Frontal fibrosing alopecia (FFA): background and latest understanding

Frontal fibrosing alopecia is a primary scarring (cicatricial) alopecia that typically presents with progressive recession of the frontal and temporoparietal hairline and frequent eyebrow loss. Kossard first delineated FFA in 1994 as a patterned variant of lichen planopilaris (LPP). Since then, case series and cohort studies from multiple regions have shown a steady rise in recognition and diagnosis, transforming FFA from a clinical curiosity into one of the most commonly encountered cicatricial alopecias in specialist hair clinics. Although most patients are post-menopausal women, the disease also affects pre-menopausal women and men.

Epidemiology and who is affected: The true population prevalence remains uncertain because many studies are clinic-based. Nevertheless, large multicentre cohorts and regional series agree that FFA predominantly affects women in mid- to later life; men present less often but may show prominent facial involvement (e.g., papules) and similar scalp patterns. The disease has been reported in all skin phototypes. Recent overviews also emphasize that FFA is a generalized process for some patients, with loss of body hair, facial papules, and peri-facial pigmentary changes alongside scalp recession.

Clinical spectrum and dermoscopy: Typical complaints include an “itchy, tight” hairline and a slowly enlarging, shiny band of hair loss anteriorly that may serrate into the forehead. Trichoscopy (dermoscopy of hair and scalp) is invaluable: the most consistent signs are perifollicular erythema, perifollicular hyperkeratosis (“peripilar casts”), disappearance of follicular openings, absence of vellus hairs at the hairline, and the “lonely hair sign” (solitary terminal hairs ahead of the recession line). Eyebrow involvement is common and may show broken hairs, dots, and reduced follicular openings rather than prominent perifollicular erythema. Depressed or prominent forehead veins—thought to reflect cutaneous atrophy—have been described as a helpful, if under-recognized, clinical clue.

Pathology: Scalp biopsy from an active margin typically shows a lichenoid lymphocytic perifolliculitis centered on the follicular infundibulum-isthmus (including the stem cell–rich bulge), with concentric perifollicular lamellar fibrosis and eventual loss of follicular structures. Importantly, similar microscopic changes may sometimes be detected in clinically less-affected scalp, supporting the view that FFA can be a broader inflammatory process rather than a purely marginal phenomenon.

Pathogenesis: what do we know now: The current model integrates autoimmunity, genetic predisposition, and environmental exposures:

• Genetics. A landmark genome-wide association study identified four risk loci (2p22.2, 6p21.1, 8q24.22, and 15q2.1). Fine-mapping implicated HLA-B*07:02 at 6p21.1 and a missense variant in CYP1B1 at 2p22.1, a xenobiotic- and hormone-metabolizing enzyme. These data support roles for antigen presentation and endocrine/xenobiotic pathways in disease susceptibility.
• Immunology and inflammation. Conceptually, FFA is part of the LPP spectrum, with loss of follicular immune privilege and a cytotoxic T-cell–mediated attack on the upper follicle. Reviews emphasize overlapping contributions from innate/adaptive immunity, neurogenic inflammation, and fibroblast activation culminating in scarring.
• Environment and leave-on products. A 2016 questionnaire study reported an association between FFA and use of sunscreens/leave-on facial products, sparking debate about photoprotective ingredients and potential hapten exposure. Subsequent reviews and analyses confirm higher reported sunscreen use among patients but do not establish causality; professional groups advise continuing sensible photoprotection while acknowledging the uncertainty.

Taken together, the emerging picture is of a genetically primed immune dysregulation in which poorly defined environmental exposures may modulate risk and phenotype.

Differential diagnosis and co-existence with other disorders: FFA can mimic or coexist with androgenetic alopecia (female pattern hair loss), traction alopecia, alopecia areata incognito, and other scarring alopecias (discoid lupus erythematosus, folliculitis decalvans, classic LPP). Dermoscopy and biopsy help distinguish these entities. Recognizing FFA-specific signs (loss of vellus hairs at the hairline, peripilar casts, lonely hairs, eyebrow involvement) is essential to avoid mislabelling as a non-scarring pattern alopecia.

Work-up and monitoring: Best practice includes targeted history (tempo, symptoms, hair-care exposures, autoimmune background), examination of scalp margins, eyebrows, sideburns, and body hair, trichoscopy documentation, and—when the diagnosis is uncertain or disease is early/atypical—punch biopsy taken tangential to the active border. Serial standardized photographs and dermoscopic scoring of perifollicular erythema and hyperkeratosis help track response to therapy.

Natural history: Progression varies. Many patients have slow, stepwise recession over years; others show periods of quiescence punctuated by flares. Symptoms (itch, trichodynia/pain sensations) and trichoscopic inflammation correlate imperfectly with imminent hairline movement, so both patient-reported activity and objective measurements are useful.

Treatment goals and evidence: FFA causes permanent follicular destruction; therefore, the primary goals are to halt progression, reduce symptoms and inflammation, and optimize restoration of hair regrowth (including eyebrows). Evidence is largely retrospective and heterogeneous, but several themes have emerged.

