Abstract
Alopecia areata (AA) is an autoimmune disease characterized clinically by round to oval well-demarcated hair loss patches and pathologically by dense lymphocytic infiltration surrounding the bulbar portion of anagen hair follicles. However, these typical manifestations can be predominantly observed in the acute phase of the disease. In chronic phase, hair follicles shift from anagen to telogen phase in response to autoimmune reaction and little inflammation can be observed. In the acute phase, hair loss is mainly caused by the destruction of the bulbar portion of the anagen hair follicles, while, in the chronic phase, club hairs are predominantly shed due to dynamic transition of most affected hair follicles from anagen to telogen phase. As the pathophysiology of AA is distinct between acute and chronic phase, treatment planning needs to be optimized considering the condition of individual cases. Those with ongoing autoimmune-mediated hair loss can benefit from direct immunosuppression by means of corticosteroid (local injection, topical application or, for rapidly progressive cases, intravenous pulse therapy), while, for chronic phase patients, alternative approaches represented by the contact immunotherapy would be more favorable. Therapeutic outcomes can be further improved with careful evaluation and elucidation of major pathophysiology causing hair loss in each patient and the selection of optimal treatments with mode-of-action which would be ideal for respective conditions.
