In the Chair: 5 Years and 4 Diagnoses

Dissecting cellulitis of the scalp is a condition that every dermatology clinician will encounter — and that patients will have already spent years trying to manage before they reach you. It is progressive, scarring, and poorly served by the treatments most likely to be tried first. It also looks like other things at first glance, which means the diagnostic clock often starts late.

This case spans 5 years in 1 patient’s life: a misdiagnosis, a correction, a cycle of partial responses and relapses, a complicating diagnosis, and finally a treatment that worked. It describes the first reported use of bimekizumab as monotherapy for dissecting cellulitis of the scalp — a dual IL-17A/F inhibitor already approved for hidradenitis suppurativa, applied here based on shared pathobiology between the 2 diseases.^1,2

Three decision points follow: recognizing DCS when it doesn’t present classically, knowing when conventional therapy has failed enough to escalate, and understanding which biologic mechanism fits this disease and why.

THE PATIENT

A 22-year-old Hispanic man first presents in May 2020 with several months of moderate focal hair loss on the scalp. Examination reveals discrete patches of alopecia and xerotic desquamating erythematous papules. He is diagnosed with alopecia areata and prescribed clobetasol 0.05% scalp solution.

At follow-up in January 2021, now under your care, he reports recurrent abscess-like lesions on the scalp that are enlarging, draining, tender, and associated with hair loss. He mentions having had similar lesions before his 2020 visit, though they were not present at the time. Examination now reveals suppurative boggy plaques on the midoccipital, right central parietal, posterior midparietal, and left central scalp.

CLINICAL DECISION POINT 1 — Establishing the Correct Diagnosis

You are looking at a young man whose scalp findings have evolved: what appeared to be alopecia areata at his last visit now presents as boggy suppurative plaques with associated hair loss and a history of draining, abscess-like lesions. He has no systemic symptoms, no relevant medical history, and no prior biopsy.

⚠️ CLINICAL CLUE

Dissecting cellulitis of the scalp primarily affects men aged 18–40, with highest prevalence in African American and Hispanic men.³ The hallmarks — painful fluctuant nodules, interconnecting sinus tracts, boggy suppurative plaques, and progressive cicatricial alopecia — localize to the vertex and occipital scalp. It is part of the follicular occlusion tetrad alongside hidradenitis suppurativa, acne conglobata, and pilonidal cysts.

📋 WHAT WOULD YOU DO?

CLINICAL DECISION POINT 2 — When Conventional Therapy Has Failed

Over the next 4 years, this patient is treated with: doxycycline 100 mg twice daily, sulfacetamide/sulfur topical cleanser, 3 rounds of intralesional triamcinolone, doxycycline 50 mg twice daily for 3 months, minocycline 100 mg twice daily, and benzoyl peroxide cleanser. Two 30-day doxycycline courses achieved complete resolution; a 30-day minocycline course achieved 75–80% improvement. But the disease returned to baseline severity between every course. Intralesional steroids produced no response. The patient has also been intermittently non-adherent, obtaining doxycycline from Mexico between clinic visits.

He returns to your care in September 2025, now 27 years old, with draining and bleeding alopecic lesions that are pruritic and painful. He describes blood staining on his clothing, car headrest, and a paper liner at the chiropractor. He has stopped going to barbers out of self-consciousness and avoids his partner touching his hair. He calls his treatment journey a discouraging cycle of intermittent therapies with no lasting relief.

📋 WHAT WOULD YOU DO?

CLINICAL DECISION POINT 3 — Which Biologic and Why

You have decided to initiate biologic therapy. Several options have published case reports in DCS: anti-TNFα agents (adalimumab), anti-IL-23 agents, IL-17A inhibitors, and JAK inhibitors. Bimekizumab, a dual IL-17A/F inhibitor approved for HS and other inflammatory conditions, has not yet been reported in DCS. The pathobiology of DCS overlaps substantially with HS, both being components of the follicular occlusion tetrad and both driven by dysregulated innate immune signaling involving IL-17, TNFα, and JAK/STAT mediators. Your patient also has concurrent acne keloidalis nuchae on the posterior inferior scalp.

