Stomatitis

STOMATITIS (from Greek stoma-mouth). Inflammation of the mucous membrane of the oral cavity. Stomatitis in relation to infection is divided into two groups: vulgar S., in which the infection is of a secondary nature (non-specific), and S., caused by specific pathogens. Clinically, both groups proceed in the form of catarrhal and more often ulcerative inflammations. Catarrhal forms often take a chronic course, while ulcerative ones recur. Clinical forms of non-specific S.: 1) Catarrhal S. (st. catarrhalis, s. simplex) as a rule begins with hyperemia of the gum margin, swelling and bleeding of the gum papillae. Subsequently, the process spreads to the mucous membrane, manifesting as redness and swelling of it (imprint of tooth crowns on the buccal mucosa), cloudiness and desquamation of the epithelium and often the appearance of petechiae. Profuse salivation. The reaction of regional glands is usually absent. Subjectively: burning in the mouth, pain when eating; in chronic cases - dryness in the mouth. 2) Aphthous S. (st. maculo-fibrinosa, s. aphthosa) - see Aphthae. 3) Vesicular S. (st. herpetica), observed in febrile patients, somewhat resembles aphthous. Clinically - a rash of small yellowish vesicles on the mucous membranes of the lips, hard palate and edges of the tongue; pain is insignificant. After several days, spontaneous healing occurs. 4) Ulcerative S., oral gangrene (st. ulcerosa, s. ulcero-membranosa, s. stomacace), often develops from the forms described above, but may also occur independently. On the reddened and swollen mucous membrane, vesicles with turbid content appear. After the vesicles burst, an ulcerative surface is exposed, covered with a foul-smelling necrotic exudate, which bleeds easily. The ulcer tends to progress in depth and width, sometimes involving bone as well. The primary localization is usually on the gum margin in the area of the lower front teeth or near gangrenous roots and cervical carious cavities. Regional glands are enlarged and painful. Temperature rises to 39-40°, chills are observed, often a severe general condition; foetor ex ore. Subjectively - severe pain, loss of appetite, poor sleep, depressed state. Patho-anatomical picture comes down to necrosis and detachment of the epithelium and the formation of a vesicle with turbid fluid. Necrosis and putrefactive decay spread to the underlying tissues, in severe cases causing gangrenous decay of muscles, necrosis and sequestration of bone and complicated by septicemia. In favorable cases, the process ends with the rejection of necrotized areas and the formation of a scar. The microflora of the process consists mainly, and sometimes in pure culture, of Bac. fusiformis and Spirochaeta perfringens (Vincenti), i.e., anaerobic. Foetor ex ore is explained by the formation of foul-smelling decay products of tissue proteins destroyed by these microbes (according to Maslov). Clinically, in the form of ulcerative S., proceed S. mercurialis (mercury stomatitis), S. bismutica (bismuth stomatitis) and water cancer (see Noma). 5) Mercury S. - see Mercury. 6) Bismuth S. is observed in the treatment of syphilis with bismuth preparations. The onset of the disease is characterized by a grayish-blue coloration of the gum margin in the area of front teeth, spots of the same color on the mucous membranes of the cheeks and tongue, and brown spots on the palate (dog palate). Subjectively - a slight increase in salivation; then ulcers of the mucous membrane with pseudo-membranous coating develop, enlargement and pain of regional glands, polyuria with excretion of bismuth. It differs from mercury stomatitis by its relatively mild course, slight salivation and less pronounced foetor ex ore. The bismuth gum margin, unlike the lead one, does not whiten when a drop of H₂O₂ is applied. 7) Scorbutic S. (st. scorbutica) - see Scurvy. 8) Pemphigus (see Pemphigus) is differentiated from aphthous stomatitis by the persistence of the disease, irregularity of the ulcer outlines, and creeping progression. The sterility and eosinophilia of punctate of pemphigus vesicles and worsening under the influence of potassium iodide decide the diagnosis in favor of pemphigus. The etiology of S. is primarily associated with general acute infections (influenza, angina), exacerbation of chronic gastrointestinal diseases, nutritional disorders, especially those related to vitamin C deficiency and monotonous food with predominance of animal proteins and flour dishes, with overwork, nervous exhaustion, absorption of salts of heavy metals (mercury, bismuth, copper), as well as disorders of the endocrine system (pregnancy) and blood diseases (malignant