Bowen’s disease is a variant of cutaneous squamous cell carcinoma (SCC) in situ that occurs on non–sun-exposed regions of the body. That strict definition is not always followed, and the term Bowen’s disease is often used interchangeably with squamous cell carcinoma in situ. SCC in situ is often derived from its precursor lesion, the actinic keratosis. Actinic keratosis is differentiated from SCC in situ and Bowen’s disease by its lack of full-thickness keratinocyte atypia, which is the hallmark of Bowen’s disease and SCC in situ.
Clinical Findings: Bowen’s disease can occur on hair-bearing and non–hair-bearing skin, and the clinical appearance in various locations can be entirely different. Bowen’s disease on hair-bearing skin often starts as a pink to red, well-demarcated patch with adherent scale. Women are most commonly affected, and it occurs later in life. Multiple lesions can occur, but it is far more common to see this as a solitary finding. Erythroplasia of Queyrat is a regional variant of Bowen’s disease that occurs on the glans penis. These lesions tend to be glistening red with crusting. The area is often well circumscribed. The diagnosis is often delayed because the lesion is easily confused with dermatitis, psoriasis, and cutaneous fungal infections. A biopsy should be performed on any nonhealing lesion or rash in the genital region. It has been estimated that up to 5% of untreated Bowen’s disease lesions will eventually develop an invasive component.
The relationship between Bowen’s disease and inter- nal malignancy has come under scrutiny; if it exists at all, it is likely a consequence of the use of arsenic in the past. Patients with a history of arsenic ingestion are at a higher risk of developing Bowen’s disease and internal malignancy. Now that arsenic exposure is limited in most developed countries, the association between Bowen’s disease and internal malignancy is thought to be unlikely.
Most SCCs in situ are found on sun-exposed areas of the skin and develop directly from an adjacent actinic keratosis. Some SCCs in situ eventually develop into an invasive form of SCC. This is clinically evident by increased thickness, bleeding, and pain associated with the lesion.
Pathogenesis: Exposure to arsenic and other carcino- gens has been implicated in the development of Bowen’s disease. Certainly, ultraviolet radiation and other forms of radiation play a role in the its pathogenesis. Human papillomavirus (HPV) has been implicated in causing many forms of SCC. The oncogenic viral types 16, 18, 31, and 33 are notorious for causing mutagenesis and malignancy in cervical and some other genital SCCs. HPV vaccines may decrease the incidence of these tumors dramatically in the future. HPV can cause cellular transformations to occur and is directly responsible for tumorigenesis.
Histology: Bowen’s disease shows full-thickness atypia of the keratinocytes within the epidermis. No dermal invasion is present. The underlying dermis may show a lymphocytic perivascular infiltrate. The atypia of the keratinocytes extends down to involve the hair follicle epithelium, and care must be taken when evaluating these lesions histologically not to mistake this finding for dermal invasion. Various amounts of cellular atypia are present.
Treatment: Treatments can be divided into surgical and nonsurgical forms. The choice depends on various factors, most importantly the location and size of the lesion. Some tumors are best treat d surgically, whereas others are best treated medically.
Simple excision or electrodessication and curettage are highly effective treatments. Cryotherapy is another destructive method that can be selectively used with good success. Medical therapies include the application of 5-fluorouracil, imiquimod, or 5-aminolevulinic acid followed by exposure to blue light. These all have been reported to be successful. The risk of recurrence is between 3 and 10% depending on the type of therapy used.