Hairy leukoplakia is a disease of the oral mucosa caused by the Epstein–Barr virus and developing against the background of immunosuppressive conditions. The pathology is most often diagnosed in patients with HIV, acute leukemia and taking immunosuppressive drugs. The lesion is a whitish or gray plaque that forms folds and plaques with a rough surface. A biopsy followed by histological analysis, smear examination and detection of HIV markers are used for diagnosis. Treatment includes taking antiviral drugs, local medication and surgical treatment.
K13.3 Hairy leukoplakia
Hairy leukoplakia is a dysplastic pathology of the oral mucosa in patients with immunodeficiency infected with Epstein-Barr virus (EBV). It got its name because of a specific histological picture: the surface parakeratic layer of pathological areas is covered with microscopic villi, which are foci of hyperkeratosis. Sometimes the disease is called “hairy”, “fleecy”, “villous” or “carpet” leukoplakia. The disease was first diagnosed in 1984 in a patient with HIV and EBV. In 25-53% of cases, patients are HIV-infected persons, with immunodeficiency of another etiology, pathology occurs in 10% of cases. Hairy leukoplakia is usually observed after the age of 40, among people over 70 years of age, its prevalence is about 8%, but the likelihood of developing pathology in children and young people cannot be excluded. 80% of patients are smokers, there are more men than women among the sick.
Currently, the main cause of the disease is considered to be EBV, which causes characteristic changes in the pathological focus during replication. When infected, the virus invades the basal epithelial cells of the pharynx and B cells, where it remains throughout the patient’s life. Up to 90% of the world’s population is infected with the EBV virus. In a healthy person, the reproduction of EBV is restrained by T-lymphocytes, but they cannot completely destroy the virus. With immunosuppression, the concentration of EBV-specific cytotoxic T-lymphocytes decreases, and active replication of the virus begins.
Usually the cause of immunodeficiency is HIV, less often acute leukemia and the use of immunosuppressive drugs for the treatment of systemic autoimmune diseases (systemic lupus erythematosus, rheumatoid arthritis, scleroderma) and for the prevention of transplant rejection. An additional factor that reduces immunity in the oral cavity is smoking. An adverse effect on the mucous membrane is caused by frequent irradiation of the oral cavity with ultraviolet light or the installation of metal prostheses, between the components of which galvanic currents occur. Permanent traumatization of tissues in the oral cavity occurs due to uneven teeth, incorrectly fixed crowns, braces and prostheses.
The disease often proceeds in an asymptomatic form, and many patients learn about it only at a dentist’s appointment. The most striking symptom is a whitish or gray plaque on the lateral borders, back or lower surface of the tongue. The mucous membrane of the cheeks and gums is less often affected, in extremely rare cases, changes affect the soft palate. Foci of hairy leukoplakia can have a unilateral and bilateral character, suddenly appear and also suddenly disappear. Patients do not complain of pain, only in rare cases there is slight discomfort, a change in taste and dry mouth. Complaints, as a rule, appear when a fungal infection is attached.
In the early stages of the disease, whitish folds with a rough surface appear, rising above the surrounding tissues and alternating with areas of a healthy mucous membrane. In appearance, the affected area of the tongue resembles a washing board. Gradually, the folds merge to form plaques with fuzzy borders. The size of the plaques varies from 1-2 mm to 3 cm. When scraping with a spatula, the appearance of the plaques does not change, and the patient himself does not feel any discomfort. When the lesion is located on the cheeks, gums or the lower surface of the tongue, the surface of the plaque does not have a characteristic “hairy” structure. In advanced cases, examination can detect cracks in the tongue, erosion and infiltrates in the affected areas.
Particular attention should be paid to the signs of immunodeficiency when collecting anamnesis: a sharp weight loss, sweating at night, prolonged causeless fevers and diarrhea, increased susceptibility to infectious diseases. It is necessary to clarify whether the patient has been tested for HIV and whether he has been on immunosuppressive therapy. Awareness of the dentist about the symptoms of pathology and timely initiation of treatment can prevent malignant degeneration of the epithelium in the affected area.
To make a diagnosis in dentistry, a complex of laboratory and instrumental studies is used. One of the key methods is a biopsy of the lesion with further histological analysis. There are 5 histological signs of the disease: hyperkeratosis of the upper epithelial layer, parakeratosis of the surface epithelial layer, acanthosis, minimal inflammation in epithelial and subepithelial tissues or its absence, and histologically normal basal epithelial layer. The presence of any one sign is not a sufficient criterion for the diagnosis of “hairy leukoplakia”.
During a biopsy of the mucous membrane in the sample examined by the immunohistochemical method, EBV is detected. Candida albicans is sown in smears from lesions in about a quarter of cases. Laboratory diagnosis of HIV is mandatory: PCR for the detection of virus RNA, immune blotting for the detection of antibodies to individual antigens, enzyme immunoassay for the detection of antibodies to HIV and the study of the immune status. With hairy leukoplakia, there is usually a decrease in the concentration of CD4 T-lymphocytes to 235-468 per ml. Differential diagnosis of the disease is carried out with other types of leukoplakia, oral candidiasis, hypertrophy of the papillae of the tongue, keratosis of the mucous membrane and genital warts.
If the disease occurs against the background of HIV infection, mandatory antiretroviral therapy with reverse transcriptase inhibitors (lamivudine, didanosine, zidovudine) and HIV protease inhibitors (saquinavir, nelfinavir, indinavir) is necessary. Specific immunotherapy (HIV-1-specific immunoglobulin, a mixture of monoclonal antibodies) is used to activate cellular immunity. With other immunodeficiency, immunotherapeutic treatment is also relevant. Antiviral drugs (acyclovir, valacyclovir, famciclovir) are used to suppress EBV replication. In the presence of concomitant candidiasis infection, antimycotics (ketoconazole, fluconazole, amphotericin B) are necessary.
For local treatment, keratolytic drugs are used, as well as retinoic acid preparations. In severe cases, surgical treatment is performed, in which the affected foci are excised using a laser. HIV-infected individuals are at risk of developing Burkitt’s lymphoma – non-Hodgkin’s lymphoma from B-lymphocytes, characterized by a high degree of malignancy. Such patients are referred for radiation therapy and chemotherapy. Regardless of the severity of the disease, it is recommended to give up smoking and follow a diet that excludes irritating food (hot, spicy, smoked). Hairy leukoplakia is prone to recurrent course, so the patient should undergo regular dental examinations.
Prognosis and prevention
In the absence of serious immunosuppression, the disease has a favorable prognosis. After the elimination of the irritating factor, the epithelial surface of the oral mucosa is completely restored within a month. However, therapy can only slow down the reproduction of EBV, but not eliminate it completely, therefore, with a decrease in immunity, relapses of the disease occur. The most severe course is observed in patients with HIV due to the risk of aggressive Burkitt’s lymphoma and malignant degeneration of the affected areas. To prevent the development of hairy leukoplakia, it is necessary to follow HIV infection prevention measures, maintain immunity, give up smoking and visit the dentist in a timely manner.