01OverviewDefinition, clinical context and the essential points that orientate the chapter.
Bowen disease remains confined to epidermis but is malignant. Record duration, growth, symptoms, previous treatments, immune state and carcinogen exposure. Examine the full plaque for a focal nodule or ulcer and the surrounding field for other cancers. A chronic scaly plaque repeatedly labelled eczema deserves histology when it remains solitary and treatment resistant.
Treatment balances cure with healing. Excision provides complete histology and is useful where invasion is possible. Curettage, cryotherapy, photodynamic therapy and topical 5-fluorouracil can treat selected in-situ lesions. Lower-leg skin with venous disease may tolerate non-surgical care better, yet large or recurrent plaques may still require specialist surgery.
Field reactions need anticipatory counselling. Fluorouracil is applied to a precisely mapped lesion and expected to cause erythema and erosion. The clinical endpoint is durable clearance after healing, not maximal inflammation. New firmness or ulceration during or after therapy needs review for previously unrecognised invasion.
Key points
- Bowen disease is SCC in situ: a persistent, slowly enlarging, well-demarcated scaly or crusted plaque, commonly on sun-exposed lower legs.
- Colour may be pink-red, violaceous or brown and is less reliable than persistent single-site scale and edge definition across skin tones.
- Biopsy when diagnosis is uncertain and whenever pain, induration, ulceration, bleeding or treatment resistance suggests invasion.
- Treatment options include excision, curettage and cautery, cryotherapy, photodynamic therapy and topical 5-fluorouracil; imiquimod is often off label.
- Choice depends on size, site, number, border, circulation, healing capacity, immune state, pathology and patient preference.
- Lower-leg lesions require vascular and oedema assessment because destructive or surgical wounds may heal slowly.
- A genital or periungual lesion needs specialist assessment for HPV association, functional anatomy and alternative malignancy.
- After treatment, review for clinical clearance and biopsy a persistent thick or ulcerated focus instead of repeating empirical therapy.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Ultraviolet damage
Cumulative ultraviolet injury is the principal driver on exposed lower legs, head, neck and hands, reflecting broader field cancerisation.
Immune suppression
Solid-organ transplantation, haematological malignancy and sustained immunosuppressive therapy increase lesion multiplicity, treatment recurrence and invasive progression risk.
Human papillomavirus
Oncogenic HPV contributes particularly to genital, periungual and selected non-sun-exposed lesions and changes their sexual-health and immune context.
Other carcinogens
Previous arsenic exposure, therapeutic radiotherapy, chronic skin injury and inherited genetic susceptibility account for a minority of presentations.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Full-thickness epidermal dysplasia
Atypical keratinocytes occupy the entire epidermis but remain above the basement membrane, defining SCC in situ.
- 2Slow lateral expansion
Dysplastic clones spread across epidermis, producing a persistent sharply demarcated scaly plaque that enlarges over months or years.
- 3Surface keratin and inflammation
Disordered maturation creates crust and scale, while inflammation causes itch and variable red, violaceous or brown colour.
- 4Invasive transformation
Basement-membrane breach creates dermal SCC, often signalled by focal thickening, pain, ulceration, bleeding or accelerated growth.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
A sharply demarcated irregular plaque remains at one site and enlarges slowly despite routine eczema care.
Scale, crust and shallow erosion vary across the lesion while the border remains clinically definable.
Brown or black in-situ SCC can mimic melanoma or pigmented BCC and requires dermoscopic and histological assessment.
A new firm nodule, pain, ulcer, spontaneous bleeding or rapid growth within the plaque suggests SCC invasion.
Genital, nail-unit, lip or ear disease has diagnostic, functional and HPV-related complexity needing specialist care.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Punch or incisional biopsyFirst step - Why
- Confirm full-thickness epidermal dysplasia and assess possible invasion.
- Interpretation and limitations
- Target the thickest, firmest or ulcerated area and include dermis; a superficial scale sample cannot exclude SCC.
- 02
Dermoscopy - Why
- Support recognition and distinguish vascular, keratin and pigment patterns from common mimics.
- Interpretation and limitations
- Dotted or glomerular vessels may support Bowen disease but histology determines invasion.
- 03
Vascular and oedema assessment - Why
- Predict healing risk before lower-leg surgery or destructive treatment.
- Interpretation and limitations
- Assess pulses and symptoms and use ABPI when compression or arterial uncertainty makes it relevant.
- 04
Histological margin review - Why
- Confirm clearance after excision and identify occult invasive disease.
