Etiology of cicatricial alopecias: a basic science point of view.
This article presents a short summary of our current knowledge of cicatricial alopecia disease pathogenesis and the hypothetical disease mechanisms that may be involved in scarring alopecia development. Several forms of scarring alopecia likely involve targeted cytotoxic action against hair follicle cells mediated by a folliculocentric inflammation. However, the specific nature of the inflammatory interference in hair follicle growth is open to question. A popular hypothesis of lymphocyte-mediated scarring alopecia development involves autoimmune targeting of hair follicle-specific self-antigens, although there is no direct evidence in support of such a view. Alternative hypotheses focus on defects in sebaceous gland function, destruction of hair follicle stem cells, and interference in the communication between hair follicle mesenchyme and epithelium. Many questions arise from these hypotheses, and addressing them with a systematic research approach may enable significant advances in understanding cicatricial alopecia etiology.
McElwee
Kevin J
KJ
Department of Dermatology and Skin Science and Vancouver Coastal Health Research Institute, University of British Columbia, Vancouver, British Columbia, Canada. kevin@keratin.com
D000505:Alopecia / Q000145:classification / Q000209:etiology*; D000818:Animals; D015703:Antigens, CD / Q000032:analysis; D015551:Autoimmunity; D002921:Cicatrix / Q000145:classification / Q000209:etiology*; D004195:Disease Models, Animal; D018859:Hair Follicle / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000209:etiology; D007633:Keratins / Q000235:genetics; D008214:Lymphocytes / Q000502:physiology; D051379:Mice; D009154:Mutation; D009504:Neutrophils / Q000502:physiology; D047495:PPAR gamma / Q000502:physiology; D012627:Sebaceous Glands / Q000502:physiology; D013234:Stem Cells / Q000473:pathology
D015703:Antigens, CD; D047495:PPAR gamma; D007633:Keratins; C042739:antigens, CD200