c tion o f m ild acids o r alkalis and therm al changes. M alalin em en t o f the teeth, the fa u lty restoration o f lost tooth structure or the non-replacem ent o f lost teeth causes m e chan ical irritation o f the tissues, w hich m a y result in a v a riety o f lesions ran gin g from a m ild infection to leukoplakia and even m alignancy. H a b it m a y result in another type o f traum a, and one o f the com m onest trau m atizin g habits is cheek biting. (F ig. 4.)
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E lectrical currents : A n um ber o f years ago, L a in ,3 o f O k lah o m a, established the fa ct th a t electrical currents cou ld be generated w ithin the m outh b y dissim ilar metals, and that a v a riety of lesions could result from burns caused b y these cu r rents. T h e lesions so produced m a y v a ry from a superficial excoriation to an ulcer or a leukoplakia patch. I h ave seen a m arkedly leukokeratotic p alate return to norm al a fte r the rem oval o f a large gold bridge. In fection : Regardless o f w h at the pre disposing cause m a y be, in fection must
Fig. I.-— Melanoblasts in gum. These were in a non-pigmented area and are brought out by means of the “ dopa” reaction. alw ays be considered an im portant ex ogenous factor. E n d o g e n o u s C a u ses. — A v ita m in o sis: V ita m in A , those o f the B com plex and vitam in C contribute m ostly to the w ell being o f the oral m ucosa. V ita m in A affects prin cip ally the epi thelium . A lack o f this foo d com ponent has a keratinizing effect, not on ly on the surface epithelium , but also, through a m etaplastic process, on that o f the ducts o f the salivary glands.
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A n avitam inosis A m a y result in leuko keratotic areas on the oral m ucosa. T h is is occasionally seen in those on strenuous w eight-reducin g diets. T h e ducts o f the m ucous and salivary glands m ay becom e keratinized and blocked, a lack o f salivary secretion and lubrication resulting. T h is causes the m ucosa to becom e dry, cracked and p ain fu l and is one o f the p rin cip al causes o f xerostomia. T hose o f the vitam in B com plex o f most interest to us are vitam ins B l3 or thiam in h ydrochloride, B 2, or riboflavin,
Fig. 2.— Sebaceous glands in submucosa of oral mucous membrane. and the pellagra preven tive factor, or nicotinic acid. W ith the exception o f a peripheral neuritis, a deficien cy in B x, as fa r as is know n, causes no oral lesions p er se. H ow ever, a d eficien cy o f this vitam in causes a loss o f appetite, and the les sened food intake w ill result in a lack of those essential factors th at w ill directly affect the oral m ucosa. T h e results o f dep rivation o f ribo flavin, described recen tly b y Sebrell and B utler,4 should be know n to all those in
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terested in the m outh. T h e lesion, w h ich th ey called “ cheilosis,” is described in their ow n w ords as fo llo w s : These lesions began as a pallor of the mucosa of the lips in the angles of the mouth without involvement of the buccal mucosa. This pallor was soon followed by maceration, and within a few days super ficial transverse fissures appeared, usually bilateral, and exactly in the angle of the mouth. These fissures extended somewhat downward from the angle and there was very little inflammatory reaction. The le sions became moist and covered with a honey-colored crust which could be scraped off without bleeding. In some instances the
Fig. 3 .—Fordyce’s disease. The word “dis ease” is a misnomer. The condition is simply an affection due to the presence of sebaceous glands and is of common occurrence. The sec tion shown in Figure 2 was taken from this case. fissures continued to extend into the skin for a distance as much as one half inch. These lesions resembled those described as per leche. A t about the time the fissures were seen, the lips became abnormally red along the line of closure. This was due appar ently to a superficial denudation of the mucosa. In addition to the cheilosis there
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was also seen a fine scaly, slightly greasy desquamation on a mildly erythematous base in the naso-labial folds, on the alae nasi, in the vestibule of the nose and on the ears. I h ave observed a n um ber o f instances o f these fissures at the m outh angles and h ave seen them involute under adequate dosages o f riboflavin. H eretofore, w e w ould h a ve called these lesions perleche and treated them as infections. T h e desquam ation, w h ich is also inter esting, m a y give us a clue as to the rea son for those cases o f true desquam ative gingivitis th at h ave up to now resisted all form s o f local treatm ent.
Fig. 4 .—Lesion produced by cheek biting. A deficiency in nicotinic acid causes pellagra. In this disease, gingivitis, stom atitis and glossitis are alw ays present and are u sually early symptoms. T h e tip and m argins o f the tongue becom e very red and are freq u en tly swollen. U lcers m ay form that are covered w ith a gray m em brane that abounds in the orga n isms o f V in cen t. In fa ct, to the u n in itiated, the severe V in c e n t’s infection m a y w ell mask the real com plaint. Jolliffe has shown a n um ber o f severe
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cases o f V in cen t’s stom atitis in pellagrins th a t w ere cured b y the adm inistration o f the p ellagra p reven tive fa cto r w ith ou t the use o f a n y specific antiseptic therapy. K in g 5 also calls attention to the relation ship betw een V in c e n t’s infection and a deficiency in n icotin ic acid . H e also foun d th a t in fo u r persons w ith norm al gums, the excretion o f n icotin ic acid in the urine o f each was fa r in excess o f that o f a patien t w ith V in cen t’s infection. More investigation a lo n g this line is necessary before conclusions can be draw n. K in g treated fo u r cases o f severe V in c e n t’s in fection successfully b y the oral adm inistration o f nicotinic acid.
