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BackgroundAlopecia areata (AA) is an autoimmune disorder characterized by patches of non-scarring alopecia affecting scalp and body hair that can be psychologically devastating. AA is clinically heterogenous, and its natural history is unpredictable. There is no preventative therapy or cure.ObjectiveThe objective of this study is to provide an evidence-based systematic review on the epidemiology and the burden of AA.Methods and selection criteriaA search was conducted of the published, peer-reviewed literature via PubMed, Embase, and Web of Science. Studies published in English within the last 51 years that measured AA’s incidence, prevalence, distribution, disability-adjusted life years (DALYs), quality of life, and associated psychiatric and medical comorbidities were included. Two authors assessed studies and extracted the data.ResultsThe lifetime incidence of AA is approximately 2% worldwide. Both formal population studies found no sex predominance. First onset is most common in the third and fourth decades of life but may occur at any age. An earlier age of first onset corresponds with an increased lifetime risk of extensive disease. Global DALYs for AA were calculated at 1,332,800 in 2010. AA patients are at risk for depression and anxiety, atopy, vitiligo, thyroid disease, and other autoimmune conditions.ConclusionAA is the most prevalent autoimmune disorder and the second most prevalent hair loss disorder after androgenetic alopecia, and the lifetime risk in the global population is approximately 2%. AA is associated with psychiatric and medical comorbidities including depression, anxiety, and several autoimmune disorders, and an increased global burden of disease.

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The advantage of this method is that it is a fast, precise way to identify even individually affected follicles in early or focal cicatricial alopecia. It also allows for the morphologic characterization of particular follicular structures.

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The rough coat (rc) spontaneous mutation causes sebaceous gland hypertrophy, hair loss and extracutaneous abnormalities including growth retardation. The rc mice have a missense mutation in the predicted immunoglobulin protein Mpzl3. In this study, we generated Mpzl3 knockout mice to determine its functions in the skin. Homozygous Mpzl3 knockout mice showed unkempt and greasy hair coat and hair loss soon after birth. Histological analysis revealed severe sebaceous gland hypertrophy and increased dermal thickness, but did not detect significant changes in the hair cycle. Mpzl3 null mice frequently developed inflammatory skin lesions; however, the early onset skin abnormalities were not the results of immune defects. The abnormalities in the Mpzl3 knockout mice resemble closely those observed in the rc/rc mice, as well as mice heterozygous for both the rc and Mpzl3 knockout alleles, indicating that rc and Mpzl3 are allelic. Using a lacZ reporter gene, we detected Mpzl3 promoter activity in the companion layer and inner root sheath of the hair follicle, sebaceous gland, and epidermis. Loss of MPZL3 function also caused a striking reduction in cutaneous and overall adipose tissue. These data reveal a complex role for Mpzl3 in the control of skin development, hair growth and adipose cell functions.

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Seborrhoeic Dermatitis (SD) is a very common chronic and/or relapsing inflammatory skin disorder whose pathophysiology remains poorly understood. Yeast of the genus Malassezia has long been regarded as a main predisposing factor, even though causal relationship has not been firmly established. Additional predisposing factors have been described, including sebaceous activity, host immunity (especially HIV infection), epidermal barrier integrity, skin microbiota, endocrine and neurologic factors, and environmental influences. Genetic studies in humans and mouse models—with particularly interesting insights from examining the Mpzl3 knockout mice and their SD‐like skin phenotype, and patients carrying a ZNF750 mutation—highlight defects in host immunity, epidermal barrier and sebaceous activity. After synthesizing key evidence from the literature, we propose that intrinsic host factors, such as changes in the amount or composition of sebum and/or defective epidermal barrier, rather than Malassezia, may form the basis of SD pathobiology. We argue that these intrinsic changes provide favourable conditions for the commensal Malassezia to over‐colonize and elicit host inflammatory response. Aberrant host immune activity or failure to clear skin microbes may bypass the initial epidermal or sebaceous abnormalities. We delineate specific future clinical investigations, complemented by studies in suitable SD animal models, that dissect the roles of different epidermal compartments and immune components as well as their crosstalk and interactions with the skin microbiota during the process of SD. This research perspective beyond the conventional Malassezia‐centric view of SD pathogenesis is expected to enable the development of better therapeutic interventions for the management of recurrent SD.