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The Mouth and Its Diseases
The Mouth and Its Diseases KURT H. THOMA, D.M.D., F.D.S.R.C.S. (ENG.) HON. F.D.S.R.C.S. (EDIN.)*
THE DEVELOPMENT OF THE MOUTH
IN THE embryonic formation of the oral cavity the frontonasal and the two maxillary processes, and the mandibular arch take part. The enclosed area develops into a pocket, the stomadeum, which is lined by ectodermal epithelium. It is separated from the anterior end of the foregut by the buccopharyngeal membrane which is formed by the apposition of the stomodeal ectoderm and the foregut endoderm. At the third week of embryonic development this membrane disappears, establishing a communication between the mouth and the future pharynx. The mandibular arch at this time is completely formed, while the upper jaw is completed later by the fusion of the globular processes, derived from the frontonasal process, with the two maxillary processes. From the maxillary arch develop the palatine processes which grow medially and fuse in midline, thus dividing the cavity into an upper, the nasal, and a lower, the buccal part. The tongue is developed in the floor of the pharynx, the buccal part being derived from a pair of lateral swellings which arise from the inner surface of the mandibular arch and meet in midline. The posterior pharyngeal part is formed from the copula. It extends forward in the shape of a V, and its limbs embrace the buccal part. At the apex of the V an invagination occurs which is represented by the foramen cecum. Anterior to the V-shaped junction are the papillae vallate. Developmental Anomalies
The faulty development and nonfusion of the various processes forming the mandibular and maxillary arches results in the formation of clefts. The most common ones are the lip cleft (harelip) and the palatal clefts. Of these there are many varieties and combinations (Fig. 11). Tongue clefts occur more rarely and are due to lack of fusion at the • Professor of Oral Surgery Emeritus, Professor of Oral Pathology Emeritus, Harvard University; Visiting Lecturer in Oral Surgery, University of Pennsylvania; Honorary Surgeon, Massachusetts General Hospital; Chief, Oral Surgery Department, Brooks Hospital, Brookline, M assachusctts.
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anterior part of the tongue. Other anomalies in this region are due to an abnormal development of the thyroid gland, giving rise to thyroglossal cysts and lingual thyroids. Median rhomboid glossitis is characterized by a:red area devoid of papillae and located in the midline of the dorsum just anterior to the circumvallate papillae. It has no pathologic significance but may be misdiagnosed as an inflammatory or neoplastic lesion. Abnormal labial and lingual frenums should also be mentioned; low attachment of the former pulls down the lip and often produces the appearance of a double lip. If the frenum is hypertrophied, a space is formed between the central incisors.
Fig. 11. Cleft palate.
Fig. 12. Ankyloglossia.
Ankyloglossia is the result of an abnormal lingual frenum which ties the tip of the tongue down to the floor of the mouth (Fig. 12). It may result in speech and feeding problems. TREATMENT OF DEVELOPMENTAL ANOMALIES. The treatment of these anomalies in most instances is surgical. Early surgical corrections are most desirable; for lip procedures, the age of two months, and for cleft palate, between the ages of one and two years is considered best. Early operation facilitates feeding and insures better speech, although in patients operated upon later orthodontic correction and speech training may still insure excellent results. In all instances the general health of an infant should be considered, and no operation should be performed until the patient is properly built up since most children with lip and palate clefts are undernourished. In older patients with cleft palates in which plastic repair is not possible or in which previous operation was unsuccessful, prosthesis may be devised that often give excellent results. THE BACTERIOLOGY OF THE MOUTH
A great variety of micro-organisms inhabit the mouth throughout life. Some of these are potentially pathogenic, others are harmless sapro-
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phytes. So~e are t~an~i~nt and oth~rs perm.anent inhabitan~s. The flora varies in dIfferent mdIvIduals, but m each It tends to remam constant. The original flora in the newborn is that found in the mother's vagina, namely, B. perfringens, B. coli and Enterococcus intestinalis. These are soon added to from the air and surroundings of the infant. The mouth flora of the adult is much more complex. It has been studied by numerous investigators such as Bibby (1938), Appleton (1950), and Mcmis (1954). The following organisms are of importance: 1. Cocci. These are the most common bacteria found. They include streptococci (viridans, salivarius and hemolyticus), Gram-negative cocci (Micrococcus catarrhalis, flavus and pharyngis) and Staphylococcus albus, aureus and citreus. 2. Bacilli. A great many gram-positive bacilli occur. Among these the lactobacilli and leptotrichia play an important part in dental caries. The Bacillus hofmanni and other diphtheroids are also found. Gram-negative bacilli are the Bacillus proteus, Bacillus lactis aerogenes and members of the Friedlander group. 3. Fusiform Bacilli. These anaerobes occur as soon as the teeth erupt. Three to four varieties are found in all adult mouths. 4. Actinomyces. Gram-positive branched organisms are found in the oral flora which have not as yet been carefully investigated. 5. Vibrios. These are motile organisms identified by darkfield investigation. Their significance is not known. 6. Spiral Organisms. These are normally found in the adult flora whenever teeth are present. The most common ones are Treponema macrodentium and T. microdentium, Borrelia vincentii and B. buccalis; and Leptospira dentium. These have been studied extensively by Ramp (1950) who found them to increase in patients with gingivitis. Re found Borrelia vincentii present in great numbers in necrotizing ulcerative (Vincent's) gingivitis. 7. Yeast and Yeastlike Fungi. Yeastlike fungi are found in most mouths, even in edentulous patients wearing dentures. Their overgrowth occurs in patients receiving antibiotics, especially penicillin troches. Parenteral administration also may change the natural balance since the drugs are secreted in the saliva. 8. Protozoa. In most filthy mouths we see at least one type of amoeba. Bass (1947) has studied the Endamoeba buccalisj it is considered a scavenger of little clinical importance. 9. Viruses. Burnett and Williams (1939) reported that they found in 90 per cent of the adults studied herpes simplex virus in the oral tissue. Lowering the tissue resistance by simple trauma, actinic rays of the sun, menstrual cycle or allergic inflammation causes aphthous ulcers or herpetic stomatitis.
Diseases Produced by Micro-organisms
Under ordinary circumstances disease is not produced by microorganisms as long as they do not become an overpowering factor and as long as the local defensive mechanism functions, but lowered local resistance, trauma, or debilitating diseases may so alter conditions that infection sets in. The defensive mechanism of the mouth against bacterial invasion consists of various factors. First, the epithelial cells lining the oral cavity havean effective phagocytic action. Cells loaded with bacteria are con-
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stantly desquamated (Fig. 13). Bacteria are removed by the cleansing effect of mastication and the action of the tongue, lips and cheek. The saliva acts as a flushing agent. It contains bacterial inhibiting factors such as lysozyme. The bacterial activity is also dependent on proper nutrient media derived from the ingested food, therefore the type of food eaten, the frequency of eating, and eating habits influence the flora. Finally, certain micro-organisms may exert an antibiotic effect on others and so help to control the flora.
Fig. 13. Desquamated epithelial cells containing streptococci in streptococcic stomatitis.
One might suggest that eventually the patient may be able to choose the micro-organisms he desires to grow in his mouth through dietary measures. Caries control is based on the dietary control of acidogenic organisms. Jay et al. (1951) and Goldsworthy and Sullivan (1955) have shown how by eliminating refined carbohydrates the caries incidence may be lowered through a marked decrease in the lactobacilli and other acidogenic organisms. TREATMENT. Today the various antibiotics furnish a very effective means to combat bacterial infection. It should be remembered, however, that there is a great variation in their effectiveness. Many oral bacteria are penicillin resistant, and even organisms which originally were penicillin sensitive have developed resistant strains. Bacillus coli is a frequent offender even when occurring in mixed infection because it produces penicillinase. In superficial infection local therapy with troches should be combined with parenteral administration since the small doses contained in the former may cause sensitization of the patient, and because the local effect is not deep enough to affect invading organisms. In all infections sensitivity tests should be made; so-called disk tests (Lind, 1953) give a
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quick result so that the most effective antibiotic can be prescribed as soon as possible. NORMAL AND PATHOLOGIC PHYSIOLOGY OF THE MOUTH
The infant, with rare exceptions, is born without erupted teeth. The oral cavity is extremely small and is occupied almost completely by the strongly developed tongue. The physiologic function of the mouth is that of sucking and not, as in the adult, that of masticating food in preparation for digestion. Sucking
The act of sucking is accomplished by a tight grasp of the nipple and depression of the tongue to produce a vacuum in the posterior part of the mouth. The milk is expressed by closure of the jaws. Then follows the act of swallowing. During the first few months the mouth is rather dry because the salivary glands are still inactive. Later, around the third month, salivation becomes activated to the extent that saliva is likely to run out of the infant's mouth until gradually it learns to swallow it. Mastication
As the teeth erupt more complex food can be utilized by the child. The mouth now takes on a more important part in the process of digestion. Mastication is the mixing of the food with saliva, reducing it to a size suitable for swallowing, and lubricating the bolus to facilitate its passage through the esophagus. A normal set of teeth is of great importance in chewing. The process is one of breaking up food not only to facilitate ingestion, but more important, to make it accessible to the action of enzymeii3 secreted in the mouth and stomach. During this process the salivary glands are stimulated and the gastric secretion becomes activated, aided by the sense of taste of substances released during the process. Proper mastication therefore promotes digestion and the efficient utilization of food. Salivation
The secretion of the salivary and mucous glands of the mouth is accelerated by reflex action. The stimulation occurs through the sensory and gustatory afferent nerves supplying the tongue and oral mucosa as well as the optic, olfactory, auditory and sympathetic nerves. Secretion is also aided by purely mechanical factors, the pressure applied by the activity of the muscles of mastication and the action of the tongue. The saliva maintains a relatively constant pH value in the mouth through its efficient buffer effect. An acid diet progressively increases its alkalinity by the secretion of bicarbonate (Wah Leung, 1951) and phosphates. The use of alkalies (dentifrices) has a depressing effect both on the amount of secretion as well as on the alkalinity.
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Ptyalin, an amylolytic ferment, is one of the most important substances in the saliva since through it the digestion of carbohydrate food is initiated in the mouth. An adequate amount of time is needed to break up the food and mix it with the saliva to allow the digestive process to be initiated. This is important since the carbohydrate digestion is soon arrested in the stomach by the action of the hydrochloric acid. FUNCTIONAL ANOMALIES
There are various factors which interfere with normal functioning of the mouth. Developmental anomalies have already been mentioned. Here additional factors will be considered. Ankylosis
Traumatic injuries such as birth trauma-several cases of injury of the mandibular joint from the use of forceps in difficult delivery have been reported (Thoma, 1946)-or arthritis may result in partial or complete ankylosis making mastication difficult or impossible. In ankylosis occurring early in life the mandible in addition remains underdeveloped on the affected side, causing facial asymmetry and malocclusion. TREATMENT. Arthroplasty with metal inserts, and osteoarthrotomy will generally restore function of the jaw. Sliding osteotomy of the mandible may be required to correct the mandibular deformity. Arthroses
Rheumatoid arthritis and traumatic arthritis of the temporomandibular joint are quite commonly seen today. The former is generally part of general arthritis, while the latter is produced by occlusal abnormalities and especially a "closed bite" due to unusual wear or loss of the supporting posterior teeth. The force which ordinarily is taken up by the teeth causes friction in the joint. The pain produced limits the function of the jaws and teeth. TREATMENT. Restoring the supporting teeth by artificial substitutes or raising the occlusion by means of splints will eliminate the cause of the joint inflammation by distraction of the joint surfaces. Advanced arthritis with bone changes visible in the x-ray and causing refractory pain requires condylectomy. Patients can get along well without the joint as long as teeth are present. DISEASES OF THE TEETH
Malocclusion
Malocclusion is often a great handicap, particularly cross bite, open bite and prognathism, but also smaller irregularities interfere with the chewing motions. TREATMENT. In most instances malocclusion can be remedied by
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orthodontic procedures during childhood. In older persons serious abnormalities in the relationship of the upper and lower jaws may be corrected by ostectomies or osteotomies (Fig. 14) in various parts of the mandible (Thoma, 1952).
B A Fig. 14. Open bite. A, before; B, after ostectomy.
