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体内肌腱病模型中由于周期性负荷导致肌腱微撕裂的证据。

Evidence of tendon microtears due to cyclical loading in an in vivo tendinopathy model.

作者信息

Nakama Leena H, King Karen B, Abrahamsson Sven, Rempel David M

机构信息

Joint Graduate Group in Bioengineering, University of California, Berkeley, CA, USA.

出版信息

J Orthop Res. 2005 Sep;23(5):1199-205. doi: 10.1016/j.orthres.2005.03.006. Epub 2005 Apr 26.

DOI:10.1016/j.orthres.2005.03.006
PMID:16140201
Abstract

Tendon injuries at the epicondyle can occur in athletes and workers whose job functions involve repetitive, high force hand activities, but the early pathophysiologic changes of tendon are not well known. The purpose of this study was to evaluate early tendon structural changes, specifically the formation of microtears, caused by cyclical loading. The Flexor Digitorum Profundus (FDP) muscle of nine New Zealand White rabbits was stimulated to contract repetitively for 80 h of cumulative loading over 14 weeks. The contralateral limb served as a control. The tendon at the medial epicondyle insertion site was harvested, sectioned, and stained. Microtears were quantified, using image analysis software, in four regions of the tendon, two regions along the enthesis and two distal to the enthesis. The tear density (loaded: 1329+/-546 tears/mm(2); unloaded: 932+/-474 tears/mm(2)) and mean tear size (loaded: 18.3+/-6.1 microm(2); unloaded: 14.0+/-4.8 microm(2)) were significantly greater in the loaded limb (p<0.0001) across all regions compared to the unloaded contralateral limb. These early microstructural changes in a repetitively loaded tendon may initiate a degenerative process that leads to tendinosis.

摘要

在从事重复性、高强度手部活动的运动员和工人中,肱骨髁上的肌腱损伤可能会发生,但肌腱早期的病理生理变化尚不为人所知。本研究的目的是评估由周期性负荷引起的肌腱早期结构变化,特别是微撕裂的形成。对9只新西兰白兔的指深屈肌(FDP)进行刺激,使其在14周内累计重复收缩80小时。对侧肢体作为对照。采集肱骨内侧髁附着点处的肌腱,进行切片和染色。使用图像分析软件对肌腱的四个区域(沿附着点的两个区域和附着点远端的两个区域)的微撕裂进行量化。与未负荷的对侧肢体相比,负荷肢体所有区域的撕裂密度(负荷:1329±546个撕裂/mm²;未负荷:932±474个撕裂/mm²)和平均撕裂大小(负荷:18.3±6.1μm²;未负荷:14.0±4.8μm²)均显著更高(p<0.0001)。重复性负荷肌腱中的这些早期微观结构变化可能引发导致肌腱病的退变过程。

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