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Possible role of the bulge region in the pathogenesis of inflammatory scarring alopecia: lichen planopilaris as the prototype
Author(s) -
Mobini Narciss,
Tam Sam,
Kamino Hideko
Publication year - 2005
Publication title -
journal of cutaneous pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 75
eISSN - 1600-0560
pISSN - 0303-6987
DOI - 10.1111/j.0303-6987.2005.00399.x
Subject(s) - pathology , scarring alopecia , hair follicle , alopecia areata , biopsy , medicine , van gieson's stain , scalp , stem cell , h&e stain , biology , dermatology , immunohistochemistry , genetics
Background: Lichen planopilaris (LPP) is the prototype of scarring alopecias that mainly target the infundibuloisthmic (bulge) region of hair follicle. Hair follicle stem cells have been shown to reside in the bulge. Methods: We carried out this study to better define the possible pathogenetic role of the bulge in LPP. Thirty‐five cases of LPP were studied. Multiple serial sections of biopsy specimens stained with hematoxylin and eosin, periodic acid Schiff‐diastase, and Elastic van Gieson. The following immunostains were applied: CD3, CD4, CD8, CD1a, and Ki‐67. Uninvolved follicles and normal scalp biopsy specimens served as normal controls. Results: All cases showed a lichenoid lymphocytic infiltrate at the bulge region. The bulb area was spared. CD8 + T cells were increased compared with CD4 + T‐cell population. Langerhans' cells were decreased. Proliferating stem cells, highlighted by Ki‐67, showed a marked decrease in the bulge compared with uninvolved follicles. Conclusion: Our study supports the finding that in LPP, the inflammatory infiltrate mainly involves the bulge region, where the stem cells reside. Once this area is damaged, the hair loses its potential of regrowth with resulting scarring alopecia. This is in contrast with inflammatory non‐scarring alopecias such as alopecia areata, where the bulb region is targeted, sparing the stem cells.