- Interpretation and limitations
- Involved margins, invasion or aggressive features return to the skin-cancer multidisciplinary pathway.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Eczema
Dermatitis is often multiple, itchy, less sharply fixed and responsive to appropriate corticosteroid, while Bowen persists at one site.
Psoriasis
Symmetrical plaques, scalp or extensor disease and nail pitting support psoriasis, though an isolated resistant plaque needs biopsy.
Superficial basal-cell carcinoma
A thin superficial BCC may have a thread-like pearly edge and dermoscopic arborising vessels or pigmented leaf-like structures.
Invasive SCC
New induration, a growing nodule, pain, ulceration or spontaneous bleeding suggests dermal invasion and changes urgency and treatment.
Tinea corporis
An advancing scaly edge and central clearing supports dermatophyte infection; scraping can prevent steroid or cancer-treatment error.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01Confirmed suitable in-situ lesionSelect site-conscious treatmentFirst stepHistology or confident specialist assessment confirms Bowen disease without invasive warning.+
- 1Assess size, site, border, circulation, healing, immune state and the patient’s priorities.
- 2Choose excision, curettage, cryotherapy, photodynamic therapy or a mapped topical course according to local expertise.
- 3Review after healing for complete clinical clearance and provide long-term skin-cancer awareness advice.
02Possible invasionBiopsy the changing focusPain, induration, nodule, ulceration, bleeding or accelerated growth appears.+
- 1Stop empirical field treatment and document the suspicious focus, nodes and immune state.
- 2Arrange urgent adequate-depth biopsy or excision and route invasive SCC through the cancer pathway.
- 3Use pathology to plan margins, nodal assessment and follow-up rather than assuming the whole plaque remains in situ.
03Persistent or recurrent diseaseReconfirm before retreatingA plaque does not clear or returns after an appropriate course.+
- 1AlternativeVerify treatment field and adherence and examine for invasion, contact reaction and an alternative diagnosis.
- 2Biopsy the most suspicious residual area and retrieve prior pathology.
- 3EscalationEscalate to excision, margin-controlled surgery or another specialist modality based on site and updated histology.
Key medicines and prescribing safety1 treatment · regimens, roles and cautions+
Fluorouracil 5% cream
Apply a thin layer once or twice daily to the precisely mapped lesion for three to four weeks or according to specialist site-specific instructions.Avoid pregnancy, eyes and mucosa; expected inflammation can be severe, and induration, infection, excessive ulceration or non-response requires review rather than automatic extension.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Invasive SCC
A minority of lesions progress through the basement membrane and acquire clinically important local destructive and metastatic potential.
Recurrence
Large, poorly defined, immune-suppression-associated or incompletely treated plaques can return after apparent clearance and may conceal invasive foci.
Treatment ulceration
Lower-leg surgery, cryotherapy and field inflammation can heal slowly where oedema or arterial disease impairs repair.
Multiple keratinocyte cancers
Bowen disease marks substantial cumulative carcinogenic exposure and predicts further actinic keratoses, invasive SCC and basal-cell carcinoma.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Review topical-treatment inflammation when clinically needed and assess clearance only after epithelial healing.
- Palpate treated skin for residual induration and biopsy persistent scale, nodule or ulcer.
- Monitor lower-leg wounds closely where venous oedema, diabetes or arterial disease delays repair.
- Continue whole-skin surveillance proportional to immune state, field damage and previous cancers.
- Safety-net new pain, bleeding, rapid growth or a regional node for urgent reassessment.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
In situ is still cancer
Basement membrane containment removes metastatic capability but not the need for definitive treatment and follow-up.
One eczema patch deserves thought
A solitary fixed treatment-resistant plaque is less typical of ordinary relapsing dermatitis and may need biopsy.
Lower legs heal differently
Venous oedema and limited arterial supply can make an otherwise simple destructive treatment produce a chronic wound.
Thickness changes urgency
A new indurated focus within a flat plaque is more concerning than widespread stable surface scale.
11Common pitfallsFrequent interpretation and management errors.
- 01
Prescribing repeated topical steroid for one persistent scaly plaque without securing diagnosis.
- 02
Using superficial biopsy and failing to sample an indurated focus deeply enough for invasion.
- 03
Choosing lower-leg surgery without assessing vascular and oedema-related healing risk.
- 04
Assuming a vigorous fluorouracil reaction proves histological clearance.
- 05
Retreating a recurrent ulcerated plaque without excluding invasive SCC.