Fig. 5 .—Glossitis caused by excessive use of “oxygenating” mouth washes. It is interesting to note how far this patient can extrude the tongue. This is usually a sign that the patient is constantly viewing it and is apprehensive and probably hypochondriacal. Such a person probably overuses medication of all kinds. T h is question o f a B com plex defi ciency in a ll cases o f severe V in c e n t’s infection th at h ave not a blood dyscrasia as their basis m ust alw ays be borne in mind. r e p o r t
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gingivitis and extremely fetid breath, the teeth looked elongated, the interdental soft tissue was lost and the spaces between the teeth were filled with a foul-smelling débris. Both jaws were affected. T he attack was an acute one superimposed upon a chronic one of long standing. The gums were pale and irregularly streaked with the lacy white lines seen in lichen planus. T he patient had been treated on a number of occasions for similar attacks of what she termed “ trench mouth.” Smears of the gums showed myriads of spirochetes and fusiform bacilli, to the al most total exclusion of other forms of bac teria. T he clinical signs and the smear were typical of Vincent’s infection, yet it was evident that this was just a complication. Biopsy of the whitish lined gum showed that these lines represented a mild, but defi-
Fig. 6 .—Hypertrophy of gums due to use of dilantin sodium (Kimball). (Courtesy of the Journal of the American Medical Associa tion.) nite hyperkeratosis— an uncommon finding in the buccal gum. T he woman was a chronic alcoholic. M any alcoholics are markedly deficient in their food intake and suffer from multiple vitamin deficiencies. Many of them are subclinical pellagrins. Blankenhorn and Spies6 found stomatitis and glossitis in 60 per cent of their alcoholic pellagrins, and the latter observed the rapid cure of these infections with administration of nicotinic acid. In the case under consideration, the Vincent’s infection and the keratotic white lines were simply manifestations of a deficiency disease. The reason that the patient had never been
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cured of her infection was the fact that the true predisposing causes were not suspected and eliminated. V ita m in G affects the endothelium o f the capillaries and the intercellular cem ent substance. A lack o f this vitam in causes the capillaries to becom e perm e able, allo w in g interstitial hem orrhage. T h is accounts fo r the bleeding and swollen condition o f the gum s in scurvy. S econ d ary infection, especially b y the fusospirochetal symbiosis, aga in w ill re sult in a lesion that m a y m ask the true condition. In d ealin g w ith the question o f a v it am inosis, a num ber o f im portant facts
Fig. 7.— Section of gum showing hyper trophy from use of dilantin sodium. The stroma is very dense and there is a lack of inflammatory exudate. m ust be borne in m ind. Patients w ho are d eficien t in one vitam in are usually deficient in others. T h e adm inistration o f w h a t is thought to be the missing food fa cto r m a y b rin g about on ly the am eli oration o f p a rt o f the clin ical picture. P olyvitam in therapy, plus, occasionally, the adm inistration o f the extract o f w hole liver is often indicated. A vitam inosis m a y occu r in spite o f the fa ct th a t the patient is receivin g an optim um am ount o f essential foods. Th is is seen in intestinal disease in w hich
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there is interference w ith the absorption o f the foods. E xam ples o f this are fou n d in id iopath ic steatorrhea o f children and in can cer o f th e intestines. A n avitam inosis m a y not h ave a te x t book appearance. T h ere are m a n y o f w h a t h ave been called subclinical cases and these m ust be appreciated and w atch ed for. Specific in fe c tio n s : Syphilis and tu b er culosis are the tw o principal specific in fections th a t a ffect the m outh. So m uch has been w ritten abou t the oral m an i festations o f syphilis th at it is unnecessary to go into this question now. O sier said,
Fig. 8.— Smooth “ polished” tongue with atrophy of papillae. This type of tongue is seen in pernicious anemia, in the PlummerVinson syndrome, in sprue and in other defi ciency diseases. “ syphilis is the greatest im itator o f disease.” O n e should suspect syphilis as either a cause or a com plication in every oral lesion. Tuberculosis is not alw ays considered in view in g oral disease, yet, in the past tw o years, I h a ve seen several instances o f tuberculous disease o f the m outh as a com plication o f generalized tuberculosis. In none of these cases was the oral lesion
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thought to be tuberculous, b ein g treated locally fo r aw h ile w ith ou t avail, until the correct diagnosis was m ade through biopsy. W h en oral tuberculosis is a com plication o f the system ic disease, the prognosis is usually grave and early diagnosis is im perative. M eta b o lic d istu rb an ces: In h y p o th y roidism, w hen m yxed em a is present, the patients, as a rule, h ave thick, flab b y and bloated tongues against the sides of w hich are indentations from the teeth. T h e lips are also grea tly thickened. T h e gum s a t tim es becom e sw ollen and these patients freq u en tly h ave d ifficulty in re tainin g artificial dentures. In A ddison ’ s disease, the m ucous m em -
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peripheral neuritis fro m w hich diabetics freq u en tly suffer and w h ich is evidenced in the m outh b y su bgin gival hypersen sitivity o f the teeth (M e rritt’s sig n ).7 M enstruation : T h e prem enstrual and m enstrual periods m an ifest them selves in the oral cavity. T h e extrem ely rare vicarious m enstruation from the gum s is w ell know n. H o w ever, there are a n u m ber o f less distinctive lesions. H erpes labialis an d buccalis are per haps the com m onest o f the oral lesions appearin g abou t this tim e. T h e y are quite p ain fu l and u su ally attack the same areas each m onth. T o exp lain the m od u s
Fig. 9.— Slough that quickly follows any kind of trauma in acute leukemia. In this instance, a tooth had been extracted. brance becom es pigm ented ow in g to h yp era ctivity o f the m elanoblasts. D iabetes is freq u en tly com plicated by gingivitis and pyorrhea. T h is m a y be due to an increase in the sugar in the gin gival and buccal m ucosa from the h y p e r glycem ia, w h ich in turn w ill fa v o r in fe c tion b y b acteria and fu n gi, especially yeasts. In fa u lty carbohydrate m etabolism , there is a greater dem and fo r vitam in B j. D iabetes m a y be com plicated b y this defi ciency. T h is p rob ab ly accounts fo r the
Fig. 1o.— Thrombocytopenic purpura. Blood has collected about the necks of the teeth and there are small hematomas present. o p era n d i o f these lesions is qu ite difficult. T h e y are analagous to the acne that occurs regu larly in some w om en. T h e y m a y be explained on th e basis o f a low ering o f the tissue tone o f the oral m ucosa so that the herpes virus can b e com e active. Som e w om en regu larly develop pericornal infections d u rin g the m enstrual period. In order to understand w h y these infections occu r at this tim e, it m ight
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be w ell to review certain anatom ic facts. Posterior to the m and ibu lar third m olars, is the loose areolar tissue th at contains accessory salivary glands. T h ese glands are structurally sim ilar to the v u lv o vagin al glands8 (B artholin ’s g la n d s), and also resemble som ew hat those o f the en dom etrium . T o d a y , it is established that estrogenic horm ones h a ve an effect on the oral m ucosa, and there is little doubt that the sam e horm ones a ct on the a c cessory salivary glands sim ilarly to the w a y they do on the vu lvovagin al and endom etrial ones. Also, in b ack o f the low er third m olars, there is n early alw ays a pocket, or cul-de-sac, especially should the tooth be im pacted or m alposed, th at usually contains m an y m icro-organism s, especially o f the fusospirochetal sym bi osis. I f there is an alteration in the glands from some horm onal stim ulus du rin g m enstruation, the tissue tone and im m unologic defenses becom e so changed that the bacteria alw ays present in this area can set up the pericoronal in fe c tion. T h e m on thly recurrence o f these a t tacks can be obviated on ly b y rem oval o f the tooth. In one instance, the patien t had a m on thly sw elling o f the retrom olar tissue quite aw hile a fter the tooth had been rem oved. a t r o p h ic g in g iv it is
T h ere is a type o f gingivitis ch aracter ized b y atro p h y o f large patches o f the epithelium . T h is condition has been called desquam ative gingivitis, b u t it is n ot a desquam ative lesion. H istologically, the epithelium is reduced to one or tw o thin layers o f cells, b u t m icroscopically there is no evidence o f cellu lar shedding. A trop h ic gingivitis w ou ld be a m ore a c curate nam e. T h is condition is seen in w om en chiefly, usually du rin g the m eno pause or postm enopausal periods. I saw it once in a m an. T h e use o f estrogenic horm ones locally applied a fter the m an n er ad vocated b y Ziskin has g iv en excel lent results.
