Lichen sclerosus

T his lesion is characterized by thinning of the epidermis and disappearance of rete pegs, hydropic degeneration of the basal cells, superficial hyperkeratosis, and dermal fibrosis with a scant perivascular, mononuclear inflammatory cell infiltrate (Fig. 22-5). The lesions appear clinically as smooth, white plaques or papules that in time may extend and coalesce. The surface is smoothed out and sometimes resembles parchment. When the entire vulva is affected, the labia become somewhat atrophic and stiffened, and the vaginal orifice is constricted. It occurs in all age groups but is most common in postmenopausal women. It may also be encountered elsewhere on the skin. The pathogenesis is uncertain, but the presence of activated T cells in the subepithelial inflammatory infiltrate and the increased frequency of autoimmune disorders in these women suggests an autoimmune reaction may be involved. Although the lesion in lichen sclerosus is not pre-malignant by itself, women with symptomatic lichen sclerosus have a somewhat increased chance of developing squamous cell carcinoma in their lifetime.13

Squamous cell hyperplasia

Previously called hyperplastic dystrophy, or lichen simplex chronicus, squamous cell hyperplasia is a nonspecific condition resulting from rubbing or scratching of the skin to relieve pruritus. It is marked by epithelial thickening, expansion of the stratum granulosum, and significant surface hyperkeratosis. It appears clinically as an area of leukoplakia. The epithelium may show increased mitotic activity in both the stratum basalis and spinosum. Leukocytic infiltration of the dermis is sometimes pronounced. The hyperplastic epithelial changes show no atypia (see Fig. 22-5B). There is generally no increased predisposition to cancer, but suspiciously, lichen simplex chronicus is often present at the margins of established cancer of the vulva.

Benign Exophytic Lesions

Benign raised (exophytic) or wartlike conditions of the vulva may be caused by an infection or are of unknown etiology. Condyloma acuminatum, a papillomavirus-induced lesion, also called a genital wart, and syphilitic condyloma latum (described in Chapter 8) are consequences of sexually transmitted infections. Vulvar fibroepithelial polyps, or skin tags, are similar to skin tags occurring elsewhere on the skin. Vulvar squamous papillomas are benign exophytic proliferations covered by nonkeratinized squamous epithelium, which develop on vulvar mucosal surfaces and may be single or numerous (vulvar papillomatosis). The etiology of fibroepithelial polyps and squamous papillomas is unknown; however, these lesions are not related to any known infectious agent.

Condyloma acuminatum

Condylomata acuminata are sexually transmitted, benign lesions that have a distinct verrucous gross appearance (Fig. 22-6A). Although they may be solitary, they are more frequently multifocal: they may involve vulvar, perineal, and perianal regions as well as the vagina and, less commonly, the cervix. The lesions are identical to those found on the penis and around the anus in males (Chapter 21). On histologic examination, they consist of branching, treelike cores of stroma covered by squamous epithelium with characteristic viral cytopathic changes referred to as koilocytic atypia (Fig. 22-6B). Condylomata acuminata are caused by low oncogenic risk HPVs, principally types 6 and 11, and represent productive viral infection in which HPV replicates in the squamous cells. The virus life cycle is completed in the mature superficial cells, resulting in distinct cytologic changes-koilocytotic atypia-characterized by nuclear enlargement and atypia as well as a cytoplasmic perinuclear halo (see also "Cervix"). Condylomata acuminata are not considered precancerous lesions.

Squamous Neoplastic Lesions