anemias, aleukias, agranulocytosis). Each of the listed factors has particularly great significance when the ground for the disease is prepared by the presence of local causes. The latter include untidiness of the mouth, decaying root remnants, dental deposits (tartar), poorly fitted dentures and especially artificial metal crowns. Infection in vulgar S. represents a mixed, usually saprophytic in the oral cavity microflora. In ulcerative forms, the predominance of anaerobic microbes and in particular fusospirochetal symbiosis (Bac. fusiformis and Spiroch. Vincenti) is characteristic, often found almost in pure culture. In the pathogenesis of vulgar S., the most characteristic feature is that they to a greater or lesser degree accompany all diseases that manifest as a disorder of general and local metabolism and in particular its acidotic shift, as well as causing a decrease in the immunobiological state of the body. The acid shift in metabolism, whether caused by endocrine-nervous disorders, dietary (avitaminosis C) or general intoxication, causes edema, venous stasis and deoxidation of tissues. As a result, the resistance of cellular elements to infection decreases, and the deoxidation itself favors the development of anaerobic microflora of the oral cavity. Thus, conditions are created when a local cause in the form of irritation by a prosthesis, untidiness of the oral cavity, etc. can be the trigger for the onset of the process. Clinical statistics indicate the predominant affection of S. in asthenics, i.e., individuals prone to an acid shift in metabolism and especially sensitive to hypovitaminosis C (Entin). Lesion of vessels in infectious, alimentary and dyspeptic intoxications, changing local metabolism and disturbing the nutrition of tissue elements, in the same measure contributes to the occurrence of the pathological process. In particular, products of incomplete protein digestion, so-called proteogenous amines, formed in larger than normal quantities in intestinal disorders and with excessive intake of animal proteins, sharply disrupt the function of the vascular system of the periodontal apparatus (Schwartz). Very recently, it has been experimentally established that the trophic function of the nervous system plays a major role in the pathogenesis of catarrhal and ulcerative inflammations of the oral mucosa (Entin). On this basis, the mentioned author proposes neurodystrophic stomatitis as a nosological form. Therapy of non-specific S. Etiological therapy, as always, should naturally be placed in the foreground, but it is not always possible to quickly clarify the etiology of non-specific S. Therefore, it is usually necessary to start with symptomatic therapy, which is sometimes the only one and often sufficient. In all clinical forms of S., general strengthening treatment and prescription of a diet ensuring a shift in metabolism in the alkaline direction are indicated. Food should be rich in fats and raw vegetables and fruits (vitamins A, D and C) and prepared in such a way that it does not irritate the mucosa either mechanically or chemically. Mucous and pureed soups, milk puree soups, jelly and purees from vegetables and the mandatory introduction of raw fruit and vegetable juices in sweetened form, for example juice from 200 g of tomatoes, or one lemon, or 200 g of green cabbage leaves, or 400 g of cranberries; in addition 30-50 g of brewer's yeast (vitamin B). In chronic cases, especially in chlorotic subjects, arsenic treatment gives good effect. Locally - mandatory elimination of all irritating factors, such as: temporary discontinuation of wearing removable dentures, prohibition of tobacco, alcohol and spices. Sanitation of the oral cavity is mandatory in chronic cases and is contraindicated and dangerous in acute ulcerative S. Cleansing of the oral cavity by irrigation is mandatory. For the latter, an Esmarch's mug and a sprinkling vaginal glass (ease of sterilization!) tip are used; irrigation is mandatory before and after each meal and at least 6-7 times a day. In ulcerative and especially putrefactive forms, careful (not "to blood!") wiping of ulcers with cotton wool moistened with H₂O₂ is indicated. Active mouthwashes as not achieving the goal and traumatic are contraindicated. For irrigation, pursuing mainly mechanical cleansing of the oral cavity, pure water or weak solutions of antiseptics (borax, soda, Kali hypermang., boric acid, Metaphen, Trypaflavini-iMH. etc.) are recommended. The temperature of solutions for washing and rinsing should not exceed 45-50°. After irrigation, the ulcerative surface is coated with a 3% solution of Methylenblau, Gentianviolett, Brillantgrun or Scharlachrot.