Effect of Food on the Teeth
Certain food as well as substances that are habitually chewed, such as chewing gum, lozenges, candy and tobacco, are harmful to the teeth. Acid produced from these causes decalcification and erosion, while gritty substances cause abnormal wearing of the cusps and cutting edges, a condition known as attrition. Effect of Acid on the Teeth
A pH of 6.6 causes definite etching, while a pH below 5 causes decalcification if not immediately neutralized. Marked erosion of the teeth is seen in patients who scrape out citrus fruit with their teeth. Some of the acid beverages used continuously are·also very harmful, as some have a pH as low as 2.4. Gastric acid may have a similar effect. It affects the teeth in patients who habitually regurgitate food, because of reverse peristalsis or because they do not masticate it properly. If larger pieces are present these then are chewed again, which gives rise to rumination. Other patients may vomit habitually. In all such cases the acid from the stomach decalcifies the teeth and combined with friction from the tongue, the teeth become worn down especially on the lingual surfaces. Dental Caries
Dental caries is a complex disease. It is dependent on localized action of acidogenic organisms activated by the presence of nutrient substances favorable for their exuberant growth. Of the different foods with varying chemical and physical properties which are retained in the mouth for varying periods of time, those that attach themselves to the tooth surfaces and form bacterial plaques are of course more harmful than those
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that are easily removed by the saliva. That the diet is an important factor has been demonstrated by Kite, Shaw and Sognnaes (1950) by feeding highly caries-susceptible rats a caries-producing diet through a stomach tube. These rats remained free of dental decay, whereas the normally fed control animals showed abundant caries in their teeth. It is especially the refined carbohydrates from which bacteria, through enzymatic activity, produce various organic acids that accelerates decay of the teeth. The lactobacilli have been given the greatest amount of attention, but Lennin and Sullivan (1955), who have confirmed the findings of others, state that the lactobacilli which are generally used as caries indicators are not the most important. After the acidogenic organisms have initiated the decay and cavities have formed in the teeth, food retention will give rise to flourishing bacterial activity of a great variety of organisms. The pulp of the tooth ultimately becomes infected and dentoalveolar abscesses form. The destruction of the crown of the tooth disturbs the occlusal efficiency, and because of pain the affected individual is apt to chew less vigorously. TREATMENT. In the child the production of caries-resistant teeth is of primary importance. Fluoridation of the drinking water has done a great deal to accomplish this. After the teeth are formed, dietary measures may be used to reduce or even eliminate the acidogenic flora. This can be accomplished by excluding the easily fermentable carbohydrates from the diet, and especially avoiding their use between meals. The direct elimination of the acidogenic bacteria is another approach. The use of antiseptic mouth washes and toothpastes is the older method, which, however, has been revived by the inclusion of antienzymatic agents and antibiotic substances which predominately act upon grampositive organisms. If prevention has failed, the defects produced by caries should be repaired as soon as possible. Today occlusal rehabilitation is given considerable attention; this includes the establishment of proper occlusal function besides restoration of the anatomic shape of the tooth. Periodontal Disease
Periodontal disease is the next most common oral condition which affects mastication. First the teeth become loose and painful, chewing becomes more and more difficult, and bacterial infection of deep periodontal pockets produces abundant discharge of pus (pyorrhea). Later the teeth are lost by exfoliation or extraction. Periodontal disease is conHidered the most common cause of loss of teeth today. TREATMENT. The prevention of periodontal disease is to be emphasized. Adequate blood circulation in the supporting tissues of the teeth should be fostered by the mastication of hard food. Gingival massage with the toothbrush is of great importance, especially if the initial signsgingivitis-appear. In advanced cases various procedures used by the
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periodontist, such as subgingival curettage and gingivectomy, may still salvage some of the teeth. In far advanced cases extraction may forestall the type of extensive alveolar atrophy seen after this disease, which plagues the edentulous patient who is a notoriously poor subject for artificial dentures. For such patients the implant denture, a recently introduced prosthesis, may be the salvation. Deposits on the Teeth
Various stains are found; they are usually associated with deposits on the protected tooth surfaces. Materia alba is the soft material found at the cervical margin. It is made up of cell debris, food particles, bacteria, and salivary precipitates and is found when the area has not been brushed. Green stains occur chiefly in children with poor oral hygiene and are mainly on the labial surfaces of the upper anterior teeth. Darker stains are found more on posterior teeth. The color depends on pigments from blood, food, drugs, or micro-organisms. A brown pellicle has been described on teeth of indi.viduals not using abrasive-containing dentifrices. This stain will develop if water or liquid dentifrice is used instead of pastes and powders containing abrasives. Plaques and films are found on surfaces of the tooth protected from the detergent action of food, toothbrushes, and oral soft tissues (Fig. 17). They are so-called mucinous plaques, but are bacterial masses. They can be removed only by scraping with a sharp instrument. Tobacco stains the teeth by infiltration of coal tar products into calculus, plaques and pellicles. The stain may vary from yellow to black (Fig. 29). Calculus is the hard deposit (tarter) found on teeth. It is an inorganic derivative of saliva with inclusion of 6 to 15 per cent of organic material (bacteria, cell debris, etc.). Bacteria of filamentous forms, leptotrichia, leptothrix and actinomyces, appear to be essential for attachment of calculus to the teeth. Calculus contains about 63 to 75 per cent calcium phosphate, 3 to 9 per cent calcium carbonate, and 1 to 3 per cent magnesium phosphate in the form of hydroxyapatite. The saliva appears to be supersaturated with calcium salts, and a slight increase in their concentration, a decrease of the pH of the saliva, or a decrease in the ability of mucoprotein to colloidally disperse calcium salts leads to precipitation. TREATMENT. Removal of deposits by the dentist is generally required, after which hygienic measures may prevent recurrence. ABNORMALITIES OF SALIVATION
XerostOlnia
The most important abnormality of salivation is due to decreased secretion. It results not only in inadequate carbohydrate digestion, but
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also greatly furthers dental caries. Patients complain of a dry mouth and a sore red tongue. In extreme cases speech and deglutition become difficult. Trimble, Etherington and Losch (1938) showed an inverse relationship between the volume or rate of flow of saliva and the incidence of caries. Since xerostomia frequently follows x-ray irradiation for oral carcinoma, its effect on salivation explains the typical caries seen in such patients. Xerostomia is also common, although in not so severe a form, in older individuals as a result of senile atrophy of the glands. TREATMENT. Vitamin A and estrogen in women after menopause often is helpful. The drinking of Vichy water has been found to be of benefit. Ptyalism
An increased flow of saliva is not as important and common a disease. The excess saliva frequently drools from the mouth in affected patients. Toxic substances excreted by the salivary glands, such as mercury formerly used therapeutically, produced excess saliva. Certain affections of the central nervous system, such as bulbar paralysis and hemiplegia, are frequently associated with ptyalism. TREATMENT. Ptyalism presents a great handicap during dental operations. The administration of atropine, 0.6 mg. (1/100 grain), before treatment will give temporary relief. MOUTH ODORS (HALITOSIS)
Mouth odors arise chiefly from decomposing tissue and from debris and food beneath the gingival margins and intradental spaces. The nasopharyngeal regions, the digestive tract (belching, constipation), and the bronchopulmonary region may also give rise to unpleasant odors. While most food odors arise from the mouth, some strong odors, such as that due to garlic, may come from expired air via the blood stream. Among the diseases causing characteristic oral odors are diabetes which causes an acetone or fruity breath, and uremia which produces an ammonia breath. TREATMENT. Good oral hygiene is the best defense, and regulation of the diet and digestion. DISEASES OF THE GINGIVAE
The gingivae are subject to specific diseases not always affecting the rest of the mouth. This is partly due to their close association with the teeth which they surround, and possibly to an unusual circulatory condition. The rich blood supply comes from two directions, the peridental membrane and the gingival submucosa. The anastomosis favors stasis and extravasational deposits. Hemorrhagic Diseases
The gingiva may be injured by calculus, restorations, instruments, food, toothbrushes, floss or picks with resultant bleeding. This type of
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hemorrhage is usually self-limiting. However, one must differentiate simple gingival hemorrhage from bleeding due to tumors, traumatic or extraction wounds, and the blood diatheses; and from hemorrhage originating in the nose (epistaxis), the bronchus or lungs (hemoptysis), or the stomach (hematemesis). Hemophilia is a sex-linked genetic disease characterized by failure in clotting. It is manifest in the male only, except for the rare female hemophiliac who is the offspring of a hemophiliac male and a female carrier. While the hemophiliac presents a crucial problem if surgical
Fig. 15. Petechiae and ecchymosis due to thrombocytopenic purpura. Fig. 16. Gingival hemorrhage in a patient with agranulocytosis.
procedures are contemplated, spontaneous hemorrhage from the gingivae may take place. Thrombocytopenic purpura is characterized by extravasation of blood (Fig. 15*) and enormous reduction of platelet counts. It may result from essential purpura; from secondary purpura produced by toxins such as benzol; or from leukemia, tumors, agranulocytosis (Fig. 16), anemia or polycythemia. Bleeding of the gingiva may be associated with pregnancy, dysmenorrhea or scurvy (Fig. 23). TREATMENT. In hemorrhages occurring from local inflammatory lesions, removal of the cause of the underlying condition is important. In localized or generalized · gingivitis toothbrush massage will generally effectively overcome the tendency to bleeding. In patients with a hemorrhagic disease, extreme care should be taken to prevent trauma of even a minor degree. If extraction of teeth is contemplated, multiple fresh blood transfusions before and after the procedure are of great value combined with local control of bleeding.
* Figures 15 to 26, 28 and 30 from Thoma, K. H. and Robinson, H. B. G.: Oral and Dental Diagnosis with Suggestions for Treatment. 4th Ed. Philadelphia. W. B. Saunders Co., 1955.
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Gingival Inflammation
~':Gingival inflammation occurs in a variety of forms. The following are important. Gingivitis is usually caused by locally active injurious agents. Calculus is the most important single cause with the possible exception of the oral pathogens or their toxins which invade the gingivae subjected to physical and chemical trauma, from improperly used toothbrushes, picks and floss, tobacco and foods (Fig. 17). Systemic factors contribute, .chiefly by lowering the resistance of the tissue or altering its reaction to injury (Fig. 18).
Fig. 18 Fig. 17. Simple marginal gingivitis caused by poor oral hygiene with resultant irritation by bacteria and their toxins and by fermentation products from debris. Fig. 18. Gingivitis in diabetes.
Metallic poisoning may contribute to or initiate gingivitis. Bismuth given for treatment of systemic disease may localize from the blood stream in areas of mild gingivitis by anachoresis. Lead (Fig. 19), gold, mercury, silver and other heavy metals may also become localized in regions of inflammation (halo saturnis). Necrotizing ulcerative gingivitis (Vincent's infection, trench mouth) is an acute or chronic gingival inflammation characterized by red, swollen gingivae, necrosis beginning in the interdental papillae and extending along the gingival margins, pain, hemorrhage, a necrotic odor and, often, a pseudomembrane (Fig. 20). The invading organisms are oral treponemas and fusiform bacilli, supported by cocci. Local trauma or systemic disease, or both, may have lowered the resistance permitting invasion. The disease may become chronic if neglected. Herpetic gingivitis results from infection by the herpetic virus. It may develop into herpetic gingivostomatitis. This disease results in red, swollen, tender gingivae and oral mucosa without necrosis of the interdental papillae or gingival margins. The lips are usually swollen and dry. Localized herpetic lesions may be present. The disease is highly infectious. It is differentiated from necrotizing ulcerative gingivitis by the absence
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of a fetic odor, the lack of gingival necrosis, and a high temperature . .The disease runs a course of about two weeks. . .. Desquamative gingivitis is characterized by the tendency of the surfltce epithelium to desquamate. It is readily removed by rubbing with. cotton or gauze. The gingiva appears mottled owing to areas. of recentd~squa mation which are red and other areas with natured epitheliu.lll Wlliph are whiter or a grayish red. Since the disea~e occurs most. often iriwomen during menopause, a hormonal imbalance has been cited as its cause. It also occurs in younger women and men.
