Mobini Narciss, Tam Sam, Kamino Hideko
Department of Dermatology, Section of Dermatopathology, New York University Medical Center, Suite 7J, 530 First Avenue, New York, NY 10016, USA.
J Cutan Pathol. 2005 Nov;32(10):675-9. doi: 10.1111/j.0303-6987.2005.00399.x.
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.
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.
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.
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.
扁平苔藓样毛发角化病（LPP）是瘢痕性脱发的原型，主要累及毛囊的漏斗-峡部（隆突）区域。已证实毛囊干细胞位于隆突部位。
我们开展本研究以更好地明确隆突在LPP中可能的致病作用。研究了35例LPP患者。对活检标本进行连续多个切片，分别用苏木精-伊红、过碘酸希夫-淀粉酶及弹性凡吉森染色。应用了以下免疫组化染色：CD3、CD4、CD8、CD1a和Ki-67。未受累毛囊及正常头皮活检标本作为正常对照。
所有病例在隆突区域均显示苔藓样淋巴细胞浸润。球部未受累。与CD4(+) T细胞群体相比，CD8(+) T细胞增多。朗格汉斯细胞减少。与未受累毛囊相比，Ki-67标记的增殖干细胞在隆突部位显著减少。
我们的研究支持以下发现，即在LPP中，炎症浸润主要累及干细胞所在的隆突区域。一旦该区域受损，毛发就会失去再生潜力，导致瘢痕性脱发。这与斑秃等炎症性非瘢痕性脱发相反，后者主要累及球部区域，而干细胞未受累。
