|Vulva — Lichen Planus|
|Lichen planus is a dermatologic condition
involving the glabrous skin, hair-bearing skin and scalp, nails, and mucous membranes of
the oral cavity, and vulva. Hair loss as well as a history of papular lesions on skin
surface (ankle, dorsal surface of the hands, and flexor surfaces of the wrists and
forearms) may be found. A symptom such as pruritus may be present. The age range is
approximately 30-60 years of age. A possible form of lichen planus, also known as
desquamative inflammatory vaginitis, is a sterile blistering or erosive skin disease that
occurs in the vagina. Diagnosis of this condition can sometimes be extremely difficult.
Severe atrophic vaginitis can be clinically difficult to distinguish.
Lichen planus is a disease of unknown etiology. There may be a role for an autoimmune disorder of cellular immunity. Additionally, the histologic features of lichen planus closely resemble those of another condition of immune origin, graft versus host disease.
Appearance ranges from white, reticulate papules/plaques, to uniform, white epithelium, to non-specific erosions (usually with surrounding white epithelium). Vaginal erythema is present which often results in bleeding. Late scarring with loss of labia minora and clitoral hood, occasionally resulting in obliteration of the vaginal space. Erosions of the buccal mucosa, gingivae, and/or tongue are usually present. Examination of the mouth may reveal a reticulated gray, lacy pattern of Wickham's striae. The mouth lesions may precede or follow by months or years the vulvovaginal lesions. About one third of those with vulvovaginal disease have not yet experienced the oral lesions. The gingival tissue may be diffusely swollen with interdental accentuation or actually eroded with red, scalloped borders at the gingival margins of the teeth. Keratinized skin involvement is present only rarely in erosive disease. In the absence of sexual activity or regular vaginal dilation, adhesions begin to form in the upper part of the vagina. In long-standing cases, the vagina may be totally obliterated. Contact bleeding and dyspareunia are often noted.
The diagnosis of erosive LP often made by finding characteristic skin lesions in mouth or skin biopsy. Within hair-bearing and keratinized epithelium, histopathology reveals a chronic inflammatory cell infiltrate, which consists predominantly of lymphocytes without plasma cells. The inflammation is lichenoid in that it involves the superficial dermis immediately beneath the epithelium, and extends into the basalar and parabasalar epithelium. Liquefaction necrosis is present within the basal epithelial cells; colloid bodies are present secondary to degeneration of keratinocytes. The interface at epidermal-dermal junction is obscured by the inflammatory infiltrate. The epithelium may have prominent acanthosis with a prominent granular layer and hyperkeratosis. In older lesions, acanthosis may be absent and the epithelium thinned with loss of the rete ridges. Ulceration and bullae may occur in severe lesions.
When lichen planus involves the nonkeratinized epithelium of the vestibule, the interface inflammatory infiltrate is present, but the inflammatory cell population may contain plasma cells within the preeminently lymphocytic infiltrate. Hyperkeratosis and a prominent granular layer usually are not present. Bullae and ulceration are evident in severe cases. In the presence of erosive disease a biopsy may be totally devoid of epithelium.
At times, immunofluorescent studies may be required to rule out other conditions in the differential diagnosis such as pemphigus or pemphigoid.
Direct immunofluorescence testing is superior for diagnosing pemphigus and pemphigoid. Immunofluorescence is slightly inferior to histologic evaluation for diagnosing lichen planus. Optimal criteria were IgG and C3 intercellular substance staining for pemphigus, linear C3 basement membrane zone deposits for pemphigoid, and shaggy fibrinogen basement membrane zone staining plus IgM cytoids for lichen planus.