Fig. 19. Lead line of gingiva (Burtonian line, hlllo saturnis). Fig. 20. Acute necrotizing ulcerative gingivitis (Vincent's infection) showing necrosis and pseudomembrane
TREATMENT. Simple gingivitis responds well to massage after removal of irritating etiologic factors. Infectious types are treated by antibiotics. In necrotizing ulcerative gingivitis supportive treatment to build up the resistance of the patient is of great importance. Local treatment by means of antiseptics and treatment of periodontal pockets should be given. Antibiotic therapy should be instituted at once; Aureomycin parenterally and in form of troches is most effective. In herpetic gingivostomatitis Aureomycin or Terramycin given systemically in adequate dosage has given good results. Desquamative gingivitis responds poorly to treatment, and maintenance of oral hygiene is very important. There is no specific therapy but the use of hydrocortisone ointment has given Borne promise in a few cases. In the menopausal type, estrogen therapy is useful (0.5 to 1.0 mg. stilbesterol per day) (Ziskin and Zigarelli, 1945). Gingival Hypertrophies
Hypertrophies may result from the edema and fibrosis of inflammation, or from more specific causes. Pregnancy hypertrophy is a temporary enlargement of the gingiva seen in pregnant women, apparently as a result of hormonal imbalance. It is therefore termed hormonal hypertrophy. The gingivae are enlarged, red,
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Fig. 21 Fig. 22 Fig. 21. Hormonal gingivitis and pregnancy tumors. Fig. 22. Dilantin hypertrophy.
soft, and bleed easily. The enlargement is greatest in regions of irritation. When the hormonal balance is reached after pregnancy the tissue will return to normal. In relatively rare instances these localized enlargements become sizable and are termed pregnancy tumors (Fig. 21). They are not true neoplasms, having the same microscopic appearance as pyogenic granulomas. They disappear after pregnancy unless they become too fibrous to permit regression. Dilantin ]t.YP'ertrophy is a peculiar enlargement of the gingivae which occurs frequently in' those epileptics who take Dilantin sodium for more than a year (Fig. 22). It is a fibrous enlargement, firm, painless and nontender. The tissue is not increased in redness. The enlargement begins at the interdental papillae and may cover the teeth. Scorbutic enlargement is extremely rare at the present time (Fig. 23). The gingivae are soft, red to purple, swollen, and the teeth become loose. The ascorbic acid blood level should be determined if the disease is suspected. Leukemic hypertrophy is due chiefly to the normal defensive cells (leukocytes, lymphocytes or monocytes) being replaced by afunctional tumor cells. In addition the many white cells produced engorge the blood
Fig. 23. Scorbutic gingivitis. Fig:.24. Monocytic leukemia affecting gingivae.
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stream and infiltrate the submucosa. These cells and the resultant edema usually produce enlargement of the gingivae. Bacterial infection sets in, and areas of necrosis form (Fig. 24). The gingivae bleed profusely which may be the first sign of the disease. Bleeding, ecchymosis and necrosis are oral signs suggesting the existence of leukemia but are not specific. The diagnosis is made by study of the blood count and hemapoitic pattern. TREATMENT. Underlying general causes should be treated or corrected. In all cases oral cleanliness and absence of irritation from restorations, calculus, and occlusal trauma is most important. The leukemia victim with a healthy mouth has minimal oral changes and, even in advanced leukemia, the careful elimination of irritants may result in healing. DISEASES AFFECTING PRINCIPALLY THE TONGUE
The tongue has long been considered an indicator of systemic disease, although it also presents developmental, traumatic, chemical, infectious and neoplastic diseases. Developmental Anomalies
These are present at birth or develop during infancy.
Macroglossia may be due to a developmental deviation, myxedema,
acromegaly or inflammation. It generally shows indentations along the margins corresponding to the adjacent teeth. Ankyloglossia reduces the mobility of the tongue and results in speech and feeding problems (Fig. 12). Cleft and lobulated tongue are rare congenital abnormalities. Fissured tongue is found frequently and often causes retention of food and bacteria giving rise to inflammation and odors. Other Abnormalities
Coated tongue is caused by many conditiQns including gastrointestinal upsets, fevers, stomatitis and mouth-breathing. The coating consists of desquamated epithelium, saliva, leukocytes and bacteria which adhere, chiefly because of failure of normal function. In illness salivation may be reduced with resultant decrease in the self-cleansing activity. In dehydration the coating dries, leaving an encrusted tongue. The color changes as a rel!1Ult of food, tobacco, drug and/or bacterial and blood pigments. Iron results in a brown stain, as do blackberries, licorice, or hem orrhages. In eyanosis the color is dark blue. Red color may be due to red candy or red drug dyes, or polycythemia. The red desquamated tongue with prominent lingual papillae in scarlet fever is known as strawberry tongue. Yellow colors result from tobacco or from jaundice. Black hairy tongue (lingua nigra) is a condition charaeterized by elongation of the filiform papilla and the accumulation of dark pigments (Fig. 25). It is observed in patients with anemias, leukemias, vitamin deficiencies, and after antibiotic therapy producing a disturbance of the
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balance of oral flora and resulting in a predominance of the resistant yeasts (Candida albicans). The papillae probably elongate because they are not desquamated when the patient has a sore mouth. TREATMENT. Black hairy tongue may be cured in less than one week by scraping the tongue with a wooden tongue blade twice daily using 20 strokes at each treatment. Benign migratory glossitis (geographic tongue) is an inflammation of unknown etiology. The epithelium is desquamated in annular or circinate patterns (Fig. 26) leaving red cent~rs with white borders. The
Fig. 25. Black hairy tongue.
Fig. 26. Geographic tongue.
lesions are not painful and heal from the sides, and change their locations within a matter of days. They do not respond to specific therapy. Moeller's glossitis is discussed under Deficiency Diseases, q.v. DISEASES AFFECTING THE ENTIRE MOUTH
A great variety of abnormalities of the oral mucosa occur. Developmental and Hereditary Conditions
Fordyce Disease. This.is a developmental anomaly; small, leathery spots cover the buccal or labial mucosa, which are atopic sebacious glands. Melanoplakia. Dark pigmentations occurring after puberty in irregular patches of dark brown or metallic blue color may be found on the gingivae, palate and cheeks of brunette individuals and Negroes. They are due to melanin in the epithelium. ":Melanin spots with intestinal polyposis is a hereditary syndrome reported by Jeghers, McKusick and Katz (1949). Oval, irregular patches and smaller spots of brown or black pigment are found on the lips, buccal and palatal mucosa, and the skin (Fig. 27).
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Leukoplakia Leukoplakia is characterized, clinically, by white, opaque plaques of keratinized epithelium. The lesions may be extensive, usually feel somewhat leathery, and have rather sharp margins. There is some question whether the name should be reserved for lesions showing dyskeratosis
Fig. 27 Fig. 28 Fig. 27. Oral melanotic spots in intestinal polyposis syndrome. Fig. 28. Leukoplakia of tongue with carcinoma.
microscopically, and whether leukokeratosis should be used for cases showing hyperkeratosis and inflammation only. The condition is much more common in men than in women and is found affecting the cheek, floor of the mouth, palate and tongue, in greater frequency in tobacco users or other persons with physical irritation affecting these regions. The lesions may remain in status quo for many years or may become malignant (Fig. 28). Lichen planus is a disease of unknown cause which affects the skin and mucous membranes, but oral lesions are often found without associated dermal ones. The buccal, lingual and gingival lesions are painless, porcelain-white streaks, lines and dots arranged in a lacy or filigree pattern, usually bilaterally, surrounded by or within red areas (Fig. 29). The disease does not respond to treatment. A psychosomatic background is strongly suggested, most patients having marked nervous tensions. TREATMENT. Reassurance is important to prevent cancerphobia. Remissions have occurred when the lesions have been treated daily with cortisone ointment. Brewers' yeast helps other patients. Nutritional Deficiencies Ascorbic acid deficiency (scurvy) causes marked oral changes (Fig. 22). Bloated gingivae with marked ecchymosis and spontaneous hemorrhages occur. In advanced stages the teeth become loose and painful. Vitamin B complex deficiency affects particularly the tongue. Patients
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with pellagra (nicotinamide deficiency) have a beefy red, smooth tongue. At first the borders lose their papillae and the tip and borders become red. The whole dorsum soon loses its papillation. Usually cheilosis accompanies the glossitis; the tongue may be painful or burning. Iron deficiency causing anemia results in atrophy of the lingual papillae. Often small areas only are involved. Plummer-Vinson syndrome is seen in women past middle age. It is char:wterized by anemia, dysphagia, and atrophy of the oral mucosa, ton~~,and upper portion of the gastrointestinal tract. The disease predisposes to oral carcinoma. The marked nutritional deficiency is due to the~hanges in the digestive tract.
Fig. 29 Fig. 29. Lichen planus of buccal mucosa. Fig. 30. Stomatitis nicotina with cyst and cleft formation.
Pernicious anemia is reflected in the tongues of over half of its victims, and is spoken of as Hunters' glossitis. The tongue is red and burns, is painful, and may feel numb. Atrophy of the papillae and a red color appear. The tongue has lowered resistance to infection. Moeller's glossitis is a term applied to chronic superficial irregular atrophy of the tongue. It is an inflammation which is caused by allergy, hypersensitivity, nerve disturbances, and possibly, by vitamin B complex deficiencies. Pain, especially on eating acid, spicy or hot foods, is a prominent symptom. TREATMENT. In most deficiency diseases vitamin therapy will produce remission of symptoms unless there is a metabolic interference with utilization of the vitamins. Medical treatment, in some cases injection of vitamins (B12, thiamine hydrochloride) gives excellent results. Inflammations
Stomatitis nicotina is the result of palatal irritation by smoking tobacco. It begins with the appearance of small areolae of redness around the duct orifice of the palatal glands. Soon small elevations appear (Fig. 30). The remaining palatal mucosa looks blanched. TREATMENT. Removal of the cause, the use of tobacco in particular, may result in regression of the lesions. The patient should be re-examined
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at frequent intervals and if the lesions do not continue to regress they should be removed surgically. Treatment with caustics is contraindicated. Stomatitis venenata may be caused by contact with ordinarily innocuous substances such as drugs, dentifrices, drugs used in dentistry, denture bases, lipstick, essential oils, food, and flavoring in gum and candy. The lesions occur at the part of contact only, beginning as regions of erythema which may become secondarily infected. Acrylic materials used for dentures may in some individuals cause inflammation due to excesses of a monomer which may be present in improperly cured acrylic resins. Patch tests are valuable in differential diagnosis. Stomatitis medicamentosa is due to an altered reaction (allergy) to drugs such as barbiturates, iodine, antibiotics, sulfonamides, mercury, arsenic and salicylates. The eruption usually is multiple, eroded, and painful. The history is a valuable guide in the diagnosis. Infectious stomatitis is a general term and is applied in case of a general bacterial infection. It begins with a red, itchy feeling of the mucosa; later ulcers may develop. This type is called ulcerating stomatitis. Herpetic stomatitis is the term now generally used to designate the vesicular disease of the mouth caused by the herpetic virus. The lesions have also been called aphthae, canker sores, and dyspeptic ulcers. The virus remains in the cells, apparently without attacking the host. Whenever the resistance is lowered by trauma, infection, menstruation, allergy or sensitivity, psychic factors or dietary deficiencies, the virus becomes active. The first lesion is the vesicle but inside the mouth it soon ruptures and b~comes secondarily infected. The typical lesion has a yellow, ulcerated center, a bright-red areola, and is very painful. It heals in about 10 to 14 days. Several lesions may coalesce. They occur on the tongue, lip, palate and buccal mucosa. Recurrent herpetic lesions present a greater problem. Some individuals develop one crop of herpetic lesions after the other. Episodes may occur especially with menstruation, or at times when certain foods are eaten. TREATMENT. Classically, herpetic lesions are treated by phenol or silver nitrate which stops pain. For solitary lesions, Aureomycin and Terramycin pastes have proved effective in reducing secondary infection, relieving pain, and hastening healing. For women who develop these lesions at menstruation, large doses of vitamin B complex given by mouth for a few days before the menstrual period are often effective. High vitamin B complex intake sometimes helps other patients. The use of smallpox vaccine, given either once a week for six weeks in small doses or in increasing intradermal dosage over a six week period, has benefited some subjects. Cortisone ointment has given promising results in a limited group of subjects. In some persistent cases withdrawing chocolate or citrus fruits has aided. Some cases remain recalcitrant. Necrotizing ulcerative stomatitis (Vincent's stomatitis) is the result of extension of necrotizing ulcerative gingivitis, q.v.
