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Molecular mechanisms of androgenetic alopecia
Androgenetic alopecia (Androgenetic Alopecia) is hereditary and androgen-dependent, progressive thinning of the scalp hair that follows a
defined pattern. While the genetic involvement is pronounced but poorly understood, major advances have been achieved in
understanding principal elements of the androgen metabolism involved: androgen-dependent processes are predominantly due
to the binding of dihydrotestosterone (DHT) to the androgen receptor (AR). DHT-dependent cell functions depend on the
availability of weak androgens, their conversion to more potent androgens via the action of 5alpha-reductase, low enzymatic
activity of androgen inactivating enzymes, and functionally active AR present in high numbers. The predisposed scalp exhibits
high levels of DHT, and increased expression of the AR. Conversion of testosterone to DHT within the dermal papilla plays a
central role, while androgen-regulated factors deriving from dermal papilla cells are believed to influence growth of other
components of the hair follicle. Current available treatment modalities with proven efficacy are oral finasteride, a competitive
inhibitor of type 2 5a-reductase, and topical minoxidil, an adenosine-triphosphate-sensitive potassium channel opener which
has been reported to stimulate the production of vascular endothelial growth factor in cultured dermal papilla cells. Since the
clinical success rate of treatment of Androgenetic Alopecia with modulators of androgen metabolism or hair growth promoters is limited,
sustained microscopic follicular inflammation with connective tissue remodeling, eventually resulting in permanent hair loss, is
considered a possible cofactor in the complex etiology of Androgenetic Alopecia.
http://www.derma-haarcenter.ch/files/Directory/Publikationen/Androgenetic+alopecia.pdf
Androgenetic alopecia (Androgenetic Alopecia) is hereditary and androgen-dependent, progressive thinning of the scalp hair that follows a
defined pattern. While the genetic involvement is pronounced but poorly understood, major advances have been achieved in
understanding principal elements of the androgen metabolism involved: androgen-dependent processes are predominantly due
to the binding of dihydrotestosterone (DHT) to the androgen receptor (AR). DHT-dependent cell functions depend on the
availability of weak androgens, their conversion to more potent androgens via the action of 5alpha-reductase, low enzymatic
activity of androgen inactivating enzymes, and functionally active AR present in high numbers. The predisposed scalp exhibits
high levels of DHT, and increased expression of the AR. Conversion of testosterone to DHT within the dermal papilla plays a
central role, while androgen-regulated factors deriving from dermal papilla cells are believed to influence growth of other
components of the hair follicle. Current available treatment modalities with proven efficacy are oral finasteride, a competitive
inhibitor of type 2 5a-reductase, and topical minoxidil, an adenosine-triphosphate-sensitive potassium channel opener which
has been reported to stimulate the production of vascular endothelial growth factor in cultured dermal papilla cells. Since the
clinical success rate of treatment of Androgenetic Alopecia with modulators of androgen metabolism or hair growth promoters is limited,
sustained microscopic follicular inflammation with connective tissue remodeling, eventually resulting in permanent hair loss, is
considered a possible cofactor in the complex etiology of Androgenetic Alopecia.
http://www.derma-haarcenter.ch/files/Directory/Publikationen/Androgenetic+alopecia.pdf
