Skin CancerCore · 7 min read

Squamous Cell Carcinoma in Situ (Bowen's Disease)

Full-thickness epidermal atypia recognized dermoscopically by clustered glomerular and dotted vessels on a salmon-pink background with surface scale.

By Dr. Yehonatan KaplanPublished Updated

In brief

Bowen's disease (cutaneous SCC in situ) sits between AK and invasive SCC on the keratinocyte cancer spectrum. Histologically, atypical keratinocytes occupy the full thickness of the epidermis but the basement membrane is intact. The lifetime progression rate to invasive SCC is approximately 3-5 percent for untreated lesions, higher in genital and immunocompromised sites and up to 30 percent in erythroplasia of Queyrat. Dermoscopic recognition is highly specific: clustered glomerular and dotted vessels arranged in regular focal aggregates on a salmon-pink to yellow-orange background, with surface scale, achieve diagnostic likelihood close to 98 percent. Pigmented Bowen's mimics melanoma and dysplastic nevi and is the variant where dermoscopy adds the most diagnostic value, especially with the recently described plumage sign.

Clinical content

01Non-pigmented Bowen's classic dermoscopic pattern: clustered glomerular vessels (tightly coiled like a renal glomerulus, slightly larger than dotted vessels) plus dotted vessels in regular focal aggregates over a salmon-pink, yellow, or orange background, with white-yellow surface scale. The combination has a published positive predictive value near 98 percent.

02Yellow opaque structures, white-yellow scale, and salmon-pink background reflect the histology: full-thickness atypia produces parakeratosis (yellow-white scale) and a tortuous dilated vascular plexus in the papillary dermis (the dotted-glomerular pattern). Vessels are arranged in well-defined clusters (focal density), unlike the diffuse irregular polymorphous pattern of invasive SCC.

03Pigmented Bowen's presents on legs, scrotum, and chronically sun-exposed sites in patients with skin types II-IV. Brown to gray dots and globules arranged in lines or in a fine network, plus a structureless brown-gray background, create an unsettling differential with melanoma, dysplastic nevi, lichen planus-like keratosis, and pigmented BCC. Surface scale and dotted/glomerular vessels remain the key clue that this is keratinocytic, not melanocytic.

04The plumage sign (Hurd JAAD 2025) describes pigment arranged like overlapping bird feathers in pigmented Bowen's. This is a recently reported clinical pearl helpful when the more standard pigmented Bowen's features are equivocal.

05Peripheral hyperkeratotic crust with a central erosion or a moist red patch is the characteristic clinical look on the lower leg in elderly women, often misdiagnosed as eczema, psoriasis, tinea, or stasis dermatitis. Persistence beyond 4-6 weeks of empiric topical steroid is a biopsy threshold.

06Transition from Bowen's to invasive SCC dermoscopically: the regular clustered dotted/glomerular vascular pattern becomes diffuse and polymorphous (loss of the focal clustering), white circles around follicles appear, central keratin develops, ulceration emerges, and induration appears clinically. Any of these in a known Bowen's lesion warrants re-biopsy with deep dermal sampling.

07Differential dermoscopic considerations: psoriasis plaques have regular dotted vessels in a uniform diffuse distribution (not clustered); discoid eczema vessels are sparser and surrounded by spongiotic background; superficial BCC shows short fine telangiectasias and shiny white-red structureless areas; irritated seborrheic keratosis (covered separately in the SCC mimics topic) shows hairpin vessels in a diffuse regular arrangement with multiple white halos.

08Treatment is dictated by lesion size, site, patient comorbidity, and field involvement. Surgical excision with PDEMA or Mohs is preferred for high-risk variants (digit, anogenital, large lesions, immunocompromised host, recurrent). Topical therapy (5-FU, imiquimod, photodynamic therapy with ALA or MAL) is appropriate for cosmetically sensitive sites, lower legs, and frail patients, accepting recurrence rates around 10-20 percent. Cryotherapy is acceptable for small discrete lesions but produces poor wound healing on the lower leg.

