Bowenoid papulosis is considered to be a special variant of squamous cell carcinoma (SCC) in situ that is caused by the human papillomavirus (HPV) and is located predominantly in the genital region, particularly on the penile shaft. As with other HPV-induced genital skin cancers, HPV 16, 18, 31, and 33 are the more common viral types, although many other subtypes have been found in these lesions. Bowenoid papulosis is considered by some to be a precancerous lesion with a low risk of developing invasive properties and by others as a true SCC in situ. This lesion does have a low risk of invasive transformation; if it is treated, the prognosis is excellent. It is believed that approximately 1% of all bowenoid papulosis lesions will develop into invasive SCC.
Clinical Findings: Bowenoid papulosis is most commonly found in men in the third through sixth decades of life. There is no racial preference. It is believed to be more common in patients who have had multiple sexual partners because of their increased risk for exposure to HPV. It is too soon to determine whether vaccination against HPV has resulted in any changes in the incidence of bowenoid papulosis. The lesions are most common in males on the shaft of the penis and in females on the vulva. They are typically well-circumscribed, slightly hyperpigmented macules and papules that occasionally coalesce into larger plaques. Minimal surface change is noted. They are often found in association with genital warts and can be difficult to distinguish from small genital warts. The cause of bowenoid papulosis is thought to be transformation of the keratinocyte caused by HPV, and therefore lesions of bowenoid shed HPV and are contagious.
The lesions are rarely symptomatic and are usually brought to a physician’s attention because of the patient’s concern for genital warts. For undefined reasons, circumcision appears to help prevent penile cancer. It has been theorized that the uncircumcised male is at higher risk for penile carcinoma because of retention of smegma and chronic maceration, which can provide a portal for HPV infection, in conjunction with chronic low-grade inflammation.
Pathogenesis: Almost all lesions of bowenoid papulosis have evidence of HPV. HPV subtype 16 is by far the most predominant HPV type found in bowenoid papulosis. Cells of the genital region that are chronically infected with HPV express various proteins that are critical in the transformation into cancer. The best-studied HPV oncoproteins, the E6 and E7 proteins, can disrupt normal cell signaling in the p16 (TP16) and retinoblastoma (RB) pathways. This disruption can lead to a loss of control of cell signaling and loss of normal apoptosis. These alterations eventually result in loss of the normal cell processes and the development of cancer.
Histology: The histology is almost the same as that of SCC in situ. There is full-thickness atypia of the epidermis with involvement of the adnexal structures and a well-intact basement membrane zone. Varying amounts of epidermal acanthosis and hyperkeratosis are seen. The cells are often enlarged and pleomorphic with visible mitoses. Evidence of HPV infection is almost universally seen as cells mimicking vacuolated koilocyte cells. Special techniques such as polymerase chain reaction (PCR) can be used to look for HPV subtyping.
Treatment: After biopsy has ruled out an invasive component to this tumor, the main treatment of bowenoid papulosis is to clinically remove the areas of involvement. The importance of decreasing HPV transmission to the patient’s sexual partners must be addressed. Condoms should be used at all times to help decrease the risk of transmission. Topical therapy with 5-fluorouracil or imiquimod has been advocated as the first-line therapy. Surgical treatment with electrocautery, cryotherapy, or laser ablation has also been reported to be successful. Both patients and their sexual partners should be seen for routine follow-up examinations.