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Gangrenous stomatitis (noma) is a severe fusospirochetal infection in debilitated patients. Actual gangrene occurs. Agranulocytosis (granulocytopenia) predisposes to noma. Other Lesions
Thrush (moniliasis) may occur on the labial and buccal mucosa, but is more frequent on the tongue. It produces a white, soft, rapidly spreading patch which can be removed with a curet leaving a bleeding surface. Candida albicans can be demonstrated in smears. TREATMENT. Thrush responds poorly to treatment and ordinary antibiotics are contraindicated. A new fungicidal antibiotic, Mycostatin, 500,000 U. three times a day after meals, has recently been introduced. Syphilis may result in chancres, mucous patches, or gumma. The chancre shows a necrotic center, raised margins, and induration and, as secondary infection occurs, pain is present. The mucous patches are ulcerated plaques with a milky, translucent surface. Papules have indurated bases and raised borders giving the appearance of a reddish border and a deep crater. The tongue may show atrophic changes, resulting from endartheritis, and presents a smooth surface covered by a· thin translucent epithelium producing a glassy tongue. The tertiary lesions, the gummas, may undergo malignant changes. Gummatous lesions have a predeliction for the palate. They first form as nodules which result in shallow or deep ulcers. The margins are raised and surrounded by red zones; the center of the ulcer is necrotic. The regional lymph nodes enlarge. The ulcer may perforate the palate. TREATMENT is systemic. Pemphigus is an acute or chronic disease of the skin and oral mucosa. Several types form oral lesions, vulgaris, foliaceus and vegetans. Over half the patients show oral lesions first. The initial sign is a few vesicles of small size, which soon rupture leaving a curled-up thin membrane at the edge of the ulcer (Fig. 31). Pain is prominent and the lesions soon become secondarily infected. The prognosis in many cases is grave. Erythema multiforme, one of the rarer diseases of unknown cause, produces lesions on the oral mucosa, tongue, lips, skin, conjunctiva and urethral tract. In a few days vesicles appear on the lips and oral mucosa. These become eroded within a few hours and resemble herpetic lesions, or the lesions may resemble lichen planus. In severe cases the temperature is elevated and the ulcerations are extensive and tend to coalesce. Lupus erythematosus is another one of the dermatologic diseases with acute and destructive ulcerations (Fig. 32). TUMORS OF THE MOUTH
Benign TUIllors
Benign oral tumors occur in any part of the mouth at all ages. The most common ones only will be described.
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Fig. 31 Fig. 32 Fig. 31. Pemphigus with desquamation. Fig. 32. Oral vesicular lesions in lupus erythematosus.
Hyperplasias are frequently found and are usually an exaggerated fibroblastic response to chronic irritation. They are seen associated with carious teeth, and in edentulous mouths, caused by denture irritation. Theyoccur on the palate under dentures that are improperly constructed, or, more commonly, which are worn after bone changes have made them unsuitable for use. Papillary hyperplasia may fbrm at the palatal midline. These lesions should always be biopsied as they may show early carcinomatous changes (Fig. 33). Giant cell lesions are now generally considered as giant cell reparative lesions and not as neoplasms. They are found in a younger age group than are most neoplassm. They have a purple tint, and are softer than fibromas. On the gingiva they are common, and are called giant cell epulis.
Fig. 33 Fig. 34 Fig. 33. Papillomatosis of palate (benign). Fig. 34. Fibroma of gingiva.
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Fibromas are the most common of the benign neoplasms on the gingiva, the buccal and palatal mucosa, and the tongue. They usually are firm, covered with relatively normal epithelium, and present no subjective signs. They may vary from pin-head to very large size and may be sessile or pedunculated (Fig. 34). H emangiomas are soft, blue or purple tumors that may become very large. They are found on the tongue (Fig. 35) and the cheek most commonly. There is danger of accidental injury and severe hemorrhage. Lymphangiomas are similar soft tumors affecting the tongue, but are rarer than hemangiomas and have a yellow pinkish color rather than purple.
Fig. 35
Fig. 35. Hemangioma of tongue. Fig. 36. Torus palatinus.
Lipomas are soft but may reach large size and are easily recognized by their colors. Mixed tumors form from the mucous glands of the buccal mucosa, lip and palate. The typical mixed tumor occurs on the side of the palate and grows slowly but progressively. These tumors may be present for many months or even years. They are firm but not bony hard. They are not malignant as a rule, do not metastasize, but are extremely destructive locally. They should be excised widely. Torus palatinus is found in the midline of the hard palate as a dense, hard bony enlargement which varies in form (Fig. 36). In rare instances it may interfere with speech and with denture construction. Sometimes it becomes irritated by food and ulcerated. Differential diagnosis from mixed salivary gland tumors and fibroma is important. Torus mandibularis is seen bilaterally on the inner surface of the mandible. It is a bony exostosis of no significance except interference with motion of the tongue. Osteomas occur on the oral surface of the jaws, often in multiple form. Dermoid cysts may occur benea.th the geniohyoglossus muscle in the floor of the mouth. They may reach a large size, pushing the tongue up-
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wards. They contain hair and other ectodermal structures, including teeth. Epidermoid cysts arise in a similar manner from embryonal rests but do not contain hair or teeth. Ranula and mucoceles form from the sublingual, labial and, rarely, the buccal glands. They contain mucus and are caused by occlusion of their secretory ducts. TREATMENT OF BENIGN TUMORS. All benign tumors are excised. Those that are known to recur should be excised more radically, or the tumor bed should be treated with the cautery. Any irritating factor associated with their development should be removed.
Fig. 37
Fig. 38 Fig. 39 Fig. 37. Ulcerating type of carcinoma. Fig. 38. Fibrosarcoma of mandibular gingiva. Fig. 39, Lymphosarcoma of palate.
Malignant Tumors
Malignant oral tumors occur mostly in later life, although some affect young individuals, especially sarcomas. About 15 per cent of all primary malignancies in over 200,000 patients who die each year of cancer are in the head and neck. Squamous cell carcinoma (epidermoid) is the most common intr~oral malignant lesion. Carcinoma may be preceded by papilloma or leukoplakia. It is seen mpre commonly in patients over 50 years of age. It occurs on the gingivae where it is often mistaken for an inflammatory lesion and often is aggravated by the extraction of teeth. It also forms on the lips, tongue (Fig. 28), floor of the mouth, buccal mucosa, hard and soft palates. The appearance varies greatly. We find papillomatous and ulcerating types (Fig. 37), exophytic and deeply invading lesions. Carcinoma of the antrum may invade the palate. More frequently, however, carcinomas of the mouth invade the maxillary sinus. In the mandible the bone may become extensively invaded. SmalllesioBs should be discovered by the dentist's periodic examination; unfortunately, often carcinoma is not diagnosed until the lesion is large. Pain, difficulty in swallowing, and ulceration are signs of advanced disease when generally the regional lymph nodes are involved.
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Fibrosarcoma may occur on the gingiva (Fig. 38), growing rapidly and destroying adjacent bone. It is found in younger individuals than is carcinoma. Osteogenic sarcomas may cause enlargement of the alveolar process of the jaws. Plasmocytoma and lymphosarcoma form in any part but are not very common. The latter (Fig. 39) often occurs in multiple form. Malignant melanoma is a very malignant neoplasm. It may extend from the gingiva over the palate and forms a coal-black tumor mass, rapidly growing and infiltrating. Metastases occur early and involve both the regional lymph nodes as well as the vital organs. TREATMENT. Biopsy is a most valuable aid to diagnosis, especially to differentiate benign from malignant lesions. The biopsy should be designed to secure tissue which will aid the pathologist in his examination with maximum benefit to the patient. Diagnosis of these lesions when small is of greatest importance, and contributes appreciably to the reduction of the high mortality rate of oral malignancies. In advanced cases heroic surgical measures still give hope for a cure. Radiation therapy is indicated in very radiosensitive neoplasms, such as lymphosarcoma, and often will salvage inoperable cases of squamous cell carcinoma (White, Sieniewicz, and Christensen, 1954). DISEASES AND TUMORS OF THE SALIVARY GLANDS
Developmental, functional, infectious, and neoplastic conditions occur. Sialograms are often useful in making a diagnosis. Sialadenitis may cause enlargement of the salivary glands. The infection may be ascending due to oral bacteria, and a thick, yellow exudate may be expressed. Prolonged use of potassium iodide or of mercury may be responsible for parotitis. Certain foods result in pain and inflammation in some individuals. Because the salivary glands are so readily affected by psychic influences it is surprising that so few cases have a psychic origin. Sialolithiasis is the accumulation of calcareous deposits in the salivary gland or ducts. The formation of calculi usually causes interference with the normal salivary flow. M ikulicz' s syndrome and disease are characterized by swelling of the parotid, submaxillary, sublingual, and lacrimal glands or of any comBination of these glands. Salivation is decreased greatly in most instances. Uveoparotid fever is characterized by inflammation of the parotid gland and the uveal tract of the eye. A possible relationship to Boeck's sarcoid has been postulated. Mixed tumor may be benign or malignant. The parotid gland is its most frequent site. The malignant tumors may appear as squamous cell carcinomas, adenocarcinomas, or mucoepidermoid carcinomas. These tumors are highly malignant and regional lymph node removal should be combined with wide excision.
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M alignant lymphomas may arise in the parotid or other salivary glands. Such tumors cause facial deformities and often reduce salivation SO that xerostomia results. TREATMENT. Infections are treated by the use of antibiotics; salivary stones should be excised; tumors are treated by excision or irradiation. REFERENCES Appleton, J. L. T. Jr.: Bacterial Infection, 4th Ed., Chap. XXIV. Philadelphia, Lea & Febiger, 1950. Bass, C. C.: Endameba Buccalis. Proc. Soc. Expel'. BioI. & Med. 66: 9, 1947. Bibby, B. G.: Mouth Bacteria. J. Dent. Research 17: 265,423,471, 1938. Bibby, B. G., Goldberg, H. J. and Chen, E.: Evaluation of Caries-Producing Potentialities of Various Foodstuffs. J. Am. Dent. A. 42: 491, 1951. Goldsworthy, N. E., Sullivan, H. R. and Harris, R.: Practical Caries Control. Dent. J. Australia 27: 45, 1953. Hamp, E. G.: Morphologic Characteristics of Oral Treponemas and Borrelia vincenti. J. Am. Dent. A. 40: 1, 1950. Jay, P.: Reduction of Oral Lactobacillus Acidophilus by Periodic Restriction of Carbohydrate. Am. J. Orthodontics & Oral Surg. (Oral Surg. Seet.) 33: 162, 1947. Jay, P., Beeuwkes, A. M., Blecha, E. E. and Bust, M. S.: Dietary Progress for Control of Dental Caries. Ann Arbor, Mich., the Overbeck Co., 1951. Jeghers, H., McKusick, V. A. and Katz, K. H.: Generalized Intestinal Polyposis and Melanin Spots of Oral Mucosa, Lips and Digits. New England J. Med. 241: 993, 1941. Kite, O. W., Shaw, J. H. and Sognnaes, R. F.: Prevention of Experimental Tooth Decay by Tube Feeding. J. Nutrition 42: 89, 1950. Lennin, D. F. and Sullivan, H. R.: Relative Rates of Acid Production from Refined and Natural Sugars. Dent. J. Australia 25: 67, 1955. Lind, H. E.: Rationale of Routine Antibiotic Sensitivity Determination Antibiotics & Chemotherapy 3: 672, 1953. Markowitz, H. A. and Gerry, R. G.: Temporomandibular Joint Disease. Oral Surg., Oral Med. & Oral Path. 2: 1309, 1948; 3: 1309, 1949; 4: 75, 1950. Morris, E. 0.: Bacteriology of Oral Cavity. Brit. Dent. J. 95: 77,259,1953; 96: 95, 259,1954. Orland, F. J. and others: Use of Germ-free Animal Technique in Study of Experimental Caries. I. Basic Dental Study of Rats Reared Free of All Micro-organisms. J. Dent. Research 33: 147, 1954. Thoma, K. H.: Ankylosis of Temporomandibular Joint. Am. J. Orthodontics & Oral Surg. (Oral Surg. Sect.) 32: 269, 1946. Idem: Oral Pathology, 4th Ed. St. Louis, C. V. Mosby Co., 1954. Idem: Oral Surgery, 2nd Ed. St. Louis, C. V. Mosby Co., 1949. Trimble, H. C., Etherington, J. and Losch, P. K.: Rate of Secretion and Incidence of Dental Caries. J. Dent. Research 17: 299, 1938. Wah Leung, S.: Demonstration of Importance of Bicarbonate as Salivary Buffer. J. Dent. Research 30: 403, 1951. White, G., Sieniewicz, J. and Christensen, W. R.: Improved Control of Advanced Oral Cancer with Massive Roentgen Therapy. Radiology 63: 37, 1954. Ziskin, A. and Zigarelli, E.: Chronic Desquamating Gingivitis. Am. J. Orthodontics & Oral Surg. 31: 1, 1945. 1146 Beacon Street Brookline 46, Massachusetts
THE DEVELOPMENT OF THE MOUTH
IN THE embryonic formation of the oral cavity the frontonasal and the two maxillary processes, and the mandibular arch take part. The enclosed area develops into a pocket, the stomadeum, which is lined by ectodermal epithelium. It is separated from the anterior end of the foregut by the buccopharyngeal membrane which is formed by the apposition of the stomodeal ectoderm and the foregut endoderm. At the third week of embryonic development this membrane disappears, establishing a communication between the mouth and the future pharynx. The mandibular arch at this time is completely formed, while the upper jaw is completed later by the fusion of the globular processes, derived from the frontonasal process, with the two maxillary processes. From the maxillary arch develop the palatine processes which grow medially and fuse in midline, thus dividing the cavity into an upper, the nasal, and a lower, the buccal part. The tongue is developed in the floor of the pharynx, the buccal part being derived from a pair of lateral swellings which arise from the inner surface of the mandibular arch and meet in midline. The posterior pharyngeal part is formed from the copula. It extends forward in the shape of a V, and its limbs embrace the buccal part. At the apex of the V an invagination occurs which is represented by the foramen cecum. Anterior to the V-shaped junction are the papillae vallate. Developmental Anomalies
The faulty development and nonfusion of the various processes forming the mandibular and maxillary arches results in the formation of clefts. The most common ones are the lip cleft (harelip) and the palatal clefts. Of these there are many varieties and combinations (Fig. 11). Tongue clefts occur more rarely and are due to lack of fusion at the • Professor of Oral Surgery Emeritus, Professor of Oral Pathology Emeritus, Harvard University; Visiting Lecturer in Oral Surgery, University of Pennsylvania; Honorary Surgeon, Massachusetts General Hospital; Chief, Oral Surgery Department, Brooks Hospital, Brookline, M assachusctts.
