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背景:既往对先天性马蹄内翻足骨骼及神经,肌肉病理改变的研究较多,而对畸形足周围软组织变化的研究正在探索中。目的:探讨先天性马蹄内翻足的病因、病理及发病机制与细胞外基质的关系。设计:完全随机对照实验。单位:第四军医大学全军骨科研究。对象:实验于1997-11/2003-08在第四军医大学全军骨科研究所完成,实验组深筋膜标本来自于15例手术矫正的先天性马蹄内翻足患儿。男11例,女4例,均年龄9个月。对照组选择5例非神经肌肉性疾病及非胶原病死亡患儿。年龄4～21个月,平均11个月。方法:对先天性马蹄内翻足患者及非神经肌肉病变死亡小儿的足部及小腿前外侧深筋膜进行免疫组化,切片应用LeticaQ,570c彩色图像分析仪处理系统进行量化分析。主要观察指标:两组深筋膜的Ⅰ,Ⅱ,Ⅲ型胶原阳性表达及相对含量。结果:实验组足内侧Ⅰ,Ⅱ,Ⅲ型胶原含量分别为116.43±11.80,132.91±8.88,184.40±11.82;对照组分别为169.28±8.17,176.33±9.47,194.38±5.87。先天性马蹄内翻足挛缩组织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。
BACKGROUND: There are many previous studies on the pathological changes of the foot, the nerve and muscle of congenital clubfoot. However, the research on the changes of soft tissue around the deformity foot is under exploration. Objective: To investigate the etiology, pathology and pathogenesis of congenital clubfoot and its relationship with extracellular matrix. Design: Complete randomized controlled experiment. Unit: Fourth Military Medical University, Department of Orthopedic Research. PARTICIPANTS: Experiments were performed at the Orthopedic Institute of Orthopedics, Fourth Military Medical University from November 1997 to August 2003 with deep fascia specimens from 15 patients with congenital clubfoot. There were 11 males and 4 females, all of whom were 9 months old. Control group, 5 cases of non-neuromuscular diseases and non-collagenosis were selected. Age 4 to 21 months, an average of 11 months. Methods: The hemiarthroplasty of the foot and the anterior deep fascia of the calf in patients with congenital clubfoot and non-neuromuscular lesion were examined by immunohistochemistry and quantified by LeticaQ, 570c color image analyzer processing system. MAIN OUTCOME MEASURES: The positive expression and relative content of collagen type Ⅰ, Ⅱ and Ⅲ in deep fascia of two groups. Results: The contents of collagen type Ⅰ, Ⅱ and Ⅲ in the medial group were 116.43 ± 11.80, 132.91 ± 8.88 and 184.40 ± 11.82, respectively. The control group were 169.28 ± 8.17, 176.33 ± 9.47 and 194.38 ± 5.87 respectively. Collagen content of type Ⅰ, Ⅱ and Ⅲ in congenital clubfoot contracture increased, type Ⅰ collagen increased most significantly, type Ⅲ followed, type Ⅱ increased least. And type Ⅰ, Ⅲ collagen was negatively correlated. The positive expression of type II collagen may be accompanied by the phenomenon. It has no correlation with type I and type III collagen. CONCLUSION: The change of extracellular matrix of congenital clubfoot conforms to the histopathological fibrosis and the general cicatricial fibrous connective tissue hyperplasia. Therefore, congenital clubfoot may be caused by the fibrosis of the medial foot.