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P re g n a n c y : P regn an cy is frequently accom panied b y changes in the gums. T h is m a y consist o f slight hyperem ia and sw elling o f the interdental papillae, w hich m ay b e m ild and m ay pass unnoticed. I f oral hygiene is m aintained, a disturb in g gingivitis is rarely seen. H ow ever, if the m outh is neglected, so-called “ preg n an cy gingivitis” occurs. T h e gums b e com e sw ollen and congested and the interdental pap illae are enlarged and bleed under the slightest provocation. A n oth er oral com plication o f p reg n an cy is a tum or, w h ich m a y occu r in the w ell-kept m outh, b u t here again is seen m ost often in the ill-kept one. H is tologically, it is an angiogranulom a and u sually disappears a fter parturition. T h e reason fo r the m ucous m em brane changes du rin g p regn an cy are unknown. T h e y m a y be due to horm one disturb ances, vitam in deficiencies due to an in creased dem and or a com bination of the two. A lle r g y : Sulzberger9 defines allergy as fo llo w s: “ A n y acquired specific alteration in the cap acity to react, w h ich occurs in livin g organism s or tissues upon exposure to certain livin g or inanim ate agents or substances.” A p h th ae, or canker sores, are fam iliar m anifestations o f some sensitivity to foods such as w alnuts, cheese and choco late. A n gion eu rotic edem a o f the lips is another exam ple o f allergy. These lesions usually represent the hypersensitivity o f the tissues to an internal irritant. W e do have m ou th lesions that also are caused b y actu al contact w ith an irritant. T h is is a form o f derm atitis venenata. F or exam ple, there are w om en w ho de velop cheilitis through the use o f lipstick, and oth er patients w ho are sensitive to various toothpastes or mouthwashes. (Fig- 5 -) T h e so-called denture sore m outh m ay be another exam ple o f contact derm atitis. In this instance, w e m ust be sure that the lesion is due to the denture m aterial before m akin g the patien t discard the old
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for a n ew denture.10 I h ave show n that m any o f these cases o f sore m outh u n der dentures are due to uncleanliness and th at am ong the organism s recovered, b oth fro m the plates and the tissues, was alw ays a yeast o f the M o n ilia a lbica n s type. W h en these dentures w ere prop erly cleaned, the lesions beneath them usu a lly healed w ith out chan gin g the denture m aterial. L ovem an 11 reported a case o f sore m outh from dentures in w h ich he proved th at the stomatitis w as due to the oil o f anise in the m aterial that was used to clean the plate and not to the plate itself. T h e adm inistration o f drugs and chem icals : C ertain drugs, such as phenolphthalein, quinine and m ercu ry, m ay cause disturbances w ithin the m outh that va ry from eruptions to m em branous lesions. T h ese changes are considered an allergic response. O n the oth er hand , con tact w ith bism uth and lead is usu ally not associated w ith gingivitis or stomatitis. T h e y m erely produce a characteristic line in the gin giva, w hich is caused b y the precipitation into the tissues o f the circu latin g m etal in the form o f a sulfide. I t is to be noted th a t the bism uth o r lead line is seen o n ly in the presence o f oral n eglect. In the clean, w ell-kept m outh, this line is usually missing. O f late, a n ew d ru g has been in tro d uced that has a decided effect on the gin giv al m ucosa. It is dilantin sodium ,12 an anticonvulsant used fo r the alleviation o f epileptic seizures. K im b a ll13 was the first to report an undue effect upon the gums. L ate r, T h o m a 14 and others observed sim ilar effects. A m arked hypertrop h ic gingivitis results. (F ig. 6.) T h e gum s are firm, free from p ain and do not bleed easily. K im b all th o u gh t th at there was a vitam in G deficiency as a background, b u t o f late this view has n ot been accepted. C h il dren and you n g adults are m ostly a f fected. H istologically, there is a great increase
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in collagen. T h e epithelium does not appear so m arkedly involved. W h a t in flam m ation is present is due to concom i tant infection. T h e lesion m icroscopically is sim ilar to th a t o f diffuse fibromatosis o f the gums. (F ig. 7.) T h is hypertrop hic lesion is a new clin ical en tity and one th at w e m ust sus p e ct in all cases o f h y p ertrop h y o f the gums, especially if it occurs in you n g adults or children. B lood d yscrasias: T h e term inal oral lesion o f acu te leukem ia, agranulocytosis, severe pu rpu ra and pernicious anem ia is an ulcerom em branous one, clin ically sim ilar to a severe V in c e n t’s infection. T h e early lesions, how ever, m a y present d ifferent symptoms. I n pernicious anem ia, one o f the earliest signs is fou n d in the m outh. T h is is the b u rn ing or sore tongue. A t times, the discom fort m ay fa r exceed an y visual reason fo r its existence. T h e n m a y fo l low the sm ooth, red, polished ap p ear ance o f the tongue, w ith atro p h y o f the papillae. (F ig. 8.) T h e gum s are quite pale and recurrent aph th ae are fre q u en tly noted. In acu te leukem ia, an ea rly sign is sudden h yp ertrop h y of the gum s. I t m ay be m istaken fo r an acute inflam m atory gingivitis o r for scurvy. T h e lesion is due to the deposit o f leukem ic cells in the tissue. T h e tissues soon break dow n, and secondary infection u sually results in an ulcerom em branous lesion. (F ig. 9.) Som etim es, an isolated tooth m a y b e com e p a in fu lly loosened and the gu m abou t it sw ollen and congested. A g ain , the lesion m ay be taken fo r an acute, benign periodontal one. H ere once m ore, an overw helm ing deposit o f leukem ic cells has displaced the norm al support in g structures o f the tooth. C h ro n ic leukem ia m ay also h a v e its first sym ptom s in the m outh. A sm all localized grow th , called a n epulis, m ay appear on the gum , and the pathologist exam inin g the rem oved specim en w ill consider it an inflam m atory grow th. T h is
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va riety o f lesion, analogous to those of leukem ia cutis, m a y ap p ear m onths and even years before there are definite peripheral blood changes. Purp ura, eith er o f the throm bocyto penic variety or due to secondary toxic changes, often w ill a ffect the m outh. (F ig. 10.) F requen tly, there is a con tinuous oozing fro m the gin giva, or there m a y b e hem orrhage into th e gu m tissue. W h en the latter occurs, the condition m ay closely resemble acute scurvy, and it m a y take a n um ber o f laboratory tests to distinguish betw een the two. T h e structures m a y soon Become necrotic, the condition again resulting in the m asking o f a V in cen t’ s infection. In agranulyocytosis, there is a necrotic and m em branous gingivitis w ith a stom atitis. T hese m outh lesions p la y an im po rtan t p a rt in this ofttim es fa ta l disease and the dentist m a y be the first consulted. In m y experience, w om en are m ore often affected than m en. H ypersensitivity to drugs, especially the analgesic ones, plays an im portant part in causation o f this condition. In infectious m ononucleosis and in polycythem ia vera, the m ou th is also in volved. I should like to call attention to one more blood dyscrasia th at the dentist m a y see, a m icrocytic anem ia accom panied b y dysphagia and ach lorh yd ria and sometimes know n as the Plum m erV inson syndrom e. T h e patien t is usu ally a w om an past m iddle life and is g e n erally edentulous. She is thin and has atrophic, contracted lips and a very n a r row oral opening. T h e b u ccal m ucosa is usually dull and d ry, the tongue sm ooth and atrophic and occasionally sore. T h e patien t states th at she has diffi cu lty in sw allow ing and has never been able to w ea r dentures.15 S uch a condition should be recognized, fo r the patien t is in urgen t need o f m ed i cal attention. A h lb o m 16 and others have shown th a t such patients are prone to alim en tary and p h aryn geal cancer. A p
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propriate treatm ent w ill alleviate the condition and w ill w ard off the im pend ing m alignant disease. T h e sore m ou th and the inability to w ear dentures are fo u n d often in those w ho have acquired a secondary anem ia from w h atever cause. I t is fo lly to try to m ake a n y prosthetic replacem ent in these individuals until the anem ia has been corrected. In conclusion, I w ou ld say that it is m ore necessary fo r us to correctly d iag nose the predisposing conditions than it is to treat the local lesions. W hen this is appreciated, ou r treatm ent can be re duced to the fo llo w in g : i . S top pin g pain. 2. M a k in g a correct diagnosis. 3. R e d u cin g infection. 4. R em o vin g the pre disposing causes. B IB L IO G R A P H Y
1. L a i d l a w , E. F . , and C a h n , L . R . : M elanoblasts in Gum : ] . D. Res., 12:534, June
1932 .
