Squamous cell carcinoma in situ, commonly termed Bowen's disease, represents intraepidermal malignancy with full-thickness epidermal involvement by atypical keratinocytes without invasion into dermis. This premalignant condition carries risk of progression to invasive squamous cell carcinoma (5% within 5 years, higher with extensive involvement or immunosuppression). Clinical presentation typically involves well-demarcated erythematous, scaly plaques resembling eczema or psoriasis, creating frequent diagnostic delays. Early recognition and treatment prevent progression to invasive disease and substantially reduce morbidity. Multiple treatment modalities (topical agents, surgery, phototherapy) provide excellent cure rates with appropriately selected approach based on lesion characteristics and patient factors.

Epidemiology and Etiology

Bowen's disease represents 1-5% of cutaneous malignancies. Peak incidence occurs in elderly (60-80 years). Chronic sun exposure is primary risk factor, with annual incidence increasing in lower latitudes and with cumulative lifetime UV exposure. Other risk factors include: (1) immunosuppression (30-fold increased incidence in organ transplant recipients); (2) chronic arsenic exposure (occupational, medicinal, or drinking water contamination); (3) chronic dermatologic conditions (lichen planus, psoriasis); (4) previous radiation therapy; and (5) fair skin phototype.

Human papillomavirus (HPV) association remains controversial, with variable rates of HPV detection (0-70% depending on detection methods and study population). HPV involvement may increase progression risk, particularly in immunosuppressed patients.

Clinical Presentation

Typical presentation involves solitary erythematous, scaly plaque with indistinct borders, typically 0.5-3 cm diameter (though larger lesions occur). Surface may be smooth, hyperkeratotic, or erosive. Color ranges from pink to red-brown; pigmented variants (pigmented Bowen's disease) present with brown-black coloration. Lesions are frequently asymptomatic; some patients report mild pruritus or bleeding with manipulation.

Common locations include: (1) chronically sun-exposed sites (face, ears, dorsal hands); (2) genitalia (erythroplasia of Queyrat); (3) perianal region; and (4) non-sun-exposed areas in immunosuppressed patients. Multiple synchronous lesions occur in 10-15% of cases, particularly in immunosuppressed patients with extensive field cancerization.

Diagnosis is primarily clinical; however, histopathology is essential to confirm SCC in situ diagnosis and rule out invasive SCC. Dermoscopy may aid diagnosis, showing atypical vascular patterns and pigmentation.

Histopathology

Full-thickness epidermis is replaced by atypical keratinocytes with increased nuclear-to-cytoplasmic ratio, hyperchromatism, and increased mitotic activity. Cells maintain maturation at surface (producing parakeratosis) but show significant atypia throughout epidermis. Dermal inflammatory infiltrate is variable. Critical feature distinguishing SCC in situ from invasive SCC is absence of dermal invasion; intact basement membrane separates epidermis from dermis.

Histologic variants include: (1) hyperkeratotic variant (prominent keratinization); (2) atrophic variant (thin, atrophic epidermis); (3) pigmented variant; and (4) verrucous variant.

Treatment Options

Topical Therapies: 5-Fluorouracil (5-FU) 5% cream applied twice daily for 3-8 weeks achieves 80-90% cure rate, though inflammatory response can be uncomfortable. Imiquimod 5% cream applied 3-5 times weekly for 6-16 weeks shows 75-85% efficacy with potentially better tolerability than 5-FU. Tretinoin 0.05% applied nightly shows modest efficacy (60-70%) over 12+ weeks.

Phototherapy: Photodynamic therapy (methyl aminolevulinate or aminolevulinic acid with red light activation) achieves 80-95% clearance rates with excellent cosmetic outcomes, particularly for larger lesions. Treatment requires 1-3 sessions spaced 1-3 months apart. Narrow-band UVB phototherapy (two-three times weekly for 8-12 weeks) shows 70-85% efficacy, useful for field cancerization or multiple lesions.

Surgical Intervention: Mohs micrographic surgery achieves 99% cure rate and is preferred for large lesions, recurrent disease, or cosmetically sensitive locations (face, periorbital, genitalia). Standard excision with 3-5 mm margins followed by histologic margin assessment is alternative when Mohs unavailable. Curettage and electrocautery achieves 90% cure rate for small lesions but higher recurrence (10% within 5 years) compared to other modalities.

Cryotherapy: Liquid nitrogen freezing provides 75-85% cure rate for small lesions, though less effective for large/thick lesions. Multiple freeze-thaw cycles optimize outcome.

Prognosis and Progression Risk

Untreated Bowen's disease progresses to invasive SCC in approximately 5% of cases within 5 years, with higher progression risk (15-25%) in immunosuppressed patients. Size and thickness at diagnosis influence progression risk: larger lesions and those with subclinical extension show higher progression rates. Treatment provides excellent outcomes with <5% recurrence using appropriate modalities (surgery, photodynamic therapy, topical agents).

Surveillance of treated patients includes regular dermatologic examinations (annually) and patient self-examination given elevated risk of additional primary BCC/SCC/Bowen's disease (10-15% develop second primary NMSC within 5 years).

FAQ

Q: Will Bowen's disease become cancer?
A: Yes, approximately 5% progress to invasive squamous cell carcinoma within 5 years if left untreated. Treatment is essential to prevent progression. Immunosuppressed patients have higher progression risk (15-25%).

Q: What is the best treatment for Bowen's disease?
A: Multiple effective options: Mohs surgery (99% cure), photodynamic therapy (80-95% cure), 5-FU cream (80-90% cure), imiquimod (75-85% cure). Choice depends on lesion size, location, and patient factors.

Q: Will Bowen's disease leave a scar?
A: Surgical excision may produce surgical scars depending on location and closure technique. Photodynamic therapy and topical therapies typically leave minimal scars. Cosmetic outcome depends on treatment modality selected.

Q: Can Bowen's disease come back after treatment?
A: Recurrence rates are <5% with appropriate treatment (surgery, PDT, topical therapy). However, 10-15% of patients develop new primary SCC/BCC/Bowen's elsewhere, requiring long-term surveillance.

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