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anterior part of the tongue. Other anomalies in this region are due to an abnormal development of the thyroid gland, giving rise to thyroglossal cysts and lingual thyroids. Median rhomboid glossitis is characterized by a:red area devoid of papillae and located in the midline of the dorsum just anterior to the circumvallate papillae. It has no pathologic significance but may be misdiagnosed as an inflammatory or neoplastic lesion. Abnormal labial and lingual frenums should also be mentioned; low attachment of the former pulls down the lip and often produces the appearance of a double lip. If the frenum is hypertrophied, a space is formed between the central incisors.
Fig. 11. Cleft palate.
Fig. 12. Ankyloglossia.
Ankyloglossia is the result of an abnormal lingual frenum which ties the tip of the tongue down to the floor of the mouth (Fig. 12). It may result in speech and feeding problems. TREATMENT OF DEVELOPMENTAL ANOMALIES. The treatment of these anomalies in most instances is surgical. Early surgical corrections are most desirable; for lip procedures, the age of two months, and for cleft palate, between the ages of one and two years is considered best. Early operation facilitates feeding and insures better speech, although in patients operated upon later orthodontic correction and speech training may still insure excellent results. In all instances the general health of an infant should be considered, and no operation should be performed until the patient is properly built up since most children with lip and palate clefts are undernourished. In older patients with cleft palates in which plastic repair is not possible or in which previous operation was unsuccessful, prosthesis may be devised that often give excellent results. THE BACTERIOLOGY OF THE MOUTH
A great variety of micro-organisms inhabit the mouth throughout life. Some of these are potentially pathogenic, others are harmless sapro-
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phytes. So~e are t~an~i~nt and oth~rs perm.anent inhabitan~s. The flora varies in dIfferent mdIvIduals, but m each It tends to remam constant. The original flora in the newborn is that found in the mother's vagina, namely, B. perfringens, B. coli and Enterococcus intestinalis. These are soon added to from the air and surroundings of the infant. The mouth flora of the adult is much more complex. It has been studied by numerous investigators such as Bibby (1938), Appleton (1950), and Mcmis (1954). The following organisms are of importance: 1. Cocci. These are the most common bacteria found. They include streptococci (viridans, salivarius and hemolyticus), Gram-negative cocci (Micrococcus catarrhalis, flavus and pharyngis) and Staphylococcus albus, aureus and citreus. 2. Bacilli. A great many gram-positive bacilli occur. Among these the lactobacilli and leptotrichia play an important part in dental caries. The Bacillus hofmanni and other diphtheroids are also found. Gram-negative bacilli are the Bacillus proteus, Bacillus lactis aerogenes and members of the Friedlander group. 3. Fusiform Bacilli. These anaerobes occur as soon as the teeth erupt. Three to four varieties are found in all adult mouths. 4. Actinomyces. Gram-positive branched organisms are found in the oral flora which have not as yet been carefully investigated. 5. Vibrios. These are motile organisms identified by darkfield investigation. Their significance is not known. 6. Spiral Organisms. These are normally found in the adult flora whenever teeth are present. The most common ones are Treponema macrodentium and T. microdentium, Borrelia vincentii and B. buccalis; and Leptospira dentium. These have been studied extensively by Ramp (1950) who found them to increase in patients with gingivitis. Re found Borrelia vincentii present in great numbers in necrotizing ulcerative (Vincent's) gingivitis. 7. Yeast and Yeastlike Fungi. Yeastlike fungi are found in most mouths, even in edentulous patients wearing dentures. Their overgrowth occurs in patients receiving antibiotics, especially penicillin troches. Parenteral administration also may change the natural balance since the drugs are secreted in the saliva. 8. Protozoa. In most filthy mouths we see at least one type of amoeba. Bass (1947) has studied the Endamoeba buccalisj it is considered a scavenger of little clinical importance. 9. Viruses. Burnett and Williams (1939) reported that they found in 90 per cent of the adults studied herpes simplex virus in the oral tissue. Lowering the tissue resistance by simple trauma, actinic rays of the sun, menstrual cycle or allergic inflammation causes aphthous ulcers or herpetic stomatitis.
Diseases Produced by Micro-organisms
Under ordinary circumstances disease is not produced by microorganisms as long as they do not become an overpowering factor and as long as the local defensive mechanism functions, but lowered local resistance, trauma, or debilitating diseases may so alter conditions that infection sets in. The defensive mechanism of the mouth against bacterial invasion consists of various factors. First, the epithelial cells lining the oral cavity havean effective phagocytic action. Cells loaded with bacteria are con-
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stantly desquamated (Fig. 13). Bacteria are removed by the cleansing effect of mastication and the action of the tongue, lips and cheek. The saliva acts as a flushing agent. It contains bacterial inhibiting factors such as lysozyme. The bacterial activity is also dependent on proper nutrient media derived from the ingested food, therefore the type of food eaten, the frequency of eating, and eating habits influence the flora. Finally, certain micro-organisms may exert an antibiotic effect on others and so help to control the flora.
Fig. 13. Desquamated epithelial cells containing streptococci in streptococcic stomatitis.
One might suggest that eventually the patient may be able to choose the micro-organisms he desires to grow in his mouth through dietary measures. Caries control is based on the dietary control of acidogenic organisms. Jay et al. (1951) and Goldsworthy and Sullivan (1955) have shown how by eliminating refined carbohydrates the caries incidence may be lowered through a marked decrease in the lactobacilli and other acidogenic organisms. TREATMENT. Today the various antibiotics furnish a very effective means to combat bacterial infection. It should be remembered, however, that there is a great variation in their effectiveness. Many oral bacteria are penicillin resistant, and even organisms which originally were penicillin sensitive have developed resistant strains. Bacillus coli is a frequent offender even when occurring in mixed infection because it produces penicillinase. In superficial infection local therapy with troches should be combined with parenteral administration since the small doses contained in the former may cause sensitization of the patient, and because the local effect is not deep enough to affect invading organisms. In all infections sensitivity tests should be made; so-called disk tests (Lind, 1953) give a
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quick result so that the most effective antibiotic can be prescribed as soon as possible. NORMAL AND PATHOLOGIC PHYSIOLOGY OF THE MOUTH
The infant, with rare exceptions, is born without erupted teeth. The oral cavity is extremely small and is occupied almost completely by the strongly developed tongue. The physiologic function of the mouth is that of sucking and not, as in the adult, that of masticating food in preparation for digestion. Sucking
The act of sucking is accomplished by a tight grasp of the nipple and depression of the tongue to produce a vacuum in the posterior part of the mouth. The milk is expressed by closure of the jaws. Then follows the act of swallowing. During the first few months the mouth is rather dry because the salivary glands are still inactive. Later, around the third month, salivation becomes activated to the extent that saliva is likely to run out of the infant's mouth until gradually it learns to swallow it. Mastication
As the teeth erupt more complex food can be utilized by the child. The mouth now takes on a more important part in the process of digestion. Mastication is the mixing of the food with saliva, reducing it to a size suitable for swallowing, and lubricating the bolus to facilitate its passage through the esophagus. A normal set of teeth is of great importance in chewing. The process is one of breaking up food not only to facilitate ingestion, but more important, to make it accessible to the action of enzymeii3 secreted in the mouth and stomach. During this process the salivary glands are stimulated and the gastric secretion becomes activated, aided by the sense of taste of substances released during the process. Proper mastication therefore promotes digestion and the efficient utilization of food. Salivation
The secretion of the salivary and mucous glands of the mouth is accelerated by reflex action. The stimulation occurs through the sensory and gustatory afferent nerves supplying the tongue and oral mucosa as well as the optic, olfactory, auditory and sympathetic nerves. Secretion is also aided by purely mechanical factors, the pressure applied by the activity of the muscles of mastication and the action of the tongue. The saliva maintains a relatively constant pH value in the mouth through its efficient buffer effect. An acid diet progressively increases its alkalinity by the secretion of bicarbonate (Wah Leung, 1951) and phosphates. The use of alkalies (dentifrices) has a depressing effect both on the amount of secretion as well as on the alkalinity.
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Ptyalin, an amylolytic ferment, is one of the most important substances in the saliva since through it the digestion of carbohydrate food is initiated in the mouth. An adequate amount of time is needed to break up the food and mix it with the saliva to allow the digestive process to be initiated. This is important since the carbohydrate digestion is soon arrested in the stomach by the action of the hydrochloric acid. FUNCTIONAL ANOMALIES
There are various factors which interfere with normal functioning of the mouth. Developmental anomalies have already been mentioned. Here additional factors will be considered. Ankylosis
Traumatic injuries such as birth trauma-several cases of injury of the mandibular joint from the use of forceps in difficult delivery have been reported (Thoma, 1946)-or arthritis may result in partial or complete ankylosis making mastication difficult or impossible. In ankylosis occurring early in life the mandible in addition remains underdeveloped on the affected side, causing facial asymmetry and malocclusion. TREATMENT. Arthroplasty with metal inserts, and osteoarthrotomy will generally restore function of the jaw. Sliding osteotomy of the mandible may be required to correct the mandibular deformity. Arthroses
Rheumatoid arthritis and traumatic arthritis of the temporomandibular joint are quite commonly seen today. The former is generally part of general arthritis, while the latter is produced by occlusal abnormalities and especially a "closed bite" due to unusual wear or loss of the supporting posterior teeth. The force which ordinarily is taken up by the teeth causes friction in the joint. The pain produced limits the function of the jaws and teeth. TREATMENT. Restoring the supporting teeth by artificial substitutes or raising the occlusion by means of splints will eliminate the cause of the joint inflammation by distraction of the joint surfaces. Advanced arthritis with bone changes visible in the x-ray and causing refractory pain requires condylectomy. Patients can get along well without the joint as long as teeth are present. DISEASES OF THE TEETH
Malocclusion
Malocclusion is often a great handicap, particularly cross bite, open bite and prognathism, but also smaller irregularities interfere with the chewing motions. TREATMENT. In most instances malocclusion can be remedied by
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orthodontic procedures during childhood. In older persons serious abnormalities in the relationship of the upper and lower jaws may be corrected by ostectomies or osteotomies (Fig. 14) in various parts of the mandible (Thoma, 1952).
B A Fig. 14. Open bite. A, before; B, after ostectomy.