2. F o r d y c e , J. A .: Peculiar Affection of Lips and Oral Cavity. J. Cutan. & GenitoXJrin. Dis., 14:413, 1896. 3. L a i n , E. S.: Chem ical and Electrolytic Lesions of M outh Caused by Artificial Den tures. Arch. Derm. & Syph., : , January
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4. S e b r e l l , W. H ., and B u t l e r , R. E . : Riboflavin Deficiency in M an. Pub. Health Rep., 53:2282, Dec. 30, 1938. 5. K i n g , J. D .: V incent’s Disease Treated with Nicotinic Acid. Lancet, 2 :3 1, July 13, 1940. 6. B l a n k e n h o r n , M . A ., and S p i e s , T . D . : Prevention, Treatment and Possible Nature of Peripheral Neuritis Associated with Pellagra and Chronic Alcoholism. TV. A. Am. Physi cians, 50:164, 1935. 7. M e r r i t t , A. H .: Periodontal Disease. Ed. 1. New York: T he M acmillan Co., 1930. 8. N o v a k , E . : Gynecological and Obstet rical Pathology. Philadelphia: W. B. Saunders Co., 1940. 9. S u l z b e r g e r , M . B .: Dermatologic A l lergy. Springfield, .: Charles C. Thomas, 1940.
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Denture— Sore Mouth.
Ann. Dentistry, 3:33, M arch 1936. 11. L
o vem an
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A .:
Stomatitis
Venenata.
Arch. Derm. & Syph., 37:70, January 1938. 12. M e r r i t t , H . H ., and P u t n a m , T . J.:
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Sodium Diphenyl Hydantoinate in Treatment of Convulsive Disorders. J.A .M .A., 1 1 1 : 1068, September 17, 1938. 13. K i m b a l l , O. P.: Treatment of Epilepsy. J.A .M .A., 112:1244, April 1, 1939. 14. T h o m a , K . H .: Dilantin Hyperplasia of Gingiva. Am. ] . Orthodontics, 26:394, April 1940. 15. C a h n , L. R .: Plummer-Vinson Syn-
drome Facies: O ral Pre-Cancerous Sign. Arch. Clin. & Oral Path., 2:308, September
1938. 16. A h l b o m , H. E.: Simple Achlorhydric Anaemia, Plummer Vinson Syndrome and Carcinoma of M outh, Pharynx and Oeso phagus in Women. Brit. M . 2:331, August 15, 1936. 630 West One Hundred Sixty-Eighth Street.
THE STREPTOCOCCUS AND THE CARIOUS LESION B y C . A . S crive n e r, D .D .S ., O tta w a , K a n . A L L b acterial life depends on a favorable and receptive host. T h e host or m edium inducive o f prolific gro w th in some organism s is u n favorab le to the grow th o f others. T h is fa ct is used to a d van tage in identification o f u n know n bacteria. In order to develop a desired bacterial culture, a m edium con tainin g tissue or other substance know n to be inducive o f grow th o f the p a r ticular organism should be used and conditions created sim ilar to those in w hich the organism is know n to th rive.1 In consideration o f this belief, the fo l low in g experim ents w ere conducted. A n um ber o f w hole non-carious teeth w ere extracted , carefu lly w ashed and rinsed in distilled w ater. T h e y w ere then im m ed iately placed in a hum idor and refrigerated. A large w edgew ood m ortar and pestle w ere th o rough ly cleaned and chilled. T h e teeth w ere placed in the m ortar w ith a little distilled w ater and w ere groun d to a fine paste. I t was hoped in this m ann er to retain all the elements o f the tooth structure w ith ou t loss due to heat, dehydration and putrefaction. T h e paste was washed into a porcelainlined p a n w ith an excess o f distilled w ater an d w as boiled fo r thirty m inutes. T h e broth was then filtered and divided. Jour. A .D .A ., V ol. 28, June 1941
T w e n ty per cent refined cane sugar was added to one h a lf the broth and shredded agar-a ga r o f sufficient q u an tity to p ro duce a thick je lly w as added to both solutions. T h e solutions w ere then placed in test tubes and closed w ith cotton plugs. A fte r b eing heated in the au to clave at 15 pounds pressure fo r fifteen m inutes, h a lf the tubes w ere prepared to receive “ slant” cultures and the re m ain der to receive “ stab” cultures. A d eeply involved carious tooth was extracted, ca refu lly w ashed and im m e d iately placed in a h yd rator and in cu b ated at 98° F. T h e superficial debris and carious m aterial w ere rem oved under strict aseptic conditions to prevent salivary and food contam ination, and a sam ple o f carious m aterial was rem oved from the deep p a rt o f th e c av ity w ith a sterile spoon excavator. T h is m aterial w as used to inoculate cultures in a series o f eigh t tubes, the prepared tooth-agar m edium and several com m ercial m edia, in clu d in g ord inary nutrient a ga r and Loeffler’s blood serum, b ein g used. Both surface and stab plants w ere m ade and the tubes incubated at 98° F. A fte r tw elve hours, no evidence o f grow th appeared excep t in the tw o tubes th a t contained the tooth-agar inoculated b y the stab m ethod. In these tubes, a
I
D O n ot believe th at there are such specific disease entities as, fo r e x am ple, diab etic gingivitis or pyor rhea, an d pregn an cy gingivitis. T h ere are thousands o f diabetics w h o n ever d e velop pyorrhea, and a vastly greater num ber o f w om en w ho becom e pregnant w ithout ever h a vin g gingivitis. L o ca l irritants and system ic deran ge m ent and disease m a y so underm ine the oral tissue im m unity and tone that the ever-present bacteria o f the m outh can set u p the clinical picture. M a n y o f these lesions look alike, y et their etiology is en tirely different, and in order to m ake our therapeutic measures effective, w e m ust k n ow the cause o f the trouble and the course that it w ill follow . B efore discussing oral lesions proper, I should like to m ention tw o com m only seen affections th at are due to norm al histologic conditions o f the oral mucosa. T hese are m elanin pigm entation and F o rd yce’s disease. T h e latter is a fine exam ple o f an eponym beclou d in g a sim ple anatom ic fact. In the region o f the basal layer o f the epithelium , there are den dritic cells th at in non-pigm ented areas can on ly be shown histologically b y m eans o f special stains. (Fig. i.) These cells are m elanoblasts. W hen active, th ey form m elanin, a pigm en t that is responsible fo r the brownish discoloration found n orm ally in R ead before the section on Periodontia at the Eighty-Second Annual M eeting of the American Dental Asociation, Cleveland, Ohio, September i s , 1940. •Chairm an of the Division of O ral Pathol ogy, Colum bia University Dental School.
