Traction Alopecia — Viva

Q1: Definition and the single most important intervention (2 min)

Q: Define traction alopecia in one sentence. What is the single most important intervention?

A: Traction alopecia is a form of mechanical — and eventually scarring — hair loss caused by sustained or repeated tension on hair roots from tight hairstyles, headwear, or occupational load. The single most important intervention is to discontinue the traction-inducing hairstyle; every other treatment is an adjunct layered on top of this.

Q2: Pathophysiology and the biphasic model (3 min)

Q: Describe the mechanical cascade. Why is the hairline most vulnerable?

A: Tension → follicular microtrauma → perifollicular inflammation → trichomalacia + follicular miniaturisation → perifollicular fibrosis → permanent loss of follicular ostia (scarring). The hairline is most vulnerable because marginal follicles are smaller, more superficially anchored to the galea, and bear the highest load when the hair is pulled back. The arrector pili and bulge (the follicular stem-cell niche) sit at the isthmus, and chronic traction at this level preferentially destroys the bulge, abolishing the follicle's regenerative capacity.

Q3: The 'fringe sign' (2 min)

Q: What is the 'fringe sign'? Who described it, and what is its clinical significance?

A: The fringe sign is a band of retained short, often vellus, hairs along the frontal and/or temporal rim, with thinning immediately behind it. It was described by Samrao, Price, Zedek, and Mirmirani in 2011 in Dermatology Online Journal as a sensitive and specific marker of marginal traction alopecia, useful when the hairstyle history is remote or not disclosed. Histology of the fringe shows retained sebaceous glands, decreased terminal hairs, increased vellus hairs, and fibrotic tracts — the follicles are miniaturised but not yet destroyed. The fringe therefore represents the last recoverable follicles and a clinical imperative to stop the traction immediately.

Q4: Differential diagnosis (3 min)

Q: Distinguish traction alopecia from trichotillomania, frontal fibrosing alopecia, and central centrifugal cicatricial alopecia (CCCA).

A:

• Trichotillomania — irregular patches of broken hairs of VARYING LENGTHS ('Friar Tuck' or 'tonsure' sign), psychiatric comorbidity, history of PULLING, not styling.
• Frontal fibrosing alopecia (FFA) — POST-MENOPAUSAL women, EYEBROW loss, perifollicular erythema, lymphocytic scarring, NO hairstyle history, lichenoid infiltrate at the isthmus.
• CCCA — vertex-centred scarring, may be on the SAME SPECTRUM as chronic traction alopecia in women of African descent; perifollicular fibrosis at the isthmus with premature desquamation of the inner root sheath; chemical + mechanical injury history.
• Alopecia areata — sudden patchy hair loss, EXCLAMATION-MARK hairs, non-scarring, autoimmune.

Q5: Trichoscopy and histopathology (2 min)

Q: What are the trichoscopy and histopathology findings in late, scarring traction alopecia?

A:

• Trichoscopy — loss of follicular openings (the diagnostic sign of scarring), peripilar white halos, white patches (fibrosis), pauci-follicular units (PFU), vellus hairs only.
• Histopathology (active marginal biopsy, NOT scarred centre) — trichomalacia (distorted, kinked, pigmented hair shafts within the follicular canal), perifollicular fibrosis at the isthmus, premature desquamation of the inner root sheath, reduced terminal-to-villus ratio, fibrous tracts, preserved sebaceous glands in the fringe.

Q6: Stepwise management (3 min)

Q: Outline the stepwise management of a patient with early, reversible traction alopecia. What about a patient with late, scarring disease who wants transplantation?

A:

• Early disease — Step 1: STOP THE TRACTION (loose styles, no chemicals, satin sleep cap). Step 2: treat inflammation with topical corticosteroid lotion (mometasone 0.1% or betamethasone 0.05%) or intralesional triamcinolone 2.5–5 mg/mL into the active margin. Step 3: topical minoxidil 2% (or 5%) twice daily for ≥ 6–12 months. Step 4: treat folliculitis (flucloxacillin 500 mg QDS × 7 days, or doxycycline for chronic disease). Step 5: prevention and follow-up.
• Late disease / transplantation — disease must be BURNT-OUT (no active inflammation for ≥ 12 months); occipital donor must be intact (no CCCA); patient must have realistic expectations. FUE or FUT from the occipital donor; 1500–3000 grafts per session; 70–90% graft survival at 12 months in experienced hands. Cosmetic camouflage (wigs, hairpieces, scalp micropigmentation) in the interim.

Q7: Special populations and regional differences (2 min)

Q: Name four populations at special risk and the hairstyle/headwear that drives their disease.

A: (1) Sub-Saharan African women and girls — tight braids, weaves, extensions, chemical relaxers (the highest-risk pattern). (2) Sikh men — submandibular or beard patch from the turban knot. (3) Ballet dancers — temporal rim band from the classical ballet bun. (4) Athletes (wrestlers, swimmers, cyclists, footballers) — occipital or temporal loss from headgear. (5) Hijab wearers — occipital pressure alopecia from tight underscarves. (6) Children — first onset in primary school when braids are first applied.

Q8: Complications and pitfalls (2 min)

Q: What are the disease and management complications? What is the cardinal diagnostic pitfall?

A:

• Disease complications — secondary bacterial folliculitis (Staphylococcus aureus), dissecting cellulitis of the scalp in chronic disease, permanent scarring alopecia, psychosocial distress (anxiety, depression, body-image disturbance).

• Cardinal diagnostic pitfall — misdiagnosis as alopecia areata or trichotillomania, leading to inappropriate immunosuppression or psychiatric referral. The hairstyle history is the single most diagnostic piece of information.
• Management pitfalls — transplanting into active disease (graft failure), transplanting from an occiput affected by CCCA (donor failure), prescribing minoxidil in pregnancy or breastfeeding, failing to address the hairstyle and chemical practices (recurrence after any treatment).