• Topical/intralesional corticosteroids. Widely used first-line to quiet perifollicular inflammation. Intralesional triamcinolone at the active margin has shown meaningful disease stabilization in cohorts; it is often combined with systemic agents. Eyebrows may respond particularly well to low-dose intralesional corticosteroids.
• Antimalarials (hydroxychloroquine). Frequently used steroid-sparing therapy. Response rates vary across series (from modest to meaningful stabilization), and onset is typically delayed (3–6 months). Ocular safety monitoring is required.
• Tetracyclines (e.g., doxycycline) and calcineurin inhibitors are sometimes employed for their anti-inflammatory effects, particularly in sensitive facial skin, but controlled data are limited.
• 5-α-reductase inhibitors (5-ARIs). Among systemic options, dutasteride has the most consistent real-world signal: a large multicentre practice study reported dose-dependent superiority over other systemic treatments for achieving stabilization and improvement. Subsequent analyses and 2024 updates support considering dutasteride as a leading systemic option for many patients, with individualized counselling regarding risks and reproductive planning. Finasteride is also used, particularly where dutasteride is unsuitable.
• Oral retinoids (isotretinoin/alitretinoin). Especially useful for facial papules (believed to reflect vellus follicle involvement), with multiple series and reviews noting improvement; they may also aid scalp disease in some cases. Methotrexate, mycophenolate mofetil, and cyclosporine are reserved for refractory disease; pooled analyses suggest variable efficacy and the need for careful monitoring.
• Janus kinase (JAK) inhibitors. Interest in JAK inhibition is rising based on pathophysiologic overlap with other lymphocytic alopecias. Early reports include small case series using topical ruxolitinib and oral JAK inhibitors in refractory FFA/LPP, with some patients achieving symptomatic and trichoscopic improvement. High-quality controlled trials are still lacking; current use is off-label and best confined to specialist care with shared decision-making.

Adjunctive measures and hair-care: Topical minoxidil is often added for any coexisting patterned hair loss and to maximize the caliber of remaining follicles, though it does not treat the scarring process itself. Gentle hair-care, avoidance of tractional styles, and sun-safe behaviour are sensible. Regarding the sunscreen debate, multiple reviews conclude that, while patients with FFA report higher sunscreen use, causality has not been proven; discontinuing photoprotection is not recommended. Consider fragrance-free, simple formulations if patients are concerned or patch-test positive to specific ingredients.

Eyebrows and facial features: Eyebrow loss is both diagnostically helpful and a major quality-of-life issue. Options include cautious intralesional corticosteroids, off-label bimatoprost, retinoids for associated facial papules, and cosmetic solutions (microblading/PMU by experienced practitioners, with infection/Koebnerization risks discussed). Some series suggest eyebrow regrowth is achievable in a subset when inflammation is controlled early.

Surgery and hair transplantation: Grafting into previously affected hairlines carries a risk of disease reactivation and variable long-term survival. A 2025 international expert statement advises that transplantation be considered only after prolonged inactivity (commonly more than 24 months by clinical and trichoscopic criteria) and continued medical maintenance, with meticulous patient selection and counselling.

Men and pre-menopausal disease: Men may show similar scalp patterns and a higher prevalence of facial papules; the therapeutic principles are the same, with particular attention to counselling around 5-ARIs and retinoids. Pre-menopausal women require contraceptive planning for teratogenic agents (5-ARIs, retinoids) and tailored risk-benefit discussions.

Comorbidities: Associations with thyroid disease and other autoimmune conditions have been variably reported across LPP/FFA cohorts; routine broad screening is not universally recommended, but a low threshold to test thyroid function based on symptoms or history is reasonable.

Where the field is heading: Mechanistic work continues to refine the genetics and antigen-presentation pathways underlying FFA, with recent meta-analysis pointing to interactions in peptide trimming and HLA presentation that may shape risk. Therapeutically, small studies of JAK inhibition and prospective evaluations of dutasteride and intralesional regimens are under way; international expert groups have begun to issue consensus positions on treatment principles and procedural timing.

Key take-aways: for both patients and clinicians.

• FFA is a lymphocytic scarring alopecia most often affecting the frontal/temporal hairline and eyebrows; men and younger women can also be affected. Early recognition using trichoscopy is crucial.
• Histology and genetics support an autoimmune, antigen-presentation–linked process with contributions from xenobiotic/endocrine metabolism; environmental triggers are likely but remain unproven.
• Treatment focuses on halting progression: intralesional/topical corticosteroids plus a systemic agent (often hydroxychloroquine or a 5-ARI such as dutasteride) form the backbone; retinoids help facial papules; JAK inhibitors are promising but still investigational at this point in time.
• Hair transplantation is possible in carefully selected, fully inactive disease with ongoing medical therapy.

Bottom line. FFA is a patterned LPP with the upper follicle as its Achilles’ heel. Combining early, targeted anti-inflammatory control at the advancing edge with a data-informed systemic agent – often a 5-ARI or hydroxychloroquine – likely offers the best chance to arrest progression. Layering in minoxidil and thoughtful cosmetic strategies can optimize appearance, while reserving surgery for stringently quiescent cases. With systematic monitoring and patient-centred counselling, most individuals can achieve long periods of stability and a satisfactory cosmetic outcome.

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