Jour. A .D .A ., Vol. 28, June 1941
the m ouths o f the darker races.1 T h e y m ay, how ever, be abnorm ally stim ulated into p rod u ctivity b y traum a and in A d d i son’s disease. Sebaceous glands (F ig. 2) are fre q u en tly fou n d in the corium o f the m ucous m em brane o f the inside o f the cheeks and lips, and in that o f the bu ccal gu m near the m ucobu ccal fo ld above the m axillary bicuspids. W h en in exagger ated num bers and close to the epithelium , th ey give rise to a condition erroneously th ou ght to be pathologic and w hich has been called F ord yce’s disease.2 (F ig. 3.) e t io l o g y
T h ere are exogenous and endogenous causes fo r m ost oral lesions. E x o g e n o u s Cau ses. — T r a u m a : T h e oral m ucous m em brane is subjected to constant traum a, w h ich usually is m ild and, du rin g the ord inary course o f events, can be w ithstood w ith ou t any pathologic disturbance. T h e shape o f our teeth and their contacts prevent food from in ju rin g the gin giva. T h e epithe lium o f the m ucosa w ill also, under norm al circum stances, w ithstand the a c tion o f m ild acids o r alkalis and therm al changes. M alalin em en t o f the teeth, the fa u lty restoration o f lost tooth structure or the non-replacem ent o f lost teeth causes m e chan ical irritation o f the tissues, w hich m a y result in a v a riety o f lesions ran gin g from a m ild infection to leukoplakia and even m alignancy. H a b it m a y result in another type o f traum a, and one o f the com m onest trau m atizin g habits is cheek biting. (F ig. 4.)
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E lectrical currents : A n um ber o f years ago, L a in ,3 o f O k lah o m a, established the fa ct th a t electrical currents cou ld be generated w ithin the m outh b y dissim ilar metals, and that a v a riety of lesions could result from burns caused b y these cu r rents. T h e lesions so produced m a y v a ry from a superficial excoriation to an ulcer or a leukoplakia patch. I h ave seen a m arkedly leukokeratotic p alate return to norm al a fte r the rem oval o f a large gold bridge. In fection : Regardless o f w h at the pre disposing cause m a y be, in fection must
Fig. I.-— Melanoblasts in gum. These were in a non-pigmented area and are brought out by means of the “ dopa” reaction. alw ays be considered an im portant ex ogenous factor. E n d o g e n o u s C a u ses. — A v ita m in o sis: V ita m in A , those o f the B com plex and vitam in C contribute m ostly to the w ell being o f the oral m ucosa. V ita m in A affects prin cip ally the epi thelium . A lack o f this foo d com ponent has a keratinizing effect, not on ly on the surface epithelium , but also, through a m etaplastic process, on that o f the ducts o f the salivary glands.
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A n avitam inosis A m a y result in leuko keratotic areas on the oral m ucosa. T h is is occasionally seen in those on strenuous w eight-reducin g diets. T h e ducts o f the m ucous and salivary glands m ay becom e keratinized and blocked, a lack o f salivary secretion and lubrication resulting. T h is causes the m ucosa to becom e dry, cracked and p ain fu l and is one o f the p rin cip al causes o f xerostomia. T hose o f the vitam in B com plex o f most interest to us are vitam ins B l3 or thiam in h ydrochloride, B 2, or riboflavin,
Fig. 2.— Sebaceous glands in submucosa of oral mucous membrane. and the pellagra preven tive factor, or nicotinic acid. W ith the exception o f a peripheral neuritis, a deficien cy in B x, as fa r as is know n, causes no oral lesions p er se. H ow ever, a d eficien cy o f this vitam in causes a loss o f appetite, and the les sened food intake w ill result in a lack of those essential factors th at w ill directly affect the oral m ucosa. T h e results o f dep rivation o f ribo flavin, described recen tly b y Sebrell and B utler,4 should be know n to all those in
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terested in the m outh. T h e lesion, w h ich th ey called “ cheilosis,” is described in their ow n w ords as fo llo w s : These lesions began as a pallor of the mucosa of the lips in the angles of the mouth without involvement of the buccal mucosa. This pallor was soon followed by maceration, and within a few days super ficial transverse fissures appeared, usually bilateral, and exactly in the angle of the mouth. These fissures extended somewhat downward from the angle and there was very little inflammatory reaction. The le sions became moist and covered with a honey-colored crust which could be scraped off without bleeding. In some instances the
Fig. 3 .—Fordyce’s disease. The word “dis ease” is a misnomer. The condition is simply an affection due to the presence of sebaceous glands and is of common occurrence. The sec tion shown in Figure 2 was taken from this case. fissures continued to extend into the skin for a distance as much as one half inch. These lesions resembled those described as per leche. A t about the time the fissures were seen, the lips became abnormally red along the line of closure. This was due appar ently to a superficial denudation of the mucosa. In addition to the cheilosis there
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was also seen a fine scaly, slightly greasy desquamation on a mildly erythematous base in the naso-labial folds, on the alae nasi, in the vestibule of the nose and on the ears. I h ave observed a n um ber o f instances o f these fissures at the m outh angles and h ave seen them involute under adequate dosages o f riboflavin. H eretofore, w e w ould h a ve called these lesions perleche and treated them as infections. T h e desquam ation, w h ich is also inter esting, m a y give us a clue as to the rea son for those cases o f true desquam ative gingivitis th at h ave up to now resisted all form s o f local treatm ent.
Fig. 4 .—Lesion produced by cheek biting. A deficiency in nicotinic acid causes pellagra. In this disease, gingivitis, stom atitis and glossitis are alw ays present and are u sually early symptoms. T h e tip and m argins o f the tongue becom e very red and are freq u en tly swollen. U lcers m ay form that are covered w ith a gray m em brane that abounds in the orga n isms o f V in cen t. In fa ct, to the u n in itiated, the severe V in c e n t’s infection m a y w ell mask the real com plaint. Jolliffe has shown a n um ber o f severe
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cases o f V in cen t’s stom atitis in pellagrins th a t w ere cured b y the adm inistration o f the p ellagra p reven tive fa cto r w ith ou t the use o f a n y specific antiseptic therapy. K in g 5 also calls attention to the relation ship betw een V in c e n t’s infection and a deficiency in n icotin ic acid . H e also foun d th a t in fo u r persons w ith norm al gums, the excretion o f n icotin ic acid in the urine o f each was fa r in excess o f that o f a patien t w ith V in cen t’s infection. More investigation a lo n g this line is necessary before conclusions can be draw n. K in g treated fo u r cases o f severe V in c e n t’s in fection successfully b y the oral adm inistration o f nicotinic acid.
