Concurrently, rodent models 6– 8 that faithfully recapitulate the disease in humans and have enabled functional studies have been identified, and quantitative trait locus (QTL) mapping (a technique that links variations in DNA to phenotype) 9, 10 has been performed. The registry enabled the application of genome-wide association studies (GWAS) that have identified candidate genes associated with susceptibility to alopecia areata 4, as well as an evaluation of important epidemiological and socio-medical issues, such as quality of life (QOL) 5. The generation of a National Alopecia Areata Registry 3 in the United States in 2000 provided access to data from >10,000 patients. Inflammation of the hair follicles in alopecia areata mediated by leukocytes was described over a century ago yet the involvement of the immune system in the pathogenesis of alopecia areata has only been recognized as the primary underlying cause since the late 1950s, when several immune related and several key pathogenetic effector cells were identified 1, 2. Historically, numerous hypotheses on the cause (or causes) of alopecia areata have been proposed, such as infection, a trophoneurotic hypothesis (based on the association between the time of onset alopecia areata with emotional or physical stress and/or trauma), thallium acetate poisoning (owing to a similar clinical presentation), thyroid disease and hormonal fluctuations (for example, in pregnancy or menopause). Marie Antoinette syndrome (also called canities subita): acute episode of diffuse alopecia with very sudden “overnight” greying with preferential loss of pigmented hair 205. Alopecia areata is difficult to manage medically, but recent advances in understanding the molecular mechanisms have revealed new treatments and the possibility of remission in the near future. Alopecia areata is usually diagnosed based on clinical manifestations, but dermoscopy and histopathology can be helpful. Several genetic susceptibility loci were identified associated with signaling pathways that are important to hair follicle cycling and development. Genetic studies in patients and mouse models showed that alopecia areata is a complex, polygenic disease. A breakdown of immune privilege of the hair follicle is thought to be an important driver of alopecia areata. Skin biopsies of alopecia areata affected skin show a lymphocytic infiltrate in and around the bulb or the lower part of the hair follicle in anagen (hair growth) phase. Alopecia areata affects nearly 2% of the general population at some point during their lifetime. Patchy alopecia affecting the scalp is the most common type. Hair loss can take many forms ranging from loss in well-defined patches to diffuse or total hair loss, which can affect all hair bearing sites. Alopecia areata is an autoimmune disorder characterized by transient, non-scarring hair loss and preservation of the hair follicle.
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