Vitamin D and Alopecia Areata: From Mechanism to Therapeutic Implications

Alopecia areata (AA) is an autoimmune disorder and the second most common form of non-scarring hair loss, affecting approximately 1.7-2% of the global population. Although it predominantly presents before the age of 40, AA can occur at any age and is strongly associated with genetic predisposition. Environmental, hormonal, and psychological factors have been implicated in disease onset and progression. Recent evidence highlights the immunomodulatory role of vitamin D, traditionally recognized for its functions in bone metabolism and calcium homeostasis, in skin health and immune regulation, raising interest in its potential relevance to AA pathogenesis and treatment.

This review examines the epidemiology, genetic predisposition, and immunological mechanisms underlying AA, emphasizing the loss of immune privilege in hair follicles as a key pathogenic event. Additionally, it examines the role of vitamin D and its receptor (VDR) in hair follicle homeostasis, discussing the association between vitamin D deficiency, altered VDR expression, and disease severity. Emerging clinical data suggest that vitamin D supplementation and analogs, such as calcipotriol, may serve as adjunctive therapeutic strategies, with potential benefits in mitigating disease severity and reducing relapse rates.

(1) Vitamin D serves as a critical immunomodulator in AA, regulating follicular immune privilege and key inflammatory pathways involved in disease pathogenesis. (2) Vitamin D deficiency is frequently observed in patients with AA and has been associated with increased disease severity, prolonged duration, and a higher risk of relapse. (3) Emerging evidence supports the therapeutic potential of vitamin D analogs and supplementation in AA, positioning vitamin D as a promising adjunct or primary treatment modality.