Formation process of extension knee joint contracture following external immobilization in rats.

IF 2 Q2 ORTHOPEDICS
Chen-Xu Zhou, Feng Wang, Yun Zhou, Qiao-Zhou Fang, Quan-Bing Zhang
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引用次数: 1

Abstract

Background: Current research lacks a model of knee extension contracture in rats.

Aim: To elucidate the formation process of knee extension contracture.

Methods: We developed a rat model using an aluminum external fixator. Sixty male Sprague-Dawley rats with mature bones were divided into the control group (n = 6) and groups that had the left knee immobilized with an aluminum external fixator for 1, 2, and 3 d, and 1, 2, 3, 4, 6, and 8 wk (n = 6 in each group). The passive extension range of motion, histology, and expression of fibrosis-related proteins were compared between the control group and the immobilization groups.

Results: Myogenic contracture progressed very quickly during the initial 2 wk of immobilization. After 2 wk, the contracture gradually changed from myogenic to arthrogenic. The arthrogenic contracture progressed slowly during the 1st week, rapidly progressed until the 3rd week, and then showed a steady progression until the 4rd week. Histological analyses confirmed that the anterior joint capsule of the extended fixed knee became increasingly thicker over time. Correspondingly, the level of transforming growth factor beta 1 (TGF-β1) and phosphorylated mothers against decapentaplegic homolog 2 (p-Smad2) in the anterior joint capsule also increased with the immobilization time. Over time, the cross-sectional area of muscle fibers gradually decreased, while the amount of intermuscular collagen and TGF-β1, p-Smad2, and p-Smad3 was increased. Unexpectedly, the amount of intermuscular collagen and TGF-β1, p-Smad2, and p-Smad3 was decreased during the late stage of immobilization (6-8 wk). The myogenic contracture was stabilized after 2 wk of immobilization, whereas the arthrogenic contracture was stabilized after 3 wk of immobilization and completely stable in 4 wk.

Conclusion: This rat model may be a useful tool to study the etiology of joint contracture and establish therapeutic approaches.

Abstract Image

Abstract Image

Abstract Image

大鼠外固定后伸膝关节挛缩的形成过程。
背景:目前的研究缺乏大鼠膝关节伸展挛缩的模型。目的:探讨膝关节伸展挛缩症的形成过程。方法:采用铝制外固定器制作大鼠模型。将60只骨骼成熟的雄性Sprague-Dawley大鼠分为对照组(n=6)和用铝外固定器固定左膝1、2和3天以及1、2、3、4、6和8周的组(每组n=6)。比较对照组和固定化组的被动延伸运动范围、组织学和纤维化相关蛋白的表达。结果:肌源性挛缩在固定的最初2周内进展非常快。2周后,挛缩逐渐由肌源性变为关节源性。关节源性挛缩在第1周进展缓慢,快速进展至第3周,然后稳定发展至第4周。组织学分析证实,随着时间的推移,延长固定膝关节的前关节囊越来越厚。相应地,前关节囊中转化生长因子β1(TGF-β1)和磷酸化母亲对抗偏瘫同源物2(p-Smad2)的水平也随着固定时间的增加而增加。随着时间的推移,肌肉纤维的横截面积逐渐减小,而肌间胶原和TGF-β1、p-Smad2和p-Smad3的量增加。出乎意料的是,肌间胶原和TGF-β1、p-Smad2和p-Smad3的量在固定后期(6-8周)减少。肌源性挛缩在固定2周后稳定,而关节源性挛缩则在固定3周后稳定并在4周内完全稳定。结论:该模型可作为研究关节挛缩症病因和制定治疗方法的有用工具。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
3.10
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