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肌腱蛋白-C在全髋关节置换无菌性松动中的表达

Expression of tenascin-C in aseptic loosening of total hip replacement.

作者信息

Konttinen Y T, Li T F, Michelsson O, Xu J W, Sorsa T, Santavirta S, Imai S, Virtanen I

机构信息

Department of Medicine, Helsinki University Central Hospital, Finland.

出版信息

Ann Rheum Dis. 1998 Oct;57(10):619-23. doi: 10.1136/ard.57.10.619.

Abstract

OBJECTIVE

To assess if the bonding interlayer between the implant and bone in aseptic loosening of total hip replacement (THR) is qualitatively deteriorated by excessive accumulation of anti-adhesive glycoprotein, tenascin-C.

METHODS

Alkaline phosphatase-anti-alkaline phosphatase (APAAP) method was used for immunohistochemical staining of tenascin-C in interface tissue and control synovial tissue.

RESULTS

Tenascin-C was found to be a major component of the extracellular matrix at a hitherto unrecognised site, namely the synovial membrane-like interface tissue between implant and bone in aseptic loosening of THR. The overall tenascin-C staining (median score 4.0) was greatly increased in aseptic loosening compared with synovial membrane (median score 2.0; p < 0.001) and fibrous capsule (median score 2.0; p < 0.001) from primary THR operations. Topological analysis disclosed that tenascin-C was also found at the critical implant-interface and interface-bone surfaces.

CONCLUSION

Local tenascin-C expression is increased as a result of a chronic foreign body type reaction associated with excessive cytokine production and tissue injury mediated by microtrauma and neutral endoproteinases. This qualitative and topological deterioration of the bonding interlayer by an increase of anti-adhesive tenascin-C expression may inadvertantly contribute to loosening.

摘要

目的

评估在全髋关节置换术(THR)无菌性松动中,植入物与骨之间的结合层是否因抗黏附糖蛋白腱生蛋白-C的过度积累而发生质性恶化。

方法

采用碱性磷酸酶-抗碱性磷酸酶(APAAP)法对界面组织和对照滑膜组织中的腱生蛋白-C进行免疫组织化学染色。

结果

腱生蛋白-C被发现是迄今未被认识的部位细胞外基质的主要成分,即在THR无菌性松动中植入物与骨之间的滑膜样界面组织。与初次THR手术的滑膜(中位数评分2.0;p<0.001)和纤维囊(中位数评分2.0;p<0.001)相比,无菌性松动中腱生蛋白-C的总体染色(中位数评分4.0)大大增加。拓扑分析显示,在关键的植入物界面和界面-骨表面也发现了腱生蛋白-C。

结论

由于与过度细胞因子产生以及由微创伤和中性内蛋白酶介导的组织损伤相关的慢性异物型反应,局部腱生蛋白-C表达增加。抗黏附性腱生蛋白-C表达增加导致的结合层这种质性和拓扑性恶化可能无意中促成了松动。

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The immune response to implant materials in humans.人类对植入材料的免疫反应。
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