⚠️ MECHANISTIC CONSIDERATION

In HS, mucosal-associated invariant T (MAIT) cells — highly concentrated in lesional skin — produce predominantly IL-17F through an IL-23-independent pathway. This may explain why HS responds well to IL-17A/F inhibition but less favorably to IL-23 inhibition. DCS shares this pathobiologic profile, suggesting the same mechanistic rationale applies.

📋 WHAT WOULD YOU DO?

CLINICAL TAKEAWAY: DISSECTING CELLULITIS OF THE SCALP — DIAGNOSIS, ESCALATION, AND BIOLOGIC SELECTION

✓ DCS primarily affects men aged 18–40, with highest prevalence in African American and Hispanic men; hallmarks are boggy suppurative plaques, draining sinuses, and progressive cicatricial alopecia on the vertex and occipital scalp

✓ DCS is part of the follicular occlusion tetrad alongside hidradenitis suppurativa, acne conglobata, and pilonidal cysts — shared pathobiology informs biologic selection

✓ Diagnosis is primarily clinical; biopsy is not required but can support staging and severity assessment

✓ Temporary clearance with antibiotics followed by reliable relapse is a pattern that indicates biologic escalation is warranted — not a reason to extend antibiotics indefinitely

✓ IL-17A/F inhibition is mechanistically preferred over anti-IL-23 in DCS and HS due to IL-23-independent MAIT cell-driven IL-17F production in FOT lesions

✓ Bimekizumab (320 mg Q2W × 16 weeks, then Q4W) produced complete lesion clearance and approximately 70% hair regrowth at 16 weeks in this case — the first reported use in DCS

✓ Concurrent AKN may share pathobiology with DCS; IL-17A/F inhibition reduced AKN pruritus and prevented new lesion formation in this patient

THE TAKEAWAY

This patient spent 5 years moving through diagnoses and treatments that provided temporary relief without ever addressing the underlying inflammatory mechanism. The alopecia areata diagnosis at his first visit was understandable — the characteristic suppurative plaques weren’t present yet. The 4 years of antibiotic cycling that followed reflected the absence of evidence-based guidelines and the tendency to exhaust conventional options before escalating. By the time he returned in 2025, the QOL data were unambiguous: bleeding onto his clothing, avoiding barbers, isolating from his partner.

The biologic selection in this case is worth understanding mechanistically, not just as a drug choice. The DCS-HS connection through the follicular occlusion tetrad is clinically actionable: when a patient has refractory DCS, the biologics with the strongest rationale are those that have already proven themselves in HS. The IL-17A/F specificity of bimekizumab — targeting both isoforms via an IL-23-independent pathway — is what separates it mechanistically from anti-IL-23 agents and single-isoform IL-17A inhibitors. That distinction matters when selecting therapy for a disease where the evidence base is almost entirely case reports.

No standardized guidelines exist for DCS. Every treatment decision is a clinical judgment call. Understanding the pathobiology well enough to make that judgment — and to recognize when the conventional approach has run its course — is what this case puts in your hands.

References

1. Seiter D. Case Report: Bimekizumab for dissecting cellulitis of the scalp. Front Immunol. 2026;17:1830178. Published 2026 May 19. doi:10.3389/fimmu.2026.1830178
2. Lau WC, Gerstein B, Lebwohl M. Treatment strategy for refractory dissecting cellulitis of the scalp using bimekizumab, isotretinoin, and oral antibiotics. J Drugs Dermatol. 2026;25(3):275-276. doi:10.36849/JDD.9259
3. Jaroonwanichkul S, Rajpara A. Dissecting cellulitis of the scalp. Kans J Med. 2024;17(6):160. doi:10.17161/kjm.vol17.22560