瘢痕增生机理的研究

A STUDY ON THE MECHANISM OF OVER SCARRING

增生性瘢痕（HS）和瘢痕疙瘩（K）临床表现明显不同，为探讨瘢痕增生的机理，对17例K、55例HS及55例正常皮肤（NS）标本采用actin、bFGF及其受体flg抗体免疫组化半定量分析，结合组织学淋巴细胞、皮肤附件变化情况的动态观察。结果：K和HS早期均有许多炎性细胞浸润在残留的皮肤附件和闭塞的毛细血管周围，随着瘢痕增生，皮肤附件、淋巴细胞和毛细血管逐渐减少，但在K组滞留的时间和数量远较HS组多。bFGF和flg在三组的成纤维细胞、血管内皮细胞、单核细胞和附件上皮细胞均有表达，强度依次为：K＞HS＞NS（P＜0.01），而K组flg表达明显强于bFGF。结论：组织中残留的皮肤附件、浸润的淋巴细胞和增生的毛细血管三者互为消长，由此，促进了成纤维细胞增殖和胶原沉积，K对flg敏感性增加，可能是其侵袭性生长的重要因素。

There are markedly different clinicalcharacteristics between hypertrophic scar (HS) andkeloid (K). To clarify the mechanism of over scarring, the biopsies from 17 K patients, 55 HS patientsand 55 normal skin (NS) specimens were semiquantitatively analyzed by immunohistochemistry withantibodies of actin, basic fibroblast growth factor(bFGF) and bFGF receptor ng. Meanwhile,lyynphocytes and cutaneous appendages were dynamicallyobserved by histology in the above biopsies. Numbers of innammatory cells were found infiltrating into the tissues surrounding the remaining cutaneousappendages and the occluede blood capillaries in theearly stage of both HS and K. Along with the scarring development, the cutaneous appendages, lymphocytes and blood capillaries reduced gradually,butdid much slower in K than in HS. In all the bioDsiedtissues from HS,K and normal skin ssmples respectively, both bFGF and its receptor ng were expressed by fibroblasts, vascular endothelial cells,monocytes and epithelial cells of cutaneous appendages. The bFGF and its receptor 'g's expressions were strongest in K group,while stronger inHS group than in NS group (P <0. 01). Furthermore, the bFGF receptor fig was expre88ed morethan bFGF in K group. Conclusionsl A dependentchange relationship might exist among the remainingcutaneous appendages, infiltrating lytnphocytes andblood capillaries, which could stimulate the fibroblast proliferation and collagen dePOsition in scarringprocess. overexpression of bFGF receptor ng mightbe mainly responsible for the invasive growth ofkeloid.