Cicatricial alopecia — Viva

Q1: Definition and classification (2 min)

Question: Define cicatricial alopecia and classify it.

Model answer: Cicatricial alopecia is permanent hair loss caused by destruction of hair follicles and replacement by fibrous scar tissue. The hallmark is loss of follicular ostia. It is divided into primary (inflammation targets the follicle itself) and secondary (external injury such as burns, radiation, infection or tumours). The North American Hair Research Society (NAHRS) classifies primary cases by the predominant inflammatory infiltrate on biopsy as lymphocytic (LPP, FFA, DLE, CCCA, pseudopelade of Brocq), neutrophilic (folliculitis decalvans, dissecting cellulitis) or mixed (acne keloidalis nuchae, erosive pustular dermatosis).

Q2: Clinical examination and distinguishing features (3 min)

Question: How do you distinguish scarring from non-scarring alopecia at the bedside, and what are the specific signs of LPP, FFA, folliculitis decalvans and CCCA?

Model answer: Scarring alopecia has loss of follicular ostia — the skin is smooth, shiny and atrophic, whereas non-scarring alopecia preserves follicular openings. Specific signs include:

• LPP: perifollicular erythema and perifollicular hyperkeratosis (white scale around follicles).
• FFA: frontal-temporal hairline recession with the lonely hair sign and eyebrow loss.
• Folliculitis decalvans: pustules, crusting and tufted hairs (doll's hair).
• CCCA: vertex/crown hair loss that expands centrifugally, most common in women of African ancestry.
• DLE: discoid plaques with the carpet-tack sign and follicular plugging.

Q3: Investigations (2 min)

Question: What investigations are used in suspected cicatricial alopecia?

Model answer: First-line is trichoscopy, which shows loss of follicular openings and subtype-specific patterns. Scalp biopsy from the active inflammatory margin is the gold standard for diagnosis and classification. Swab pustules for bacterial culture, including Staphylococcus aureus, and take KOH/culture if tinea is suspected. In DLE, perform autoimmune screening (ANA, anti-dsDNA, complements, FBC, renal function, urinalysis). Baseline photographs are essential for monitoring.

Q4: Management (3 min)

Question: Outline the management of lymphocytic and neutrophilic cicatricial alopecia.

Model answer: For lymphocytic disease use potent topical corticosteroids, intralesional triamcinolone and hydroxychloroquine; add doxycycline, mycophenolate, pioglitazone or JAK inhibitors for refractory disease. For FFA, add a 5-alpha-reductase inhibitor. For neutrophilic disease, use antistaphylococcal therapy: the classic regimen is rifampicin 300 mg twice daily plus clindamycin 300 mg twice daily for 10–12 weeks, with maintenance doxycycline or macrolides. For dissecting cellulitis, isotretinoin is first-line, with TNF inhibitors for refractory cases. Surgery and hair transplantation are reserved for stable, burnt-out disease.

Q5: Complications, prognosis and counselling (2 min)

Question: What is the prognosis, and what must you tell the patient?

Model answer: Established scar is permanent; destroyed follicles cannot regrow hair. The goal of treatment is to stop inflammation and preserve remaining hair. Early treatment improves the chance of halting progression. Complications include psychosocial distress, secondary infection, and keloid formation; long-standing scarring lesions warrant ongoing surveillance for secondary change. Patients need realistic expectations, trigger avoidance, regular follow-up and photographs to monitor progression.^[2]