Key dermoscopic features

Clustered glomerular vessels
Defining feature of non-pigmented Bowen's. Tightly coiled vessel resembling a renal glomerulus, in tight focal aggregates.Multiple discrete, well-defined clusters of red coiled vessels separated by paler background.
Clustered dotted vessels
Often coexists with glomerular vessels in Bowen's. Smaller pinpoint red dots in regular focal density.Tight aggregates of regularly spaced red dots, not diffuse polymorphous.
White-yellow scale (often peripheral)
Reflects parakeratosis. Often seen at the lesion edge with central exposure of vessels.White or yellow-white surface scale, sometimes thick and crusted at periphery.
Salmon-pink to yellow-orange background
Color of vascularized tissue beneath partially keratinized atypia. Highly characteristic of Bowen's.Soft pink-orange wash interrupted by clustered vessels and scale; not the bright red of poorly differentiated invasive SCC.
Yellow opaque structures
Areas of orthokeratosis and parakeratosis without follicular plugging.Yellow homogeneous structureless zones distinct from white circles.
Brown to gray dots/globules in lines (pigmented Bowen's)
Pigment incontinence in a stippled pattern reflecting the basal/full-thickness atypical keratinocytes carrying melanin. Linear arrangement is characteristic.Multiple small brown or slate-gray dots aligned in linear, sometimes parallel, arrangements; often overlying glomerular vessels.
Plumage sign (pigmented Bowen's)
Recently described feature (Hurd 2025). Pigment arranged like overlapping bird feathers. When seen, biopsy almost always returns pigmented Bowen's.Brown pigment in radiating, slightly curved lines resembling a bird's plumage; highly suggestive of pigmented Bowen's disease.
Peripheral hyperkeratotic crust
Reflects long-standing accumulation of parakeratotic material at the lesion margin.Thick yellow-white crust around the periphery with central erythematous moist surface.
Transition signs to invasion
Loss of clustered focal vessel pattern in favor of diffuse polymorphous vessels, white circles, central keratin, ulceration. Trigger for re-biopsy.Polymorphous diffuse vessels replacing clustered glomerular pattern; white circles around follicles; ulceration; central keratin mass.

High yield clinical points15 pearls in 5 groups

Recognition & pattern analysis

3 points
1
Clustered glomerular plus dotted vessels with scale = Bowen's until proven otherwise. Cameron and Rosendahl reported this combination has a diagnostic likelihood of 98 percent for Bowen's disease (Arch Dermatol 2012).
2
Focal clustering distinguishes Bowen's vessels from invasive SCC. Bowen's vessels are arranged in well-defined focal aggregates with intervening pale background; invasive SCC shows diffuse, irregular, polymorphous distribution. This single distinction reorganizes the differential.
3
Yellow opaque structures and salmon-pink background distinguish Bowen's from psoriasis. Psoriasis plaques have a more uniform red background with diffuse regular dotted vessels and silvery (not yellow) scale.

Management & treatment

6 points
1
Bowen's lifetime invasive progression risk is roughly 3-5 percent untreated. Higher in immunocompromised hosts, anogenital sites (HPV-driven), and erythroplasia of Queyrat (up to 30 percent lifetime invasion risk). The figure is lifetime, not per-year, and is the rationale for definitive treatment of recognized lesions.
2
Topical 5-FU clearance rates are about 70-90 percent at 12 months. Imiquimod approximately 73-90 percent; PDT initial clearance 80-98 percent with durable response 48-89 percent (Morton, Salim trials). Surgery remains the gold standard for high-risk sites and recurrent disease.
3
Cryotherapy works for small discrete Bowen's but heals poorly on lower legs. Recurrence rates 1-13 percent, but ulcer healing on shins can take months. Prefer 5-FU or PDT for lower leg lesions.
4
Erythroplasia of Queyrat is glans/prepuce Bowen's. HPV-driven. Treat aggressively (Mohs or topical 5-FU/imiquimod) given proximity to functional structures and meaningful invasion risk.
5
Bowenoid papulosis is a separate entity to keep in mind. Multiple pigmented papules on the genitalia in younger sexually active patients, HPV-16 driven. Histologically resembles Bowen's but has a much lower invasion risk and may regress. Manage less aggressively, but monitor.
6
Photodynamic therapy is excellent for cosmetic field disease. Two sessions of MAL-PDT or ALA-PDT achieve 80-98 percent clearance of Bowen's with superior cosmesis vs cryotherapy or surgery; useful for face and lower leg in non-frail patients.