Fig. 5 .—Glossitis caused by excessive use of “oxygenating” mouth washes. It is interesting to note how far this patient can extrude the tongue. This is usually a sign that the patient is constantly viewing it and is apprehensive and probably hypochondriacal. Such a person probably overuses medication of all kinds. T h is question o f a B com plex defi ciency in a ll cases o f severe V in c e n t’s infection th at h ave not a blood dyscrasia as their basis m ust alw ays be borne in mind. r e p o r t
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gingivitis and extremely fetid breath, the teeth looked elongated, the interdental soft tissue was lost and the spaces between the teeth were filled with a foul-smelling débris. Both jaws were affected. T he attack was an acute one superimposed upon a chronic one of long standing. The gums were pale and irregularly streaked with the lacy white lines seen in lichen planus. T he patient had been treated on a number of occasions for similar attacks of what she termed “ trench mouth.” Smears of the gums showed myriads of spirochetes and fusiform bacilli, to the al most total exclusion of other forms of bac teria. T he clinical signs and the smear were typical of Vincent’s infection, yet it was evident that this was just a complication. Biopsy of the whitish lined gum showed that these lines represented a mild, but defi-
Fig. 6 .—Hypertrophy of gums due to use of dilantin sodium (Kimball). (Courtesy of the Journal of the American Medical Associa tion.) nite hyperkeratosis— an uncommon finding in the buccal gum. T he woman was a chronic alcoholic. M any alcoholics are markedly deficient in their food intake and suffer from multiple vitamin deficiencies. Many of them are subclinical pellagrins. Blankenhorn and Spies6 found stomatitis and glossitis in 60 per cent of their alcoholic pellagrins, and the latter observed the rapid cure of these infections with administration of nicotinic acid. In the case under consideration, the Vincent’s infection and the keratotic white lines were simply manifestations of a deficiency disease. The reason that the patient had never been
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cured of her infection was the fact that the true predisposing causes were not suspected and eliminated. V ita m in G affects the endothelium o f the capillaries and the intercellular cem ent substance. A lack o f this vitam in causes the capillaries to becom e perm e able, allo w in g interstitial hem orrhage. T h is accounts fo r the bleeding and swollen condition o f the gum s in scurvy. S econ d ary infection, especially b y the fusospirochetal symbiosis, aga in w ill re sult in a lesion that m a y m ask the true condition. In d ealin g w ith the question o f a v it am inosis, a num ber o f im portant facts
Fig. 7.— Section of gum showing hyper trophy from use of dilantin sodium. The stroma is very dense and there is a lack of inflammatory exudate. m ust be borne in m ind. Patients w ho are d eficien t in one vitam in are usually deficient in others. T h e adm inistration o f w h a t is thought to be the missing food fa cto r m a y b rin g about on ly the am eli oration o f p a rt o f the clin ical picture. P olyvitam in therapy, plus, occasionally, the adm inistration o f the extract o f w hole liver is often indicated. A vitam inosis m a y occu r in spite o f the fa ct th a t the patient is receivin g an optim um am ount o f essential foods. Th is is seen in intestinal disease in w hich
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there is interference w ith the absorption o f the foods. E xam ples o f this are fou n d in id iopath ic steatorrhea o f children and in can cer o f th e intestines. A n avitam inosis m a y not h ave a te x t book appearance. T h ere are m a n y o f w h a t h ave been called subclinical cases and these m ust be appreciated and w atch ed for. Specific in fe c tio n s : Syphilis and tu b er culosis are the tw o principal specific in fections th a t a ffect the m outh. So m uch has been w ritten abou t the oral m an i festations o f syphilis th at it is unnecessary to go into this question now. O sier said,
Fig. 8.— Smooth “ polished” tongue with atrophy of papillae. This type of tongue is seen in pernicious anemia, in the PlummerVinson syndrome, in sprue and in other defi ciency diseases. “ syphilis is the greatest im itator o f disease.” O n e should suspect syphilis as either a cause or a com plication in every oral lesion. Tuberculosis is not alw ays considered in view in g oral disease, yet, in the past tw o years, I h a ve seen several instances o f tuberculous disease o f the m outh as a com plication o f generalized tuberculosis. In none of these cases was the oral lesion
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thought to be tuberculous, b ein g treated locally fo r aw h ile w ith ou t avail, until the correct diagnosis was m ade through biopsy. W h en oral tuberculosis is a com plication o f the system ic disease, the prognosis is usually grave and early diagnosis is im perative. M eta b o lic d istu rb an ces: In h y p o th y roidism, w hen m yxed em a is present, the patients, as a rule, h ave thick, flab b y and bloated tongues against the sides of w hich are indentations from the teeth. T h e lips are also grea tly thickened. T h e gum s a t tim es becom e sw ollen and these patients freq u en tly h ave d ifficulty in re tainin g artificial dentures. In A ddison ’ s disease, the m ucous m em -
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peripheral neuritis fro m w hich diabetics freq u en tly suffer and w h ich is evidenced in the m outh b y su bgin gival hypersen sitivity o f the teeth (M e rritt’s sig n ).7 M enstruation : T h e prem enstrual and m enstrual periods m an ifest them selves in the oral cavity. T h e extrem ely rare vicarious m enstruation from the gum s is w ell know n. H o w ever, there are a n u m ber o f less distinctive lesions. H erpes labialis an d buccalis are per haps the com m onest o f the oral lesions appearin g abou t this tim e. T h e y are quite p ain fu l and u su ally attack the same areas each m onth. T o exp lain the m od u s
Fig. 9.— Slough that quickly follows any kind of trauma in acute leukemia. In this instance, a tooth had been extracted. brance becom es pigm ented ow in g to h yp era ctivity o f the m elanoblasts. D iabetes is freq u en tly com plicated by gingivitis and pyorrhea. T h is m a y be due to an increase in the sugar in the gin gival and buccal m ucosa from the h y p e r glycem ia, w h ich in turn w ill fa v o r in fe c tion b y b acteria and fu n gi, especially yeasts. In fa u lty carbohydrate m etabolism , there is a greater dem and fo r vitam in B j. D iabetes m a y be com plicated b y this defi ciency. T h is p rob ab ly accounts fo r the
Fig. 1o.— Thrombocytopenic purpura. Blood has collected about the necks of the teeth and there are small hematomas present. o p era n d i o f these lesions is qu ite difficult. T h e y are analagous to the acne that occurs regu larly in some w om en. T h e y m a y be explained on th e basis o f a low ering o f the tissue tone o f the oral m ucosa so that the herpes virus can b e com e active. Som e w om en regu larly develop pericornal infections d u rin g the m enstrual period. In order to understand w h y these infections occu r at this tim e, it m ight
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be w ell to review certain anatom ic facts. Posterior to the m and ibu lar third m olars, is the loose areolar tissue th at contains accessory salivary glands. T h ese glands are structurally sim ilar to the v u lv o vagin al glands8 (B artholin ’s g la n d s), and also resemble som ew hat those o f the en dom etrium . T o d a y , it is established that estrogenic horm ones h a ve an effect on the oral m ucosa, and there is little doubt that the sam e horm ones a ct on the a c cessory salivary glands sim ilarly to the w a y they do on the vu lvovagin al and endom etrial ones. Also, in b ack o f the low er third m olars, there is n early alw ays a pocket, or cul-de-sac, especially should the tooth be im pacted or m alposed, th at usually contains m an y m icro-organism s, especially o f the fusospirochetal sym bi osis. I f there is an alteration in the glands from some horm onal stim ulus du rin g m enstruation, the tissue tone and im m unologic defenses becom e so changed that the bacteria alw ays present in this area can set up the pericoronal in fe c tion. T h e m on thly recurrence o f these a t tacks can be obviated on ly b y rem oval o f the tooth. In one instance, the patien t had a m on thly sw elling o f the retrom olar tissue quite aw hile a fter the tooth had been rem oved. a t r o p h ic g in g iv it is
T h ere is a type o f gingivitis ch aracter ized b y atro p h y o f large patches o f the epithelium . T h is condition has been called desquam ative gingivitis, b u t it is n ot a desquam ative lesion. H istologically, the epithelium is reduced to one or tw o thin layers o f cells, b u t m icroscopically there is no evidence o f cellu lar shedding. A trop h ic gingivitis w ou ld be a m ore a c curate nam e. T h is condition is seen in w om en chiefly, usually du rin g the m eno pause or postm enopausal periods. I saw it once in a m an. T h e use o f estrogenic horm ones locally applied a fter the m an n er ad vocated b y Ziskin has g iv en excel lent results.
