Noma: causes, symptoms, diagnosis, treatment

Noma (cancrum oris) is a disease in which, as a result of necrosis, extensive defects of the soft and bone tissues of the orofacial region arise - a kind of wet gangrene, currently found almost exclusively in underdeveloped and developing countries.

Usually, only isolated cases of noma are observed, but sometimes, when social and living conditions worsen, after severe infectious diseases, the number of diseases increases. Thus, in the early 20s of the last century, due to the dire situation of the population of Russia (intervention, civil war, crop failure, famine) in some regions (Perm, Astrakhan, etc.), the number of cases of noma increased significantly. With noma, the mucous membrane of the oral cavity is most often primarily affected. Dentists identify noma with ulcerative necrotic gingivitis, which for one reason or another has acquired a malignant form of the course. Currently, ulcerative necrotic gingivitis can be considered a precursor disease of noma.

Noma mainly affects children aged 2 to 15 years. According to A.I. Makarenko (1933), I.M. Sobol (1936), A.T. Pulatov (1956) and others, noma usually develops in weakened children, exhausted during or after infectious diseases such as measles, whooping cough, dysentery, scarlet fever, diphtheria, pneumonia, typhus, leishmaniasis, influenza, etc. In adults, noma is much less common, despite the fact that adults are much more likely to suffer from ulcerative necrotic gingivitis.

Cause of noma. Taking into account the above-mentioned conditions and risk factors, most authors associate noma with an infectious origin. Thus, various bacteria, spirochetes, cocci, fungi, and anaerobes have been isolated from noma.

According to some authors, B. perfringens plays an important role in the etiology of noma, causing the development of local necrotic processes. However, most authors believe that noma is associated with fusospirochetal microbiota (Plaut-Vincent symbiosis). Some authors attach etiological significance to factors such as the special enzymatic action of saliva and vitamin deficiency. At present, the action of other microorganisms and viruses is assumed, such as Prevotella intermtdia, Fusobacterium spirochetae, hemolytic streptococcus, and viruses from the Herpes family. The contagiousness of noma remains questionable, despite the fact that there are observations of noma diseases in one family or in one focus. However, the occurrence of noma should not be associated with a specific pathogen, but mainly with unfavorable living, social, sanitary conditions, the consequences of infectious diseases that sharply reduce the body's immunobiological resistance, with vitamin deficiency and other risk factors.

Pathological anatomy and clinical course. With noma, the oral mucosa is most often affected, a severe form of gangrenous stomatitis (gingivitis, periodontitis) develops with rapid, during the first 3-5 days, spread of the necrotic process in breadth and depth. As a result, significant areas of affected tissue are destroyed and fall off. Noma can also occur on the auricle, neck, genitals, in the anus area, etc. Beginning, as a rule, on the distal part of the alveolar process in the form of ulcerative necrotic gingivitis, noma can quickly spread to the lips, cheeks and nose. In a few days, all bone tissue in the cheek area can be completely exposed due to the destruction of soft tissues.

The disease begins with the appearance of a bluish-red blister on the skin or mucous membrane, followed by a dark blue spot, the skin around which acquires a waxy color with a pearlescent tint - the so-called waxy zone. The tissues surrounding this zone acquire the appearance of a glassy edema, are dense to the touch and quickly undergo necrotic decay, emitting an unpleasant putrid odor. The affected areas with noma are painless (similar to leprosy), bleeding is almost absent. The affected area on the side of the oral cavity quickly increases, the cervical zones of the teeth become necrotic, and the teeth become loose and fall out (super-lightning form of periodontitis). In the most severe cases, the process moves to the tongue, palate, lip and to the opposite side. The gangrenous process also spreads to the skin of the face, affecting the entire cheek, the pyramid of the nose, and can spread to the eye socket and, like a creeping, unstoppable ulcer, spread to the eyeball and bone formations of the upper jaw. A.I. Makarenko (1961) describes the process of destruction of the nomadic facial area as follows.

The tissue decay progresses, the resulting cheek defect increases, the jaws, teeth, and tongue are exposed; the release of putrefactive exudate and abundant salivation are noted.

The general condition of the patient is severe, due to severe intoxication. Patients are usually indifferent to their surroundings, clouding of consciousness is often observed, body temperature is of the continua type, reaching 39-40°C.

Ingestion of tissue decay products causes gastrointestinal disorders, and their aspiration leads to pulmonary complications (pneumonia, pulmonary gangrene). However, noma can also proceed benignly. In a benign course, the process may be limited to ulceration of a section of the oral mucosa or the formation of a defect in the cheek and wing of the nose of greater or lesser size with subsequent scarring. However, the process of wound surface cleansing and wound scarring proceeds slowly, resembling a similar process in cases of damage by ionizing radiation. Deep defects are formed at the site of dead tissue. Scars after noma disfigure the face and cause contracture of the temporomandibular joint. These organic defects are subsequently, as far as possible, eliminated by plastic surgery.

In malignant cases, the necrotic process progresses rapidly and leads to rapid death of the patient. Due to complications and concomitant diseases, the mortality rate currently ranges from 70 to 90%.

Diagnosis of noma in the developed process does not present difficulties. In some cases, in small children in the initial period of noma, which affected the mucous membrane of the oral cavity, the disease remains unnoticed and is detected by others only by an unusual putrid odor from the mouth. Differential diagnostics is difficult in the initial stage of the disease. According to G.M. Babiyak (2004), the clinical picture in this period of noma is so erased (especially in recent years) that it can be distinguished from many other noma-like diseases only by the absence of vitreous edema around the inflammation site, which is specific to noma.

Treatment of noma is carried out in a hospital with certain measures of anti-infection protection of medical personnel and other patients, taking into account the age, prevalence of the local process and the severity of the general condition of the patient.

It includes the prescription of broad-spectrum antibiotics, taking into account the type of microbiota and its sensitivity to the treatment used. Much attention should be paid to the local necrotic process, timely removal of necrotic tissue, the use of proteolytic enzymes, local antiseptics and careful toilet of the affected anatomical structures. At the same time, drugs are prescribed to strengthen the immune system, the general condition of the body, vitamins. Detoxification therapy is carried out up to plasmapheresis and UFO or laser autohemotherapy. Symptomatic treatment - according to indications.

Prevention of noma consists of hygienic care of the oral cavity in children with infectious diseases, especially those accompanied by exhaustion, and general strengthening and immunocorrective treatment.

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