The role of the vitamin D receptor (VDR) in the hair cycle was first suggested by the observation of alopecia in patients with type II vitamin D dependent rickets (VDDR IIA), an autosomal recessive disorder that, due to a defect in the VDR, is characterized by hypokalemia, hypophosphatemia, hyperparathyroidism, rickets, osteomalacia, dental caries, and alopecia universalis. Further hydroxylation in the liver leads to 25-hydroxyvitamin-D3 (25OHD3) and subsequently in the kidney to the active hormone 1-25-dihydroxyvitamin-D3 (1-25(OH)2D3, calcitriol). Vitamin D is synthesized in the epidermal keratinocytes from 7-Dehydrocholesterol by ultraviolet B light (290-315 nm) or is acquired through the diet and dietary supplements. The role of vitamin D in the proliferation and differentiation of keratinocytes has been extensively studied and well established in the literature. The collapse of mechanisms that maintain the HFIP renders the HF susceptible to inflammatory assault, contributing to the development of AA, while growing evidence implicates interferon gamma in triggering HFIP collapse. This HF immune privilege (HFIP) is important for the protection of anagen- and melanogenesis-associated antigens from immune recognition by autoreactive CD8+ T cells. During the anagen segment of the hair cycle, HF epithelium generates and maintains an area of immune privilege, which is mainly characterized by the low expression of major histocompatibility complex class Ia antigens and local production of immunosuppressive agents. HF is a micro-organ with its own immune and hormonal microenvironment. The likelihood of complete spontaneous regrowth in AA is estimated to be less than 10%, but even then, relapses are common and frustrating. Pediatric age and more extensive disease with resistance to initial therapies with corticosteroids may sometimes benefit from a cocktail of established therapies. Management of the disease can be challenging, and despite multiple treatment modalities, no successful treatment is available. Its prevalence among the young and adult population is 0.7%-3.8%, significantly affecting patients’ lives and having psychosocial implications. Alopecia areata (AA) is a non-scarring T-cell mediated autoimmune disease directed at the hair follicle (HF), either limited to patchy hair loss over the scalp (Focalis, AF), total loss of scalp hair (Totalis, AT), or loss of both scalp and body hair (Universalis, AU).
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