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P re g n a n c y : P regn an cy is frequently accom panied b y changes in the gums. T h is m a y consist o f slight hyperem ia and sw elling o f the interdental papillae, w hich m ay b e m ild and m ay pass unnoticed. I f oral hygiene is m aintained, a disturb in g gingivitis is rarely seen. H ow ever, if the m outh is neglected, so-called “ preg n an cy gingivitis” occurs. T h e gums b e com e sw ollen and congested and the interdental pap illae are enlarged and bleed under the slightest provocation. A n oth er oral com plication o f p reg n an cy is a tum or, w h ich m a y occu r in the w ell-kept m outh, b u t here again is seen m ost often in the ill-kept one. H is tologically, it is an angiogranulom a and u sually disappears a fter parturition. T h e reason fo r the m ucous m em brane changes du rin g p regn an cy are unknown. T h e y m a y be due to horm one disturb ances, vitam in deficiencies due to an in creased dem and or a com bination of the two. A lle r g y : Sulzberger9 defines allergy as fo llo w s: “ A n y acquired specific alteration in the cap acity to react, w h ich occurs in livin g organism s or tissues upon exposure to certain livin g or inanim ate agents or substances.” A p h th ae, or canker sores, are fam iliar m anifestations o f some sensitivity to foods such as w alnuts, cheese and choco late. A n gion eu rotic edem a o f the lips is another exam ple o f allergy. These lesions usually represent the hypersensitivity o f the tissues to an internal irritant. W e do have m ou th lesions that also are caused b y actu al contact w ith an irritant. T h is is a form o f derm atitis venenata. F or exam ple, there are w om en w ho de velop cheilitis through the use o f lipstick, and oth er patients w ho are sensitive to various toothpastes or mouthwashes. (Fig- 5 -) T h e so-called denture sore m outh m ay be another exam ple o f contact derm atitis. In this instance, w e m ust be sure that the lesion is due to the denture m aterial before m akin g the patien t discard the old
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for a n ew denture.10 I h ave show n that m any o f these cases o f sore m outh u n der dentures are due to uncleanliness and th at am ong the organism s recovered, b oth fro m the plates and the tissues, was alw ays a yeast o f the M o n ilia a lbica n s type. W h en these dentures w ere prop erly cleaned, the lesions beneath them usu a lly healed w ith out chan gin g the denture m aterial. L ovem an 11 reported a case o f sore m outh from dentures in w h ich he proved th at the stomatitis w as due to the oil o f anise in the m aterial that was used to clean the plate and not to the plate itself. T h e adm inistration o f drugs and chem icals : C ertain drugs, such as phenolphthalein, quinine and m ercu ry, m ay cause disturbances w ithin the m outh that va ry from eruptions to m em branous lesions. T h ese changes are considered an allergic response. O n the oth er hand , con tact w ith bism uth and lead is usu ally not associated w ith gingivitis or stomatitis. T h e y m erely produce a characteristic line in the gin giva, w hich is caused b y the precipitation into the tissues o f the circu latin g m etal in the form o f a sulfide. I t is to be noted th a t the bism uth o r lead line is seen o n ly in the presence o f oral n eglect. In the clean, w ell-kept m outh, this line is usually missing. O f late, a n ew d ru g has been in tro d uced that has a decided effect on the gin giv al m ucosa. It is dilantin sodium ,12 an anticonvulsant used fo r the alleviation o f epileptic seizures. K im b a ll13 was the first to report an undue effect upon the gums. L ate r, T h o m a 14 and others observed sim ilar effects. A m arked hypertrop h ic gingivitis results. (F ig. 6.) T h e gum s are firm, free from p ain and do not bleed easily. K im b all th o u gh t th at there was a vitam in G deficiency as a background, b u t o f late this view has n ot been accepted. C h il dren and you n g adults are m ostly a f fected. H istologically, there is a great increase
s s o c ia t io n
in collagen. T h e epithelium does not appear so m arkedly involved. W h a t in flam m ation is present is due to concom i tant infection. T h e lesion m icroscopically is sim ilar to th a t o f diffuse fibromatosis o f the gums. (F ig. 7.) T h is hypertrop hic lesion is a new clin ical en tity and one th at w e m ust sus p e ct in all cases o f h y p ertrop h y o f the gums, especially if it occurs in you n g adults or children. B lood d yscrasias: T h e term inal oral lesion o f acu te leukem ia, agranulocytosis, severe pu rpu ra and pernicious anem ia is an ulcerom em branous one, clin ically sim ilar to a severe V in c e n t’s infection. T h e early lesions, how ever, m a y present d ifferent symptoms. I n pernicious anem ia, one o f the earliest signs is fou n d in the m outh. T h is is the b u rn ing or sore tongue. A t times, the discom fort m ay fa r exceed an y visual reason fo r its existence. T h e n m a y fo l low the sm ooth, red, polished ap p ear ance o f the tongue, w ith atro p h y o f the papillae. (F ig. 8.) T h e gum s are quite pale and recurrent aph th ae are fre q u en tly noted. In acu te leukem ia, an ea rly sign is sudden h yp ertrop h y of the gum s. I t m ay be m istaken fo r an acute inflam m atory gingivitis o r for scurvy. T h e lesion is due to the deposit o f leukem ic cells in the tissue. T h e tissues soon break dow n, and secondary infection u sually results in an ulcerom em branous lesion. (F ig. 9.) Som etim es, an isolated tooth m a y b e com e p a in fu lly loosened and the gu m abou t it sw ollen and congested. A g ain , the lesion m ay be taken fo r an acute, benign periodontal one. H ere once m ore, an overw helm ing deposit o f leukem ic cells has displaced the norm al support in g structures o f the tooth. C h ro n ic leukem ia m ay also h a v e its first sym ptom s in the m outh. A sm all localized grow th , called a n epulis, m ay appear on the gum , and the pathologist exam inin g the rem oved specim en w ill consider it an inflam m atory grow th. T h is
C ahn— L
e s io n s o f
L
o c a l an d
va riety o f lesion, analogous to those of leukem ia cutis, m a y ap p ear m onths and even years before there are definite peripheral blood changes. Purp ura, eith er o f the throm bocyto penic variety or due to secondary toxic changes, often w ill a ffect the m outh. (F ig. 10.) F requen tly, there is a con tinuous oozing fro m the gin giva, or there m a y b e hem orrhage into th e gu m tissue. W h en the latter occurs, the condition m ay closely resemble acute scurvy, and it m a y take a n um ber o f laboratory tests to distinguish betw een the two. T h e structures m a y soon Become necrotic, the condition again resulting in the m asking o f a V in cen t’ s infection. In agranulyocytosis, there is a necrotic and m em branous gingivitis w ith a stom atitis. T hese m outh lesions p la y an im po rtan t p a rt in this ofttim es fa ta l disease and the dentist m a y be the first consulted. In m y experience, w om en are m ore often affected than m en. H ypersensitivity to drugs, especially the analgesic ones, plays an im portant part in causation o f this condition. In infectious m ononucleosis and in polycythem ia vera, the m ou th is also in volved. I should like to call attention to one more blood dyscrasia th at the dentist m a y see, a m icrocytic anem ia accom panied b y dysphagia and ach lorh yd ria and sometimes know n as the Plum m erV inson syndrom e. T h e patien t is usu ally a w om an past m iddle life and is g e n erally edentulous. She is thin and has atrophic, contracted lips and a very n a r row oral opening. T h e b u ccal m ucosa is usually dull and d ry, the tongue sm ooth and atrophic and occasionally sore. T h e patien t states th at she has diffi cu lty in sw allow ing and has never been able to w ea r dentures.15 S uch a condition should be recognized, fo r the patien t is in urgen t need o f m ed i cal attention. A h lb o m 16 and others have shown th a t such patients are prone to alim en tary and p h aryn geal cancer. A p
9 J7
S y s t e m i c O r ig in
propriate treatm ent w ill alleviate the condition and w ill w ard off the im pend ing m alignant disease. T h e sore m ou th and the inability to w ear dentures are fo u n d often in those w ho have acquired a secondary anem ia from w h atever cause. I t is fo lly to try to m ake a n y prosthetic replacem ent in these individuals until the anem ia has been corrected. In conclusion, I w ou ld say that it is m ore necessary fo r us to correctly d iag nose the predisposing conditions than it is to treat the local lesions. W hen this is appreciated, ou r treatm ent can be re duced to the fo llo w in g : i . S top pin g pain. 2. M a k in g a correct diagnosis. 3. R e d u cin g infection. 4. R em o vin g the pre disposing causes. B IB L IO G R A P H Y
1. L a i d l a w , E. F . , and C a h n , L . R . : M elanoblasts in Gum : ] . D. Res., 12:534, June
1932 .