Effect of Food on the Teeth
Certain food as well as substances that are habitually chewed, such as chewing gum, lozenges, candy and tobacco, are harmful to the teeth. Acid produced from these causes decalcification and erosion, while gritty substances cause abnormal wearing of the cusps and cutting edges, a condition known as attrition. Effect of Acid on the Teeth
A pH of 6.6 causes definite etching, while a pH below 5 causes decalcification if not immediately neutralized. Marked erosion of the teeth is seen in patients who scrape out citrus fruit with their teeth. Some of the acid beverages used continuously are·also very harmful, as some have a pH as low as 2.4. Gastric acid may have a similar effect. It affects the teeth in patients who habitually regurgitate food, because of reverse peristalsis or because they do not masticate it properly. If larger pieces are present these then are chewed again, which gives rise to rumination. Other patients may vomit habitually. In all such cases the acid from the stomach decalcifies the teeth and combined with friction from the tongue, the teeth become worn down especially on the lingual surfaces. Dental Caries
Dental caries is a complex disease. It is dependent on localized action of acidogenic organisms activated by the presence of nutrient substances favorable for their exuberant growth. Of the different foods with varying chemical and physical properties which are retained in the mouth for varying periods of time, those that attach themselves to the tooth surfaces and form bacterial plaques are of course more harmful than those
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that are easily removed by the saliva. That the diet is an important factor has been demonstrated by Kite, Shaw and Sognnaes (1950) by feeding highly caries-susceptible rats a caries-producing diet through a stomach tube. These rats remained free of dental decay, whereas the normally fed control animals showed abundant caries in their teeth. It is especially the refined carbohydrates from which bacteria, through enzymatic activity, produce various organic acids that accelerates decay of the teeth. The lactobacilli have been given the greatest amount of attention, but Lennin and Sullivan (1955), who have confirmed the findings of others, state that the lactobacilli which are generally used as caries indicators are not the most important. After the acidogenic organisms have initiated the decay and cavities have formed in the teeth, food retention will give rise to flourishing bacterial activity of a great variety of organisms. The pulp of the tooth ultimately becomes infected and dentoalveolar abscesses form. The destruction of the crown of the tooth disturbs the occlusal efficiency, and because of pain the affected individual is apt to chew less vigorously. TREATMENT. In the child the production of caries-resistant teeth is of primary importance. Fluoridation of the drinking water has done a great deal to accomplish this. After the teeth are formed, dietary measures may be used to reduce or even eliminate the acidogenic flora. This can be accomplished by excluding the easily fermentable carbohydrates from the diet, and especially avoiding their use between meals. The direct elimination of the acidogenic bacteria is another approach. The use of antiseptic mouth washes and toothpastes is the older method, which, however, has been revived by the inclusion of antienzymatic agents and antibiotic substances which predominately act upon grampositive organisms. If prevention has failed, the defects produced by caries should be repaired as soon as possible. Today occlusal rehabilitation is given considerable attention; this includes the establishment of proper occlusal function besides restoration of the anatomic shape of the tooth. Periodontal Disease
Periodontal disease is the next most common oral condition which affects mastication. First the teeth become loose and painful, chewing becomes more and more difficult, and bacterial infection of deep periodontal pockets produces abundant discharge of pus (pyorrhea). Later the teeth are lost by exfoliation or extraction. Periodontal disease is conHidered the most common cause of loss of teeth today. TREATMENT. The prevention of periodontal disease is to be emphasized. Adequate blood circulation in the supporting tissues of the teeth should be fostered by the mastication of hard food. Gingival massage with the toothbrush is of great importance, especially if the initial signsgingivitis-appear. In advanced cases various procedures used by the
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periodontist, such as subgingival curettage and gingivectomy, may still salvage some of the teeth. In far advanced cases extraction may forestall the type of extensive alveolar atrophy seen after this disease, which plagues the edentulous patient who is a notoriously poor subject for artificial dentures. For such patients the implant denture, a recently introduced prosthesis, may be the salvation. Deposits on the Teeth
Various stains are found; they are usually associated with deposits on the protected tooth surfaces. Materia alba is the soft material found at the cervical margin. It is made up of cell debris, food particles, bacteria, and salivary precipitates and is found when the area has not been brushed. Green stains occur chiefly in children with poor oral hygiene and are mainly on the labial surfaces of the upper anterior teeth. Darker stains are found more on posterior teeth. The color depends on pigments from blood, food, drugs, or micro-organisms. A brown pellicle has been described on teeth of indi.viduals not using abrasive-containing dentifrices. This stain will develop if water or liquid dentifrice is used instead of pastes and powders containing abrasives. Plaques and films are found on surfaces of the tooth protected from the detergent action of food, toothbrushes, and oral soft tissues (Fig. 17). They are so-called mucinous plaques, but are bacterial masses. They can be removed only by scraping with a sharp instrument. Tobacco stains the teeth by infiltration of coal tar products into calculus, plaques and pellicles. The stain may vary from yellow to black (Fig. 29). Calculus is the hard deposit (tarter) found on teeth. It is an inorganic derivative of saliva with inclusion of 6 to 15 per cent of organic material (bacteria, cell debris, etc.). Bacteria of filamentous forms, leptotrichia, leptothrix and actinomyces, appear to be essential for attachment of calculus to the teeth. Calculus contains about 63 to 75 per cent calcium phosphate, 3 to 9 per cent calcium carbonate, and 1 to 3 per cent magnesium phosphate in the form of hydroxyapatite. The saliva appears to be supersaturated with calcium salts, and a slight increase in their concentration, a decrease of the pH of the saliva, or a decrease in the ability of mucoprotein to colloidally disperse calcium salts leads to precipitation. TREATMENT. Removal of deposits by the dentist is generally required, after which hygienic measures may prevent recurrence. ABNORMALITIES OF SALIVATION
XerostOlnia
The most important abnormality of salivation is due to decreased secretion. It results not only in inadequate carbohydrate digestion, but
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also greatly furthers dental caries. Patients complain of a dry mouth and a sore red tongue. In extreme cases speech and deglutition become difficult. Trimble, Etherington and Losch (1938) showed an inverse relationship between the volume or rate of flow of saliva and the incidence of caries. Since xerostomia frequently follows x-ray irradiation for oral carcinoma, its effect on salivation explains the typical caries seen in such patients. Xerostomia is also common, although in not so severe a form, in older individuals as a result of senile atrophy of the glands. TREATMENT. Vitamin A and estrogen in women after menopause often is helpful. The drinking of Vichy water has been found to be of benefit. Ptyalism
An increased flow of saliva is not as important and common a disease. The excess saliva frequently drools from the mouth in affected patients. Toxic substances excreted by the salivary glands, such as mercury formerly used therapeutically, produced excess saliva. Certain affections of the central nervous system, such as bulbar paralysis and hemiplegia, are frequently associated with ptyalism. TREATMENT. Ptyalism presents a great handicap during dental operations. The administration of atropine, 0.6 mg. (1/100 grain), before treatment will give temporary relief. MOUTH ODORS (HALITOSIS)
Mouth odors arise chiefly from decomposing tissue and from debris and food beneath the gingival margins and intradental spaces. The nasopharyngeal regions, the digestive tract (belching, constipation), and the bronchopulmonary region may also give rise to unpleasant odors. While most food odors arise from the mouth, some strong odors, such as that due to garlic, may come from expired air via the blood stream. Among the diseases causing characteristic oral odors are diabetes which causes an acetone or fruity breath, and uremia which produces an ammonia breath. TREATMENT. Good oral hygiene is the best defense, and regulation of the diet and digestion. DISEASES OF THE GINGIVAE
The gingivae are subject to specific diseases not always affecting the rest of the mouth. This is partly due to their close association with the teeth which they surround, and possibly to an unusual circulatory condition. The rich blood supply comes from two directions, the peridental membrane and the gingival submucosa. The anastomosis favors stasis and extravasational deposits. Hemorrhagic Diseases
The gingiva may be injured by calculus, restorations, instruments, food, toothbrushes, floss or picks with resultant bleeding. This type of
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hemorrhage is usually self-limiting. However, one must differentiate simple gingival hemorrhage from bleeding due to tumors, traumatic or extraction wounds, and the blood diatheses; and from hemorrhage originating in the nose (epistaxis), the bronchus or lungs (hemoptysis), or the stomach (hematemesis). Hemophilia is a sex-linked genetic disease characterized by failure in clotting. It is manifest in the male only, except for the rare female hemophiliac who is the offspring of a hemophiliac male and a female carrier. While the hemophiliac presents a crucial problem if surgical
Fig. 15. Petechiae and ecchymosis due to thrombocytopenic purpura. Fig. 16. Gingival hemorrhage in a patient with agranulocytosis.
procedures are contemplated, spontaneous hemorrhage from the gingivae may take place. Thrombocytopenic purpura is characterized by extravasation of blood (Fig. 15*) and enormous reduction of platelet counts. It may result from essential purpura; from secondary purpura produced by toxins such as benzol; or from leukemia, tumors, agranulocytosis (Fig. 16), anemia or polycythemia. Bleeding of the gingiva may be associated with pregnancy, dysmenorrhea or scurvy (Fig. 23). TREATMENT. In hemorrhages occurring from local inflammatory lesions, removal of the cause of the underlying condition is important. In localized or generalized · gingivitis toothbrush massage will generally effectively overcome the tendency to bleeding. In patients with a hemorrhagic disease, extreme care should be taken to prevent trauma of even a minor degree. If extraction of teeth is contemplated, multiple fresh blood transfusions before and after the procedure are of great value combined with local control of bleeding.
* Figures 15 to 26, 28 and 30 from Thoma, K. H. and Robinson, H. B. G.: Oral and Dental Diagnosis with Suggestions for Treatment. 4th Ed. Philadelphia. W. B. Saunders Co., 1955.
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Gingival Inflammation
~':Gingival inflammation occurs in a variety of forms. The following are important. Gingivitis is usually caused by locally active injurious agents. Calculus is the most important single cause with the possible exception of the oral pathogens or their toxins which invade the gingivae subjected to physical and chemical trauma, from improperly used toothbrushes, picks and floss, tobacco and foods (Fig. 17). Systemic factors contribute, .chiefly by lowering the resistance of the tissue or altering its reaction to injury (Fig. 18).
Fig. 18 Fig. 17. Simple marginal gingivitis caused by poor oral hygiene with resultant irritation by bacteria and their toxins and by fermentation products from debris. Fig. 18. Gingivitis in diabetes.
Metallic poisoning may contribute to or initiate gingivitis. Bismuth given for treatment of systemic disease may localize from the blood stream in areas of mild gingivitis by anachoresis. Lead (Fig. 19), gold, mercury, silver and other heavy metals may also become localized in regions of inflammation (halo saturnis). Necrotizing ulcerative gingivitis (Vincent's infection, trench mouth) is an acute or chronic gingival inflammation characterized by red, swollen gingivae, necrosis beginning in the interdental papillae and extending along the gingival margins, pain, hemorrhage, a necrotic odor and, often, a pseudomembrane (Fig. 20). The invading organisms are oral treponemas and fusiform bacilli, supported by cocci. Local trauma or systemic disease, or both, may have lowered the resistance permitting invasion. The disease may become chronic if neglected. Herpetic gingivitis results from infection by the herpetic virus. It may develop into herpetic gingivostomatitis. This disease results in red, swollen, tender gingivae and oral mucosa without necrosis of the interdental papillae or gingival margins. The lips are usually swollen and dry. Localized herpetic lesions may be present. The disease is highly infectious. It is differentiated from necrotizing ulcerative gingivitis by the absence
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of a fetic odor, the lack of gingival necrosis, and a high temperature . .The disease runs a course of about two weeks. . .. Desquamative gingivitis is characterized by the tendency of the surfltce epithelium to desquamate. It is readily removed by rubbing with. cotton or gauze. The gingiva appears mottled owing to areas. of recentd~squa mation which are red and other areas with natured epitheliu.lll Wlliph are whiter or a grayish red. Since the disea~e occurs most. often iriwomen during menopause, a hormonal imbalance has been cited as its cause. It also occurs in younger women and men.
