The Role of Fibrosis in Androgenetic Alopecia: Mechanisms and Implications

Androgenetic alopecia (AGA) is a common pattern hair loss in which perifollicular fibrosis drives hair follicle miniaturization. Inflammatory-fibrotic cross talk centered on TGF-β/Smad, with input from Wnt/β-catenin and Notch, disrupts epithelial-mesenchymal communication and impairs regeneration.

We summarize evidence linking chronic inflammation to fibroblast/myofibroblast activation and excessive extracellular matrix deposition around hair follicles, highlight dermoscopic features that may reflect fibrotic burden, and outline a continuum between AGA and fibrosing patterned alopecias. We review anti-fibrotic strategies directed at TGF-β, Wnt/β-catenin, and Notch signaling, and how combining antiandrogenic, anti-inflammatory, and anti-fibrotic approaches could address both hormonal and structural drivers.

Perifollicular fibrosis is integral to AGA progression and may underlie incomplete treatment responses. Dermoscopic signs such as perifollicular hyperpigmentation and whitish perifollicular structures may correlate with histologic fibrosis and merit validation. Pathway-directed anti-fibrotic agents targeting TGF-β and Wnt/Notch show anti-fibrotic activity in other organs but require AGA-specific testing.