2. F o r d y c e , J. A .: Peculiar Affection of Lips and Oral Cavity. J. Cutan. & GenitoXJrin. Dis., 14:413, 1896. 3. L a i n , E. S.: Chem ical and Electrolytic Lesions of M outh Caused by Artificial Den tures. Arch. Derm. & Syph., : , January
2 5 21
1932 -
4. S e b r e l l , W. H ., and B u t l e r , R. E . : Riboflavin Deficiency in M an. Pub. Health Rep., 53:2282, Dec. 30, 1938. 5. K i n g , J. D .: V incent’s Disease Treated with Nicotinic Acid. Lancet, 2 :3 1, July 13, 1940. 6. B l a n k e n h o r n , M . A ., and S p i e s , T . D . : Prevention, Treatment and Possible Nature of Peripheral Neuritis Associated with Pellagra and Chronic Alcoholism. TV. A. Am. Physi cians, 50:164, 1935. 7. M e r r i t t , A. H .: Periodontal Disease. Ed. 1. New York: T he M acmillan Co., 1930. 8. N o v a k , E . : Gynecological and Obstet rical Pathology. Philadelphia: W. B. Saunders Co., 1940. 9. S u l z b e r g e r , M . B .: Dermatologic A l lergy. Springfield, .: Charles C. Thomas, 1940.
111
10. C
ahn,
L. R .:
Denture— Sore Mouth.
Ann. Dentistry, 3:33, M arch 1936. 11. L
o vem an
,
A .:
Stomatitis
Venenata.
Arch. Derm. & Syph., 37:70, January 1938. 12. M e r r i t t , H . H ., and P u t n a m , T . J.:
9 í8
T
he
J
ournal of th e
A m e r ic a n D e n t a l A s s o c ia t io n
Sodium Diphenyl Hydantoinate in Treatment of Convulsive Disorders. J.A .M .A., 1 1 1 : 1068, September 17, 1938. 13. K i m b a l l , O. P.: Treatment of Epilepsy. J.A .M .A., 112:1244, April 1, 1939. 14. T h o m a , K . H .: Dilantin Hyperplasia of Gingiva. Am. ] . Orthodontics, 26:394, April 1940. 15. C a h n , L. R .: Plummer-Vinson Syn-
drome Facies: O ral Pre-Cancerous Sign. Arch. Clin. & Oral Path., 2:308, September
1938. 16. A h l b o m , H. E.: Simple Achlorhydric Anaemia, Plummer Vinson Syndrome and Carcinoma of M outh, Pharynx and Oeso phagus in Women. Brit. M . 2:331, August 15, 1936. 630 West One Hundred Sixty-Eighth Street.
THE STREPTOCOCCUS AND THE CARIOUS LESION B y C . A . S crive n e r, D .D .S ., O tta w a , K a n . A L L b acterial life depends on a favorable and receptive host. T h e host or m edium inducive o f prolific gro w th in some organism s is u n favorab le to the grow th o f others. T h is fa ct is used to a d van tage in identification o f u n know n bacteria. In order to develop a desired bacterial culture, a m edium con tainin g tissue or other substance know n to be inducive o f grow th o f the p a r ticular organism should be used and conditions created sim ilar to those in w hich the organism is know n to th rive.1 In consideration o f this belief, the fo l low in g experim ents w ere conducted. A n um ber o f w hole non-carious teeth w ere extracted , carefu lly w ashed and rinsed in distilled w ater. T h e y w ere then im m ed iately placed in a hum idor and refrigerated. A large w edgew ood m ortar and pestle w ere th o rough ly cleaned and chilled. T h e teeth w ere placed in the m ortar w ith a little distilled w ater and w ere groun d to a fine paste. I t was hoped in this m ann er to retain all the elements o f the tooth structure w ith ou t loss due to heat, dehydration and putrefaction. T h e paste was washed into a porcelainlined p a n w ith an excess o f distilled w ater an d w as boiled fo r thirty m inutes. T h e broth was then filtered and divided. Jour. A .D .A ., V ol. 28, June 1941
T w e n ty per cent refined cane sugar was added to one h a lf the broth and shredded agar-a ga r o f sufficient q u an tity to p ro duce a thick je lly w as added to both solutions. T h e solutions w ere then placed in test tubes and closed w ith cotton plugs. A fte r b eing heated in the au to clave at 15 pounds pressure fo r fifteen m inutes, h a lf the tubes w ere prepared to receive “ slant” cultures and the re m ain der to receive “ stab” cultures. A d eeply involved carious tooth was extracted, ca refu lly w ashed and im m e d iately placed in a h yd rator and in cu b ated at 98° F. T h e superficial debris and carious m aterial w ere rem oved under strict aseptic conditions to prevent salivary and food contam ination, and a sam ple o f carious m aterial was rem oved from the deep p a rt o f th e c av ity w ith a sterile spoon excavator. T h is m aterial w as used to inoculate cultures in a series o f eigh t tubes, the prepared tooth-agar m edium and several com m ercial m edia, in clu d in g ord inary nutrient a ga r and Loeffler’s blood serum, b ein g used. Both surface and stab plants w ere m ade and the tubes incubated at 98° F. A fte r tw elve hours, no evidence o f grow th appeared excep t in the tw o tubes th a t contained the tooth-agar inoculated b y the stab m ethod. In these tubes, a