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Eyebrow Madarosis: An Updated Review of the Etiology and Management, Part II- Scarring Disorders.

Created on 05 Sep 2026

Authors

Janaya Nelson, Adam Friedman

Published in

Journal of drugs in dermatology : JDD. Volume 25. Issue 9. Pages 852-856. Sep 01, 2026.

Abstract

Eyebrows play an essential role in facial symmetry, communication, and aesthetic identity. Scarring eyebrow alopecia results from inflammatory, autoimmune, infectious, genetic, traumatic, and iatrogenic processes that irreversibly damage follicular stem cells and limit regrowth potential. Despite its clinical and psychosocial impact, evidence-based guidance for diagnosis and management remains limited.
A comprehensive PubMed search (1960–2025) was performed using terms related to "eyebrow alopecia," "eyebrow madarosis," and etiology-specific conditions. English-language original studies evaluating eyebrow involvement and reporting diagnostic or therapeutic outcomes were included. Review articles without original patient data and studies limited to scalp alopecia were excluded.
Scarring eyebrow alopecia included autoimmune conditions such as discoid lupus erythematosus and localized scleroderma; infectious etiologies such as lepromatous leprosy; genetic disorders including keratosis follicularis spinulosa decalvans; and inflammatory dermatoses such as ulerythema ophryogenes. Additional causes included radiation therapy, trauma, and hematologic malignancies. Reported treatments included corticosteroids, calcineurin inhibitors, antimalarials, methotrexate, mycophenolate, retinoids, JAK inhibitors, phototherapy, and reconstructive approaches. Emerging therapies, including biologics and regenerative techniques, have shown limited but evolving benefit.
Scarring eyebrow madarosis involves diverse irreversible etiologies. Early diagnosis and etiology-directed treatment are essential to limit progression, highlighting the need for standardized management algorithms and eyebrow-specific outcome measures.  .

PMID:
42696332
Bibliographic data and abstract were imported from PubMed on 05 Sep 2026.

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