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Morphological analysis of hair follicles in alopecia areata
Author(s) -
Tobin Desmond J.
Publication year - 1997
Publication title -
microscopy research and technique
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 118
eISSN - 1097-0029
pISSN - 1059-910X
DOI - 10.1002/(sici)1097-0029(19970815)38:4<443::aid-jemt12>3.0.co;2-j
Subject(s) - alopecia areata , hair follicle , pathology , vellus hair , hair cycle , involution (esoterism) , biology , hair disease , anatomy , scalp , medicine , microbiology and biotechnology , immunology , neuroscience , consciousness
This study characterizes hair follicles from early alopecia areata lesions at both the light and electron microscopic levels and describes how affected hair follicles differ from normal hair growth. The study focuses on acute and active lesions where hair follicles show greatest divergence from the normal growth pattern and are most likely to display features of primary pathology. Morphologic analysis revealed regressive changes in the hair bulbs of anagen hair follicles in alopecia areata. While tissue injury did not appear to be cell type specific, pre‐cortical keratinocytes and hair bulb melanocytes were primarily affected. Three distinct patterns of cell degeneration, of variable frequency, are described including “dark cell” transformation, apoptosis, and necrosis. Abnormal melanogenesis was a common finding in this study, which may explain some of the associated pigmentary anomalies seen clinically in acute alopecia areata. Tissue damage, which was not always associated with a mononuclear cell infiltrate, may explain the premature involution of suboptimal anagen hair follicles into an early resting phase in alopecia areata. Finally, scanning electron microscopic, light microscopic, and transmission electron microscopic studies describe defective cortex differentiation in characteristic “exclamation‐mark” hair shafts. These hairs may result from a transient phase of cell degeneration among pre‐cortical keratinocytes. Microsc. Res. Tech. 38:443–451, 1997. © 1997 Wiley‐Liss, Inc.