Evaluation of apoptosis regulatory markers in AGA

Background  Androgenetic alopecia (AGA) is a common androgen-induced progressive disorder; the pathways of which are regulated by local genetic codes and hormonal control. Meanwhile, it is unclear whether an altered proliferation or increased apoptosis could contribute to its pathogenesis. Aims  To evaluate the role of some apoptosis regulatory markers and follicular proliferation in the pathogenesis of AGA.

Patients/Methods  Thirty biopsies were taken from the frontal (bald) area and occipital (hair-bearing) area of 15 male patients with AGA, as well as five specimens from the frontal area of five age-matched controls. The biopsies were stained with apoptosis regulatory markers (Bcl-2, p53, Bax & Fas) and PCNA (proliferating cell nuclear antigen), as well as TUNEL (terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling) staining for the detection of DNA fragmentation in apoptotic cells.

Results  Bcl-2 expression was localized to epidermal basal layer and follicular dermal papilla with highly significant correlation with PCNA expres​sion(P < 0.001). Perifollicular lymphocytic infiltrate of the bald area showed significant expression of Bcl-2. However, pro-apoptotic Bax and Fas were expressed in the epidermis and not in the hair follicles which does not show any apoptotic keratinocytes by TUNEL staining.

Conclusion  The low proliferation rate in the bald area of patients, together with persistent perifollicular inflammatory infiltrate as evidenced by the anti-apoptotic Bcl-2 expression in dermal lymphocytes, would result in follicular miniaturization and fibrosis.

http://www.ncbi.nlm.nih.gov/pubmed/21122044

Pronounced perifollicular lymphocytic infiltrates in alopecia areata are associated with poor treatment response to diphencyprone.
Freyschmidt-Paul P, et al

Some authors have reported that severe destruction of follicular structures and even scarring patterns occur in those patients with hair loss due to alopecia areata (AA) who fail to respond with regrowth to treatment with contact sensitizers, such as diphencyprone (DCP). Other studies, however, gave contradictory results. Therefore, we re-examined histopathological changes in scalp samples obtained from 85 patients with severe hair loss before initiation of DCP treatment (40 responders and 45 non-responders in terms of hair regrowth). The following parameters were evaluated: i) perifollicular lymphocytic infiltration; ii) perifollicular fibrosis, and iii) miniaturized hair follicles. No difference between responders and non-responders could be observed in the degree of miniaturization of hair follicles and proliferation of perifollicular fibrous tissue. In neither group was there any evidence of scarring or severe follicular destruction. 18 non-responders who did not regrow hair but only 6 responders to hair loss treatment showed a very dense perifollicular lymphocytic infiltration. In contrast, a particularly scarce infiltrate was seen in 9 non-regrowers and in 19 responders. We conclude that non-responders tend to have pronounced inflammatory reactions with dense perifollicular lymphocytic infiltrates

http://www.md.st/index.php?blog=2&title ... &tb=1&pb=1