S2 FEMALE PATTERN HAIR LOSS AND ITS RELATIONSHIP TO ANDROGENETIC ALOPECIA
Sinclair R
University of Melbourne, Australia

Recent gene association investigations have heightened the requirement for accurate definition of baldness, patterned hair loss and androgenetic alopecia so the patients can be correctly assigned as affected or un-affected. Female pattern hair loss (FPHL) is the result of a progressive patterned hair follicle miniaturization that only occurs in genetically susceptible individuals in genetically predisposed follicles. The pattern of hair loss differs from male pattern hair loss (MPHL). Four separate but interrelated factors determine whether a person develops significant hair loss, namely susceptibility to androgenetic alopecia, age of onset, rate of progression and pattern of hair loss. The lower age related prevalence of MPHL and higher proportion of men with a Ludwig pattern hair loss among Koreans, and twin concordance studies in males indicate that all four factors are genetic. The inheritance is most likely polygenic. In contrast, whether someone is considered bald, and in particular prematurely bald is in part a subjective assessment. Many people with early evolving MPHL or FPHL would not be considered bald. The process by which MPHL occurs is androgen- mediated conversion of innately susceptible terminal hairs into vellus hairs and has been termed androgenetic alopecia. The lack of MPHL in eunuchs, pseudohermaphrodites and androgen insensitivity syndrome affected individuals confirms that testicular androgen production, the type II, 5a-reductase enzyme and functional androgen receptors are prerequisites for MPHL. Hair follicle transplantation/relocation studies reveal that the response of each individual follicle to androgens is maintained irrespective of where on the skin the follicle is moved. The histology or the hair loss seen in women is indistinguishable from that seen in men. While the subject of recent debate, the process of hair loss in women also appears to involve androgen dependant miniaturization of terminal hair follicles and is therefore also androgenetic alopecia. The relationship of FPHL to ovarian androgen production, 5a-reductase and functional androgen receptors has not been accurately defined and is complicated by the finding of an identical pattern of hair loss in females without androgens, indicating that other non-androgen dependant mechanisms produce hair loss that mimics androgenetic alopecia. Furthermore fundamental differences in the genetics of male and female pattern hair loss are emerging in relation to gene associations with polymorphisms of the androgen receptor gene and polymorphisms of the aromatase gene.