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Annals of Clinical & Laboratory Science 33:107-112 (2003)
© 2003 Association of Clinical Scientists

An Investigation of Apoptosis in Androgenetic Alopecia

Michael B. Morgan1 and Paul Rose2
1 Department of Pathology and 2 Department of Dermatology, College of Medicine, University of South Florida,Tampa, Florida

Address correspondence to Michael B. Morgan, M.D., 16124 Chastain Road, Odessa, FL 33556, USA; tel 813 971 0775; fax 813 971 6675; e-mail mbkmmorgan{at}aol.com.

While the androgens, including dihydrotestosterone (DHT), have been implicated in the development of androgenetic alopecia (AGA), the exact mechanism by which they exert their effect(s) is unknown. Since apoptosis is an integral component of the normal cycling of human hair, we investigated individuals clinically affected by AGA to assess whether objective differences in the expression of apoptosis-related immunohistochemical markers could be observed in scalp biopsies. Specimens from 16 alopecic male patients were stained with bcl-2 and the terminal deoxynucleotidyltransferase dUTP fluorescein nick end-labeling (TUNEL) method was used to assess apoptotic activity in affected and unaffected areas of the scalp. Immunoreactivity was analyzed by quantifying staining differences within the same individual. Sections from 3 human volunteers were used to establish the method validity. Significant differences in the bcl-2 staining index (0.67 versus 0.42, p <0.05) and TUNEL expression (5.7 versus 10.2, p <0.05) were observed between the areas of the scalp that were clinically affected (frontal) and unaffected (occipital) by AGA. The Gaussian distributions of bcl-2 and TUNEL staining suggest that a relatively uniform population of follicles exists at the frontal hairline and/or that synchrony of follicular cycling occurs in AGA. The apoptosis "hot spot" revealed by TUNEL staining in the bulge-isthmus region of the murine follicle is also identifiable in the human follicle.

Keywords: alopecia, baldness, bcl-2, testosterone, TUNEL, apoptosis, hair follicle






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