Two main pathophysiological pathways are currently understood to contribute to development of<unk> —human papillomavirus (HPV) infection and chronic inflammation or autoimmunity affecting the<unk>  area. HPV DNA can be found in up to 87% of<unk>  intraepithelial neoplasia (VIN) and 29% of invasive<unk> s; HPV 16 is the most commonly detected subtype in VIN and<unk> , followed by HPV 33 and HPV 18. VIN is a superficial lesion of the skin that has not invaded the basement membrane—or a pre-cancer. VIN may progress to carcinoma in situ and, eventually, squamous cell<unk> . Chronic inflammatory conditions of the<unk> that may be precursors to<unk>  include lichen sclerosus, which can predispose to differentiated VIN. Risk factors Risk factors for<unk>  are largely related to the causal pathways above, involving exposure or infection with the HPV virus and/or acquired or innate auto-immunity. * Increasing age *History of<unk>  or cervical intraepithelial neoplasia *Increased number of male sexual partners *Prior history pre-invasive or invasive cervical<unk>  * History of cigarette smoking * Infection with human immunodeficiency virus (HIV)<unk>  lichen sclerosus * Immunodeficiency syndromes * Northern European ancestry
Vulvar cancer
Lichen sclerosus
Genital ulcer
Hyperplasia
Amurca
Bartholin's cyst
Anal cancer
Atrophic vaginitis