Many authors recommend cauterizing the ulcerous surface with lunar caustic, chromic acid, zinc chloride, copper sulfate, etc. In this case, high concentrations should be avoided, limiting to a maximum of 10%. Based on the fact that Spirochaeta Vincenti is always found in the microflora of ulcers, the application of a suspension of salvarsan in glycerine, the administration of 3-5 tablets (0.5 each) of preparation 594, Spirocid, and injections of Hydr. oxycyanati no 0.01x3 have been proposed. Autovaccination and autogenous hemotherapy are used, as well as compresses from Bezredka's antivirus (not for tubercular and lupus ulcers!). Lukomsky recommends pilocarpine injections. Bauer applies 0.5 erythema doses of X-rays to increase the bactericidal properties of the blood. For mercurial stomatitis, rinsing, resp. irrigation, with a 2% solution of Berthollet's salt is beneficial; during mercury therapy, this rinse is also prescribed prophylactically. Etiological therapy comes down to treating the underlying disease that has manifested as a local process in the oral cavity. Thus, for chronic avitaminosis and intestinal intoxications - appropriate diet, for helminth invasions - anthelmintic treatment, for endocrine disorders - organotherapy, for functional disorders of the nervous system - strengthening sanatorium-resort treatment, etc. Specific Stomatites. Acute. 1. Gonorrheal stomatitis (st. gonorrhoica) is rare in adults (coitus praeternaturalis), more common in newborns. In the latter, no later than the end of the first and beginning of the second week, a bluish discoloration of the oral mucosa appears, followed by ulcers with a pseudomembranous yellowish coating, localized on the transitional fold of the lips, root of the tongue, and palatine arches. In adults, the diagnosis is determined by bacterioscopy. Therapy: locally 0.5% lunar caustic or 1% protargol. The condition responds quickly to treatment. 2) Diphtheritic stomatitis (st. diphtherica) - see Diphtheria. 3) Erysipelas stomatitis (st. erysipelatosa) is most often observed as a transition of facial erysipelas to the mucous membrane. Primary localization on the mucosa is rare (according to Maslov). Bright redness and dryness of the mucosa are characteristic. Unlike cutaneous forms, the redness does not have sharp outlines. General condition is severe, with fever and delirium. Duration is 8-10 days. Complications: spread to accessory cavities, meninges, and vocal cords (asphyxia). Tendency to relapses. Therapy - administration of serum, which often quickly cures the disease. 4) Hemorrhagic stomatitis (st. haemorrhagica); causative agent - Leptospira icteroides; accompanies yellow fever. On the 3rd-6th day of the incubation period, hemorrhages of the gums and palate mucosa appear, which quickly ulcerate. The prognosis is poor due to the general disease. Local therapy - usual care for the oral cavity, as in stomatitis. General therapy - see Yellow fever. 5) Thrush (st. oidica, s. soor). Causative agent - the fungus Oidium albicans - see Thrush. Chronic specific stomatites almost exclusively encompass stomatogenic manifestations of syphilis and tuberculosis. Some authors include leukoplakia in this group without sufficient reason (see). For tuberculosis and syphilis of the oral cavity - see Mouth _t oral cavity.