Fig. 19. Lead line of gingiva (Burtonian line, hlllo saturnis). Fig. 20. Acute necrotizing ulcerative gingivitis (Vincent's infection) showing necrosis and pseudomembrane
TREATMENT. Simple gingivitis responds well to massage after removal of irritating etiologic factors. Infectious types are treated by antibiotics. In necrotizing ulcerative gingivitis supportive treatment to build up the resistance of the patient is of great importance. Local treatment by means of antiseptics and treatment of periodontal pockets should be given. Antibiotic therapy should be instituted at once; Aureomycin parenterally and in form of troches is most effective. In herpetic gingivostomatitis Aureomycin or Terramycin given systemically in adequate dosage has given good results. Desquamative gingivitis responds poorly to treatment, and maintenance of oral hygiene is very important. There is no specific therapy but the use of hydrocortisone ointment has given Borne promise in a few cases. In the menopausal type, estrogen therapy is useful (0.5 to 1.0 mg. stilbesterol per day) (Ziskin and Zigarelli, 1945). Gingival Hypertrophies
Hypertrophies may result from the edema and fibrosis of inflammation, or from more specific causes. Pregnancy hypertrophy is a temporary enlargement of the gingiva seen in pregnant women, apparently as a result of hormonal imbalance. It is therefore termed hormonal hypertrophy. The gingivae are enlarged, red,
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Fig. 21 Fig. 22 Fig. 21. Hormonal gingivitis and pregnancy tumors. Fig. 22. Dilantin hypertrophy.
soft, and bleed easily. The enlargement is greatest in regions of irritation. When the hormonal balance is reached after pregnancy the tissue will return to normal. In relatively rare instances these localized enlargements become sizable and are termed pregnancy tumors (Fig. 21). They are not true neoplasms, having the same microscopic appearance as pyogenic granulomas. They disappear after pregnancy unless they become too fibrous to permit regression. Dilantin ]t.YP'ertrophy is a peculiar enlargement of the gingivae which occurs frequently in' those epileptics who take Dilantin sodium for more than a year (Fig. 22). It is a fibrous enlargement, firm, painless and nontender. The tissue is not increased in redness. The enlargement begins at the interdental papillae and may cover the teeth. Scorbutic enlargement is extremely rare at the present time (Fig. 23). The gingivae are soft, red to purple, swollen, and the teeth become loose. The ascorbic acid blood level should be determined if the disease is suspected. Leukemic hypertrophy is due chiefly to the normal defensive cells (leukocytes, lymphocytes or monocytes) being replaced by afunctional tumor cells. In addition the many white cells produced engorge the blood
Fig. 23. Scorbutic gingivitis. Fig:.24. Monocytic leukemia affecting gingivae.
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stream and infiltrate the submucosa. These cells and the resultant edema usually produce enlargement of the gingivae. Bacterial infection sets in, and areas of necrosis form (Fig. 24). The gingivae bleed profusely which may be the first sign of the disease. Bleeding, ecchymosis and necrosis are oral signs suggesting the existence of leukemia but are not specific. The diagnosis is made by study of the blood count and hemapoitic pattern. TREATMENT. Underlying general causes should be treated or corrected. In all cases oral cleanliness and absence of irritation from restorations, calculus, and occlusal trauma is most important. The leukemia victim with a healthy mouth has minimal oral changes and, even in advanced leukemia, the careful elimination of irritants may result in healing. DISEASES AFFECTING PRINCIPALLY THE TONGUE
The tongue has long been considered an indicator of systemic disease, although it also presents developmental, traumatic, chemical, infectious and neoplastic diseases. Developmental Anomalies
These are present at birth or develop during infancy.
Macroglossia may be due to a developmental deviation, myxedema,
acromegaly or inflammation. It generally shows indentations along the margins corresponding to the adjacent teeth. Ankyloglossia reduces the mobility of the tongue and results in speech and feeding problems (Fig. 12). Cleft and lobulated tongue are rare congenital abnormalities. Fissured tongue is found frequently and often causes retention of food and bacteria giving rise to inflammation and odors. Other Abnormalities
Coated tongue is caused by many conditiQns including gastrointestinal upsets, fevers, stomatitis and mouth-breathing. The coating consists of desquamated epithelium, saliva, leukocytes and bacteria which adhere, chiefly because of failure of normal function. In illness salivation may be reduced with resultant decrease in the self-cleansing activity. In dehydration the coating dries, leaving an encrusted tongue. The color changes as a rel!1Ult of food, tobacco, drug and/or bacterial and blood pigments. Iron results in a brown stain, as do blackberries, licorice, or hem orrhages. In eyanosis the color is dark blue. Red color may be due to red candy or red drug dyes, or polycythemia. The red desquamated tongue with prominent lingual papillae in scarlet fever is known as strawberry tongue. Yellow colors result from tobacco or from jaundice. Black hairy tongue (lingua nigra) is a condition charaeterized by elongation of the filiform papilla and the accumulation of dark pigments (Fig. 25). It is observed in patients with anemias, leukemias, vitamin deficiencies, and after antibiotic therapy producing a disturbance of the
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balance of oral flora and resulting in a predominance of the resistant yeasts (Candida albicans). The papillae probably elongate because they are not desquamated when the patient has a sore mouth. TREATMENT. Black hairy tongue may be cured in less than one week by scraping the tongue with a wooden tongue blade twice daily using 20 strokes at each treatment. Benign migratory glossitis (geographic tongue) is an inflammation of unknown etiology. The epithelium is desquamated in annular or circinate patterns (Fig. 26) leaving red cent~rs with white borders. The
Fig. 25. Black hairy tongue.
Fig. 26. Geographic tongue.
lesions are not painful and heal from the sides, and change their locations within a matter of days. They do not respond to specific therapy. Moeller's glossitis is discussed under Deficiency Diseases, q.v. DISEASES AFFECTING THE ENTIRE MOUTH
A great variety of abnormalities of the oral mucosa occur. Developmental and Hereditary Conditions
Fordyce Disease. This.is a developmental anomaly; small, leathery spots cover the buccal or labial mucosa, which are atopic sebacious glands. Melanoplakia. Dark pigmentations occurring after puberty in irregular patches of dark brown or metallic blue color may be found on the gingivae, palate and cheeks of brunette individuals and Negroes. They are due to melanin in the epithelium. ":Melanin spots with intestinal polyposis is a hereditary syndrome reported by Jeghers, McKusick and Katz (1949). Oval, irregular patches and smaller spots of brown or black pigment are found on the lips, buccal and palatal mucosa, and the skin (Fig. 27).
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Leukoplakia Leukoplakia is characterized, clinically, by white, opaque plaques of keratinized epithelium. The lesions may be extensive, usually feel somewhat leathery, and have rather sharp margins. There is some question whether the name should be reserved for lesions showing dyskeratosis
Fig. 27 Fig. 28 Fig. 27. Oral melanotic spots in intestinal polyposis syndrome. Fig. 28. Leukoplakia of tongue with carcinoma.
microscopically, and whether leukokeratosis should be used for cases showing hyperkeratosis and inflammation only. The condition is much more common in men than in women and is found affecting the cheek, floor of the mouth, palate and tongue, in greater frequency in tobacco users or other persons with physical irritation affecting these regions. The lesions may remain in status quo for many years or may become malignant (Fig. 28). Lichen planus is a disease of unknown cause which affects the skin and mucous membranes, but oral lesions are often found without associated dermal ones. The buccal, lingual and gingival lesions are painless, porcelain-white streaks, lines and dots arranged in a lacy or filigree pattern, usually bilaterally, surrounded by or within red areas (Fig. 29). The disease does not respond to treatment. A psychosomatic background is strongly suggested, most patients having marked nervous tensions. TREATMENT. Reassurance is important to prevent cancerphobia. Remissions have occurred when the lesions have been treated daily with cortisone ointment. Brewers' yeast helps other patients. Nutritional Deficiencies Ascorbic acid deficiency (scurvy) causes marked oral changes (Fig. 22). Bloated gingivae with marked ecchymosis and spontaneous hemorrhages occur. In advanced stages the teeth become loose and painful. Vitamin B complex deficiency affects particularly the tongue. Patients
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with pellagra (nicotinamide deficiency) have a beefy red, smooth tongue. At first the borders lose their papillae and the tip and borders become red. The whole dorsum soon loses its papillation. Usually cheilosis accompanies the glossitis; the tongue may be painful or burning. Iron deficiency causing anemia results in atrophy of the lingual papillae. Often small areas only are involved. Plummer-Vinson syndrome is seen in women past middle age. It is char:wterized by anemia, dysphagia, and atrophy of the oral mucosa, ton~~,and upper portion of the gastrointestinal tract. The disease predisposes to oral carcinoma. The marked nutritional deficiency is due to the~hanges in the digestive tract.
Fig. 29 Fig. 29. Lichen planus of buccal mucosa. Fig. 30. Stomatitis nicotina with cyst and cleft formation.
Pernicious anemia is reflected in the tongues of over half of its victims, and is spoken of as Hunters' glossitis. The tongue is red and burns, is painful, and may feel numb. Atrophy of the papillae and a red color appear. The tongue has lowered resistance to infection. Moeller's glossitis is a term applied to chronic superficial irregular atrophy of the tongue. It is an inflammation which is caused by allergy, hypersensitivity, nerve disturbances, and possibly, by vitamin B complex deficiencies. Pain, especially on eating acid, spicy or hot foods, is a prominent symptom. TREATMENT. In most deficiency diseases vitamin therapy will produce remission of symptoms unless there is a metabolic interference with utilization of the vitamins. Medical treatment, in some cases injection of vitamins (B12, thiamine hydrochloride) gives excellent results. Inflammations
Stomatitis nicotina is the result of palatal irritation by smoking tobacco. It begins with the appearance of small areolae of redness around the duct orifice of the palatal glands. Soon small elevations appear (Fig. 30). The remaining palatal mucosa looks blanched. TREATMENT. Removal of the cause, the use of tobacco in particular, may result in regression of the lesions. The patient should be re-examined
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at frequent intervals and if the lesions do not continue to regress they should be removed surgically. Treatment with caustics is contraindicated. Stomatitis venenata may be caused by contact with ordinarily innocuous substances such as drugs, dentifrices, drugs used in dentistry, denture bases, lipstick, essential oils, food, and flavoring in gum and candy. The lesions occur at the part of contact only, beginning as regions of erythema which may become secondarily infected. Acrylic materials used for dentures may in some individuals cause inflammation due to excesses of a monomer which may be present in improperly cured acrylic resins. Patch tests are valuable in differential diagnosis. Stomatitis medicamentosa is due to an altered reaction (allergy) to drugs such as barbiturates, iodine, antibiotics, sulfonamides, mercury, arsenic and salicylates. The eruption usually is multiple, eroded, and painful. The history is a valuable guide in the diagnosis. Infectious stomatitis is a general term and is applied in case of a general bacterial infection. It begins with a red, itchy feeling of the mucosa; later ulcers may develop. This type is called ulcerating stomatitis. Herpetic stomatitis is the term now generally used to designate the vesicular disease of the mouth caused by the herpetic virus. The lesions have also been called aphthae, canker sores, and dyspeptic ulcers. The virus remains in the cells, apparently without attacking the host. Whenever the resistance is lowered by trauma, infection, menstruation, allergy or sensitivity, psychic factors or dietary deficiencies, the virus becomes active. The first lesion is the vesicle but inside the mouth it soon ruptures and b~comes secondarily infected. The typical lesion has a yellow, ulcerated center, a bright-red areola, and is very painful. It heals in about 10 to 14 days. Several lesions may coalesce. They occur on the tongue, lip, palate and buccal mucosa. Recurrent herpetic lesions present a greater problem. Some individuals develop one crop of herpetic lesions after the other. Episodes may occur especially with menstruation, or at times when certain foods are eaten. TREATMENT. Classically, herpetic lesions are treated by phenol or silver nitrate which stops pain. For solitary lesions, Aureomycin and Terramycin pastes have proved effective in reducing secondary infection, relieving pain, and hastening healing. For women who develop these lesions at menstruation, large doses of vitamin B complex given by mouth for a few days before the menstrual period are often effective. High vitamin B complex intake sometimes helps other patients. The use of smallpox vaccine, given either once a week for six weeks in small doses or in increasing intradermal dosage over a six week period, has benefited some subjects. Cortisone ointment has given promising results in a limited group of subjects. In some persistent cases withdrawing chocolate or citrus fruits has aided. Some cases remain recalcitrant. Necrotizing ulcerative stomatitis (Vincent's stomatitis) is the result of extension of necrotizing ulcerative gingivitis, q.v.
