What is the pathophysiology of androgenetic alopecia?

vina

Achin

@sarkarsatarupa Androgenetic alopecia is a genetically determined disorder and is progressive through the gradual conversion of terminal hairs into indeterminate hairs and finally to vellus hairs. Patients with androgenetic alopecia have a reduction in the terminal-to-vellus hair ratio, normally about 4:1. Following miniaturization of the follicles, fibrous tracts remain. Patients with this disorder usually have a typical patterned distribution of hair loss.

In androgenetic alopecia, studies have indicated a self-renewal of the hair follicle via keratinocyte stem cells located at the area of the bulge of the hair follicle. In addition, a series of studies using mice has indicated that interfollicular keratinocyte stem cells could generate de novo hair follicles in adult mouse skin. These regenerated hair follicles cycled through stages of telogen to anagen. However, these transitions between bulge and epidermal keratinocytes have not been seen yet in human studies.

Another report has indicated that mice lacking in functional vitamin D receptors develop a functional first coat of hair but lack the cyclic regeneration of hair follicles, leading to the development of alopecia. Whether these findings will lead to a new area of exploration into the cause of androgenetic alopecia in humans is unknown at this time.

A lymphocytic microfolliculitis targeting the bulge epithelium, along with deposits of epithelial basement membrane zone immunoreactants, are frequently seen in androgenetic alopecia in both sexes. Those cases with a positive immunoreactant profile respond better to combined-modality therapy than do those with a negative result.

Numerous studies have identified 2 major genetic risk loci for androgenetic alopecia. These are the X-chromosomal AR/EDA2R locus and the PAX1/FOXA2 locus on chromosome 20. A recent genome-wide association study compared move than 1100 severely affected cases of androgenetic alopecia and controls to note differences in the 2 groups. The study indicated that HDAC9 is the third androgenetic alopecia susceptibility gene. The results of this German study were further analyzed by fine-mapping and then individually replicated in an Australian sample.