先天性马蹄内翻足深筋膜胶原的免疫组化研究  

The observation of immunohistochemistry with collagen polysaccharide on deep fasciae of congenital clubfoot

作　　者：赵东风[1] 岳勇[1] 黄耀添[2] 赵黎[2] 葛杰[1] 杨柏[1] 

机构地区：[1]中国人民解放军第二一○医院骨科,大连市116021 [2]第四军医大学西京医院骨科研究所,西安市710033

出　　处：《中华小儿外科杂志》2004年第2期182-184,F003,共4页Chinese Journal of Pediatric Surgery

摘　　要：目的　探讨先天性马蹄内翻足 (congenitalclubfoot,CCF)的病因、病理及发病机制与细胞外基质 (extracellularmatrix ,ECM )的关系。方法　对 15例先天性马蹄内翻足患者及对照组 5例非神经、肌肉及胶原病死亡小儿 ,足内侧及小腿前外侧深筋膜的Ⅰ、Ⅱ、Ⅲ型胶原进行免疫组化研究。切片应用LeticaQ5 70c彩色图像分析仪处理系统进行量化分析 ,并经统计学处理。结果　先天性马蹄内翻足挛缩侧Ⅰ、Ⅱ、Ⅲ型胶原含量均有增加 ,Ⅰ型胶原增加最显著 ,Ⅲ型次之 ,Ⅱ型增加最少 ,且Ⅰ、Ⅲ型胶原呈负相关。Ⅱ型胶原的阳性表达可能为伴随现象 ,它与Ⅰ、Ⅲ型胶原无相关性。结论　先天性马蹄内翻足细胞外基质的改变符合组织器官纤维化及一般瘢痕性纤维结缔组织增生。故认为先天性马蹄内翻足可能为足内侧的纤维化所引起。Objective To investigate the pathogenesis, pathology and mechanism of formation of congenital club foot (CCF) and their relationship with extracellular matrix (ECM). Methods The collagen type Ⅰ?Ⅱ?Ⅲ of CCF group (15 patients) and control group (5 cases) (from corpses of infants without neural, muscular and collagenous diseases) were studied immunohistochemically. The quantitative an- alysis of collagen type I?Ⅱ?III were performed by Leica Q570c imagine analyzer and the results were analyzed with standard statistical methods. Results The content of collagen increased in the contractured side of CCF group in the following order: typeI>typeIII>typeⅡ. Collagen type I was negatively related to collagen III. The positive effect of collegen II may probably just be an accompanying phenomenon and had no relation with types I and III collegens Conclusions The ECM from the contracture side of CCF is consistent with tissue fribrosis and fibroelastosis. Therefore, fibrosis of inner aspect of the foot may be the cause of CCF.

关 键 词：先天性马蹄内翻足 筋膜 胶原 免疫组化法 发病机制 细胞外基质 

分 类 号：R726.8[医药卫生—儿科]