Pitfalls & mimics

1 point
1
Pigmented Bowen's on the leg mimics melanoma. Look for brown-gray dots in lines plus clustered glomerular vessels plus surface scale. The presence of scale on a pigmented lesion is a strong argument for keratinocytic rather than melanocytic origin.

When to biopsy

4 points
1
Suspect Bowen's on persistent eczema-like patches on the lower leg. Especially in elderly women, the lower leg Bowen's is the great impostor of eczema, psoriasis, and tinea. Biopsy any unilateral persistent scaly patch that fails 4-6 weeks of topical steroid.
2
White circles inside a Bowen's lesion herald invasion. White circles around follicles appear in invasive SCC, not in pure in-situ disease. If you see them in a lesion you have been managing as Bowen's, repeat biopsy with deep reticular dermal sampling.
3
Image-guided biopsy when surface keratin obscures dermoscopy. Gentle curettage or alcohol/saline application can clear surface scale and reveal the underlying vascular pattern, which often clarifies Bowen's vs psoriasis vs SCC.
4
Always biopsy anogenital Bowen's. HPV-driven anogenital SCC in situ has a higher invasion risk and benefits from definitive surgery (Mohs preferred) plus HPV testing and partner evaluation. Topical imiquimod is an alternative for non-surgical candidates.

Recent changes (2022 onward)

1 point
1
Plumage sign indicates pigmented Bowen's. Hurd (JAAD 2025) described feather-like radiating pigment arrangements that have a high specificity for pigmented Bowen's disease in case observations.

Lectures covering this topic4 lectures

Notable updates & conceptual milestones5 updates

Plumage sign for pigmented Bowen's

2025

Hurd (JAAD 2025) described feather-like pigment arrangements that strongly suggest pigmented Bowen's, addressing a long-standing diagnostic challenge in distinguishing pigmented Bowen's from melanoma, lichen planus-like keratosis, and dysplastic nevi.

Daylight PDT for large field Bowen's

2018-2024

Daylight-activated PDT (after MAL application) provides outpatient treatment of multiple Bowen's lesions across a cosmetic field with less pain than conventional PDT. Effectiveness comparable to conventional PDT for thinner lesions.

Combined ablative laser plus MAL-PDT

2017-2023

Erbium:YAG or fractional CO2 ablation followed by MAL-PDT improves clearance rates for hyperkeratotic Bowen's by enhancing photosensitizer penetration. Choi et al (JAMA Dermatol 2017) showed 12-month clearance significantly higher than PDT alone.

RCM and OCT for non-invasive Bowen's confirmation

2020-2025

Reflectance confocal microscopy reveals atypical honeycomb pattern through the full epidermis with intact dermal-epidermal junction. OCT confirms no breach of the DEJ. Useful for monitoring topical or PDT response without re-biopsy.

AI-augmented dermoscopic Bowen's recognition

2023-2025

Convolutional neural networks trained on dermoscopic images of Bowen's are reaching 90+ percent accuracy in distinguishing Bowen's from psoriasis, eczema, and superficial BCC, particularly useful in primary care triage.

Bottom line

Full-thickness epidermal atypia recognized dermoscopically by clustered glomerular and dotted vessels on a salmon-pink background with surface scale.

15 clinical points · 5 recent updates · 11 references

Source content

AAD 2026 · U004 · #01

Real-Time Identification and Management of Actinic Keratoses (covers SCCIS)

Drew A. Emge, MD, MSc · University of Kansas Medical Center, Kansas City, Kansas

References

Sources cited in the lecture content or that underpin the clinical points above. Verify with primary sources before practice changes.

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