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[关节纤维化中VI型胶原蛋白的表达。一项免疫组织化学研究]

[Expression of type VI collagen in arthrofibrosis. An immunohistochemical study].

作者信息

Zeichen J, van Griensven M, Lobenhoffer P, Bosch U

机构信息

Unfallchirurgische Klinik, Medizinische Hochschule Hannover.

出版信息

Unfallchirurg. 2000 Aug;103(8):640-4. doi: 10.1007/s001130050597.

Abstract

Arthrofibrosis is a disabling complication after trauma and surgery due to massive connective tissue proliferation. The etiology and pathogenesis have never been fully understood. A strong immune response may lead to activation and proliferation of fibroblasts with excessive and disordered deposition of matrix proteins. In similar pathological conditions, like lung fibrosis or superficial fibromatoses with fibrotic transformation an increased expression of collagen type VI has been reported. We investigated fibrotic tissue samples taken from 18 patients (average age: 32.7 years), who underwent arthrolysis of the knee joint because of symptomatic arthrofibrosis following ligament injury. The mean interval between trauma and arthrolysis was 13.8 months (range 4-50 months). Tissue samples were taken from the infrapatellar fat pad and intercondylar connective tissue. All samples were stained with HE. The expression of type III and VI collagen was studied immunohistochemically using an immunoperoxidase method for light microscopic visualization. Histologic analysis from patients with arthrofibrosis showed a synovial hyperplasia with cell infiltration and vascular proliferation compared to synovial tissue samples from knee joints without any detectable pathology. Subsynovial an increased deposition of matrix proteins was visible. Type VI collagen was widely distributed as a network subsynovial and around capillary walls. Type III collagen showed a diffuse distribution. Arthrofibrotic tissue is, similar to pathological conditions with fibrotic transformation characterized by an increased expression of collagen type VI. Collagen type VI may play an important role in matrix homeostasis. It serves as an anchoring element between collagen fibers and as a cell binding structure.

摘要

关节纤维化是创伤和手术后因大量结缔组织增生而导致的致残性并发症。其病因和发病机制尚未完全明确。强烈的免疫反应可能导致成纤维细胞活化和增殖,伴有基质蛋白过度且无序的沉积。在类似的病理状况下,如肺纤维化或伴有纤维化转变的浅表纤维瘤病,已有报道称VI型胶原表达增加。我们研究了18例患者(平均年龄:32.7岁)的纤维化组织样本,这些患者因韧带损伤后出现症状性关节纤维化而接受了膝关节松解术。创伤与膝关节松解术之间的平均间隔时间为13.8个月(范围4 - 50个月)。组织样本取自髌下脂肪垫和髁间结缔组织。所有样本均进行苏木精 - 伊红(HE)染色。采用免疫过氧化物酶法进行免疫组织化学研究III型和VI型胶原的表达,以用于光镜观察。与无任何可检测病理的膝关节滑膜组织样本相比,关节纤维化患者的组织学分析显示滑膜增生伴细胞浸润和血管增殖。滑膜下可见基质蛋白沉积增加。VI型胶原作为滑膜下网络和毛细血管壁周围广泛分布。III型胶原呈弥漫性分布。关节纤维化组织与伴有纤维化转变的病理状况相似,其特征为VI型胶原表达增加。VI型胶原可能在基质稳态中起重要作用。它作为胶原纤维之间的锚定元件以及细胞结合结构。

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