Oral hairy leukoplakia is a corrugated white lesion that usually occurs on the lateral or ventral surfaces of the tongue in patients with severe immunodeficiency.The most common disease associated with oral hairy leukoplakia is HIV infection.Oral hairy leukoplakia is reported in about 25% of adults with HIV infection but is not as common in HIVinfected children. Its prevalence reaches as high as 80% in patients with acquired immunodeficiency syndrome (AIDS).
Epstein-Barr virus (EBV) is implicated as the causative agent in oral hairy leukoplakia.A positive correlation with decreasing cluster designation 4 (CD4) cell counts has been established in HIV-positive patients. The presence of this lesion has been associated with the subsequent development of AIDS in a large percentage of HIV positive patients.
Hairy leukoplakia has also occasionally been reported in patients with other immunosuppressive conditions, such as patients undergoing organ transplantation and patients undergoing prolonged steroid therapy.Rare cases may occur in immunocompetent persons after topical steroid therapy.
TYPICAL FEATURES
Oral hairy leukoplakia most commonly involves the lateral border of the tongue but may extend to the ventral or dorsal surfaces. Lesions on the tongue are usually corrugated and may have a shaggy or frayed appearance, mimicking lesions caused by tongue chewing (Figure 5-14). Oral hairy leukoplakia may also present as a plaquelike lesion and is often bilateral. Histopathologic examination of the epithelium reveals severe hyperparakeratosis with an irregular surface, acanthosis with superficial edema, and numerous koilocytic cells (virally affected
“balloon” cells) in the spinous layer. The characteristic microscopic feature is the presence of homogeneous viral nuclear inclusions with a residual rim of normal chromatin.
The definitive diagnosis can be established by demonstrating the presence of EBV through in situ hybridization, electron microscopy, or polymerase chain reaction (PCR).
DIFFERENTIAL DIAGNOSIS
The definitive diagnosis can be established by demonstrating the presence of EBV through in situ hybridization, electron microscopy, or polymerase chain reaction (PCR).
DIFFERENTIAL DIAGNOSIS
It is important to differentiate this lesion from other clinically similar entities such as hyperplastic candidiasis, idiopathic leukoplakia, leukoplakia induced by tongue chewing, tobaccoassociated leukoplakia, lichen planus, lupus erythematosus, WSN, and verrucous leukoplakia. Since oral hairy leukoplakia is considered to be highly predictive of the development of AIDS, differentiation from other lesions is critical.
TREATMENT AND PROGNOSIS
No treatment is indicated. The condition usually disappears when antiviral medications such as zidovudine, acyclovir, or gancyclovir are used in the treatment of the HIV infection and its complicating viral infections.Topical application of podophyllin resin or tretinoin has led to short-term resolution of the lesions, but relapse is often seen.The probability of patients developing AIDS was found to be 48% at 16 months and as high as 83% at 31 months after the initial diagnosis of oral hairy leukoplakia.
TREATMENT AND PROGNOSIS
No treatment is indicated. The condition usually disappears when antiviral medications such as zidovudine, acyclovir, or gancyclovir are used in the treatment of the HIV infection and its complicating viral infections.Topical application of podophyllin resin or tretinoin has led to short-term resolution of the lesions, but relapse is often seen.The probability of patients developing AIDS was found to be 48% at 16 months and as high as 83% at 31 months after the initial diagnosis of oral hairy leukoplakia.
