Abstract
Condyloma acuminatum, intraepithelial neoplasia, and squamous cell carcinoma are three relatively frequent vulvar lesions. Condyloma acuminatum is induced by low risk genotypes of human papillomavirus (HPV). Vulvar intraepithelial neoplasia (VIN) and squamous cell carcinoma have different etiopathogenic pathways and are related or not with high risk HPV types. The goal of this paper is to review the main pathological and clinical features of these lesions. A special attention has been paid also to epidemiological data, pathological classification, and clinical implications of these diseases.
Highlights
Vulvar human papillomavirus (HPV) infection is responsible for the development of benign tumors, of one type of preneoplastic lesions, and of certain types of squamous cell carcinoma (SCC) [1]
Genetic mutations in TP53 [42, 43] or PTEN [44] and epigenetic alterations such as hypermethylation of the MGMT, RASSF2A, or TSP1 gene promoters [45] have frequently been detected in Differentiated VIN (dVIN) and vulvar SCC, suggesting that the alteration of these genes contributes to vulvar carcinogenesis
Differentiated/simplex Vulvar intraepithelial neoplasia (VIN) can be seen as focal discoloration, ill-defined white plaques, or discrete elevated nodules but they are typically less bulky than usual VIN (uVIN) lesions [4]
Summary
Vulvar human papillomavirus (HPV) infection is responsible for the development of benign tumors (condylomata acuminata), of one type of preneoplastic lesions, and of certain types of squamous cell carcinoma (SCC) [1]. Most of the vulvar (pre)neoplastic lesions are induced by HPV infection (most commonly HPV 16), except for the “differentiated” (simplex) type of VIN. DVIN type and non-HPV-related vulvar SCC occur commonly in elderly women [9]. Up to 20% of people with genital warts will present other STDs. The following risk factors have been described, including smoking, hormonal contraceptives, multiple sexual partners, and early coital age. Viral DNA replication in the intermediate and superficial cell layers of the squamous epithelium occurs independently of host chromosomal DNA synthesis This allows large amounts of intact virions to be formed, leading to typical morphological aspects such as “koilocytic changes.”. These two HPV types are responsible for over 90% of CA [17, 18]
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