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Gangrenous stomatitis (noma) is a severe fusospirochetal infection in debilitated patients. Actual gangrene occurs. Agranulocytosis (granulocytopenia) predisposes to noma. Other Lesions
Thrush (moniliasis) may occur on the labial and buccal mucosa, but is more frequent on the tongue. It produces a white, soft, rapidly spreading patch which can be removed with a curet leaving a bleeding surface. Candida albicans can be demonstrated in smears. TREATMENT. Thrush responds poorly to treatment and ordinary antibiotics are contraindicated. A new fungicidal antibiotic, Mycostatin, 500,000 U. three times a day after meals, has recently been introduced. Syphilis may result in chancres, mucous patches, or gumma. The chancre shows a necrotic center, raised margins, and induration and, as secondary infection occurs, pain is present. The mucous patches are ulcerated plaques with a milky, translucent surface. Papules have indurated bases and raised borders giving the appearance of a reddish border and a deep crater. The tongue may show atrophic changes, resulting from endartheritis, and presents a smooth surface covered by a· thin translucent epithelium producing a glassy tongue. The tertiary lesions, the gummas, may undergo malignant changes. Gummatous lesions have a predeliction for the palate. They first form as nodules which result in shallow or deep ulcers. The margins are raised and surrounded by red zones; the center of the ulcer is necrotic. The regional lymph nodes enlarge. The ulcer may perforate the palate. TREATMENT is systemic. Pemphigus is an acute or chronic disease of the skin and oral mucosa. Several types form oral lesions, vulgaris, foliaceus and vegetans. Over half the patients show oral lesions first. The initial sign is a few vesicles of small size, which soon rupture leaving a curled-up thin membrane at the edge of the ulcer (Fig. 31). Pain is prominent and the lesions soon become secondarily infected. The prognosis in many cases is grave. Erythema multiforme, one of the rarer diseases of unknown cause, produces lesions on the oral mucosa, tongue, lips, skin, conjunctiva and urethral tract. In a few days vesicles appear on the lips and oral mucosa. These become eroded within a few hours and resemble herpetic lesions, or the lesions may resemble lichen planus. In severe cases the temperature is elevated and the ulcerations are extensive and tend to coalesce. Lupus erythematosus is another one of the dermatologic diseases with acute and destructive ulcerations (Fig. 32). TUMORS OF THE MOUTH
Benign TUIllors
Benign oral tumors occur in any part of the mouth at all ages. The most common ones only will be described.
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Fig. 31 Fig. 32 Fig. 31. Pemphigus with desquamation. Fig. 32. Oral vesicular lesions in lupus erythematosus.
Hyperplasias are frequently found and are usually an exaggerated fibroblastic response to chronic irritation. They are seen associated with carious teeth, and in edentulous mouths, caused by denture irritation. Theyoccur on the palate under dentures that are improperly constructed, or, more commonly, which are worn after bone changes have made them unsuitable for use. Papillary hyperplasia may fbrm at the palatal midline. These lesions should always be biopsied as they may show early carcinomatous changes (Fig. 33). Giant cell lesions are now generally considered as giant cell reparative lesions and not as neoplasms. They are found in a younger age group than are most neoplassm. They have a purple tint, and are softer than fibromas. On the gingiva they are common, and are called giant cell epulis.
Fig. 33 Fig. 34 Fig. 33. Papillomatosis of palate (benign). Fig. 34. Fibroma of gingiva.
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Fibromas are the most common of the benign neoplasms on the gingiva, the buccal and palatal mucosa, and the tongue. They usually are firm, covered with relatively normal epithelium, and present no subjective signs. They may vary from pin-head to very large size and may be sessile or pedunculated (Fig. 34). H emangiomas are soft, blue or purple tumors that may become very large. They are found on the tongue (Fig. 35) and the cheek most commonly. There is danger of accidental injury and severe hemorrhage. Lymphangiomas are similar soft tumors affecting the tongue, but are rarer than hemangiomas and have a yellow pinkish color rather than purple.
Fig. 35
Fig. 35. Hemangioma of tongue. Fig. 36. Torus palatinus.
Lipomas are soft but may reach large size and are easily recognized by their colors. Mixed tumors form from the mucous glands of the buccal mucosa, lip and palate. The typical mixed tumor occurs on the side of the palate and grows slowly but progressively. These tumors may be present for many months or even years. They are firm but not bony hard. They are not malignant as a rule, do not metastasize, but are extremely destructive locally. They should be excised widely. Torus palatinus is found in the midline of the hard palate as a dense, hard bony enlargement which varies in form (Fig. 36). In rare instances it may interfere with speech and with denture construction. Sometimes it becomes irritated by food and ulcerated. Differential diagnosis from mixed salivary gland tumors and fibroma is important. Torus mandibularis is seen bilaterally on the inner surface of the mandible. It is a bony exostosis of no significance except interference with motion of the tongue. Osteomas occur on the oral surface of the jaws, often in multiple form. Dermoid cysts may occur benea.th the geniohyoglossus muscle in the floor of the mouth. They may reach a large size, pushing the tongue up-
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wards. They contain hair and other ectodermal structures, including teeth. Epidermoid cysts arise in a similar manner from embryonal rests but do not contain hair or teeth. Ranula and mucoceles form from the sublingual, labial and, rarely, the buccal glands. They contain mucus and are caused by occlusion of their secretory ducts. TREATMENT OF BENIGN TUMORS. All benign tumors are excised. Those that are known to recur should be excised more radically, or the tumor bed should be treated with the cautery. Any irritating factor associated with their development should be removed.
Fig. 37
Fig. 38 Fig. 39 Fig. 37. Ulcerating type of carcinoma. Fig. 38. Fibrosarcoma of mandibular gingiva. Fig. 39, Lymphosarcoma of palate.
Malignant Tumors
Malignant oral tumors occur mostly in later life, although some affect young individuals, especially sarcomas. About 15 per cent of all primary malignancies in over 200,000 patients who die each year of cancer are in the head and neck. Squamous cell carcinoma (epidermoid) is the most common intr~oral malignant lesion. Carcinoma may be preceded by papilloma or leukoplakia. It is seen mpre commonly in patients over 50 years of age. It occurs on the gingivae where it is often mistaken for an inflammatory lesion and often is aggravated by the extraction of teeth. It also forms on the lips, tongue (Fig. 28), floor of the mouth, buccal mucosa, hard and soft palates. The appearance varies greatly. We find papillomatous and ulcerating types (Fig. 37), exophytic and deeply invading lesions. Carcinoma of the antrum may invade the palate. More frequently, however, carcinomas of the mouth invade the maxillary sinus. In the mandible the bone may become extensively invaded. SmalllesioBs should be discovered by the dentist's periodic examination; unfortunately, often carcinoma is not diagnosed until the lesion is large. Pain, difficulty in swallowing, and ulceration are signs of advanced disease when generally the regional lymph nodes are involved.
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Fibrosarcoma may occur on the gingiva (Fig. 38), growing rapidly and destroying adjacent bone. It is found in younger individuals than is carcinoma. Osteogenic sarcomas may cause enlargement of the alveolar process of the jaws. Plasmocytoma and lymphosarcoma form in any part but are not very common. The latter (Fig. 39) often occurs in multiple form. Malignant melanoma is a very malignant neoplasm. It may extend from the gingiva over the palate and forms a coal-black tumor mass, rapidly growing and infiltrating. Metastases occur early and involve both the regional lymph nodes as well as the vital organs. TREATMENT. Biopsy is a most valuable aid to diagnosis, especially to differentiate benign from malignant lesions. The biopsy should be designed to secure tissue which will aid the pathologist in his examination with maximum benefit to the patient. Diagnosis of these lesions when small is of greatest importance, and contributes appreciably to the reduction of the high mortality rate of oral malignancies. In advanced cases heroic surgical measures still give hope for a cure. Radiation therapy is indicated in very radiosensitive neoplasms, such as lymphosarcoma, and often will salvage inoperable cases of squamous cell carcinoma (White, Sieniewicz, and Christensen, 1954). DISEASES AND TUMORS OF THE SALIVARY GLANDS
Developmental, functional, infectious, and neoplastic conditions occur. Sialograms are often useful in making a diagnosis. Sialadenitis may cause enlargement of the salivary glands. The infection may be ascending due to oral bacteria, and a thick, yellow exudate may be expressed. Prolonged use of potassium iodide or of mercury may be responsible for parotitis. Certain foods result in pain and inflammation in some individuals. Because the salivary glands are so readily affected by psychic influences it is surprising that so few cases have a psychic origin. Sialolithiasis is the accumulation of calcareous deposits in the salivary gland or ducts. The formation of calculi usually causes interference with the normal salivary flow. M ikulicz' s syndrome and disease are characterized by swelling of the parotid, submaxillary, sublingual, and lacrimal glands or of any comBination of these glands. Salivation is decreased greatly in most instances. Uveoparotid fever is characterized by inflammation of the parotid gland and the uveal tract of the eye. A possible relationship to Boeck's sarcoid has been postulated. Mixed tumor may be benign or malignant. The parotid gland is its most frequent site. The malignant tumors may appear as squamous cell carcinomas, adenocarcinomas, or mucoepidermoid carcinomas. These tumors are highly malignant and regional lymph node removal should be combined with wide excision.
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M alignant lymphomas may arise in the parotid or other salivary glands. Such tumors cause facial deformities and often reduce salivation SO that xerostomia results. TREATMENT. Infections are treated by the use of antibiotics; salivary stones should be excised; tumors are treated by excision or irradiation. REFERENCES Appleton, J. L. T. Jr.: Bacterial Infection, 4th Ed., Chap. XXIV. Philadelphia, Lea & Febiger, 1950. Bass, C. C.: Endameba Buccalis. Proc. Soc. Expel'. BioI. & Med. 66: 9, 1947. Bibby, B. G.: Mouth Bacteria. J. Dent. Research 17: 265,423,471, 1938. Bibby, B. G., Goldberg, H. J. and Chen, E.: Evaluation of Caries-Producing Potentialities of Various Foodstuffs. J. Am. Dent. A. 42: 491, 1951. Goldsworthy, N. E., Sullivan, H. R. and Harris, R.: Practical Caries Control. Dent. J. Australia 27: 45, 1953. Hamp, E. G.: Morphologic Characteristics of Oral Treponemas and Borrelia vincenti. J. Am. Dent. A. 40: 1, 1950. Jay, P.: Reduction of Oral Lactobacillus Acidophilus by Periodic Restriction of Carbohydrate. Am. J. Orthodontics & Oral Surg. (Oral Surg. Seet.) 33: 162, 1947. Jay, P., Beeuwkes, A. M., Blecha, E. E. and Bust, M. S.: Dietary Progress for Control of Dental Caries. Ann Arbor, Mich., the Overbeck Co., 1951. Jeghers, H., McKusick, V. A. and Katz, K. H.: Generalized Intestinal Polyposis and Melanin Spots of Oral Mucosa, Lips and Digits. New England J. Med. 241: 993, 1941. Kite, O. W., Shaw, J. H. and Sognnaes, R. F.: Prevention of Experimental Tooth Decay by Tube Feeding. J. Nutrition 42: 89, 1950. Lennin, D. F. and Sullivan, H. R.: Relative Rates of Acid Production from Refined and Natural Sugars. Dent. J. Australia 25: 67, 1955. Lind, H. E.: Rationale of Routine Antibiotic Sensitivity Determination Antibiotics & Chemotherapy 3: 672, 1953. Markowitz, H. A. and Gerry, R. G.: Temporomandibular Joint Disease. Oral Surg., Oral Med. & Oral Path. 2: 1309, 1948; 3: 1309, 1949; 4: 75, 1950. Morris, E. 0.: Bacteriology of Oral Cavity. Brit. Dent. J. 95: 77,259,1953; 96: 95, 259,1954. Orland, F. J. and others: Use of Germ-free Animal Technique in Study of Experimental Caries. I. Basic Dental Study of Rats Reared Free of All Micro-organisms. J. Dent. Research 33: 147, 1954. Thoma, K. H.: Ankylosis of Temporomandibular Joint. Am. J. Orthodontics & Oral Surg. (Oral Surg. Sect.) 32: 269, 1946. Idem: Oral Pathology, 4th Ed. St. Louis, C. V. Mosby Co., 1954. Idem: Oral Surgery, 2nd Ed. St. Louis, C. V. Mosby Co., 1949. Trimble, H. C., Etherington, J. and Losch, P. K.: Rate of Secretion and Incidence of Dental Caries. J. Dent. Research 17: 299, 1938. Wah Leung, S.: Demonstration of Importance of Bicarbonate as Salivary Buffer. J. Dent. Research 30: 403, 1951. White, G., Sieniewicz, J. and Christensen, W. R.: Improved Control of Advanced Oral Cancer with Massive Roentgen Therapy. Radiology 63: 37, 1954. Ziskin, A. and Zigarelli, E.: Chronic Desquamating Gingivitis. Am. J. Orthodontics & Oral Surg. 31: 1, 1945. 1146 Beacon Street Brookline 46, Massachusetts