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股内侧肌肌力减弱导致的髌股关节接触压力变化。

Changes in patellofemoral joint contact pressures caused by vastus medialis muscle weakness.

作者信息

Sawatsky Andrew, Bourne Doug, Horisberger Monika, Jinha Azim, Herzog Walter

机构信息

Human Performance Laboratory, Faculty of Kinesiology, University of Calgary, Calgary, Alberta, Canada.

出版信息

Clin Biomech (Bristol). 2012 Jul;27(6):595-601. doi: 10.1016/j.clinbiomech.2011.12.011. Epub 2012 Jan 5.

DOI:10.1016/j.clinbiomech.2011.12.011
PMID:22226076
Abstract

BACKGROUND

Patellofemoral joint pain is a common knee disorder, but its underlying causes remain unknown. One proposed mechanism is an imbalance in force in the knee extensor muscles. Specifically, the vastus medialis and vastus lateralis are thought to play a crucial role in proper patellar tracking, and weakness in vastus medialis is thought to lead to a lateral shift in the patella causing increased contact pressures and pain. The purpose of this study was to create an animal model of vastus medialis weakness and to test the effect of this weakness on patellofemoral contact pressures.

METHODS

Experiments were performed using New Zealand white rabbits (mass 4.9-7.7 kg, n=12). Loading of the patellofemoral joint was produced by femoral nerve stimulation of the knee extensor muscles. Knee extensor imbalance was produced by vastus medialis ablation. Fuji pressure sensitive film was used to record contact area, shape and pressures for maximal and sub-maximal, matched-force contractions at knee angles of 30°, 60°, and 90°.

FINDINGS

Patellofemoral peak pressures, average pressures, contact areas and contact shapes were the same across all loading conditions for matched-force contractions before and after elimination of vastus medialis.

INTERPRETATION

We conclude that vastus medialis weakness does not cause changes in patellofemoral contact pressures. Since the muscular and knee joint geometry in rabbits and humans is similar, we question the idea of vastus medialis weakness as a cause of patellar mal-tracking and patellofemoral joint pain.

摘要

背景

髌股关节疼痛是一种常见的膝关节疾病,但其潜在病因尚不清楚。一种提出的机制是膝关节伸肌力量失衡。具体而言,股内侧肌和股外侧肌被认为在髌骨正常轨迹中起关键作用,股内侧肌无力被认为会导致髌骨向外移位,从而增加接触压力并引起疼痛。本研究的目的是创建股内侧肌无力的动物模型,并测试这种无力对髌股接触压力的影响。

方法

使用新西兰白兔(体重4.9 - 7.7千克,n = 12)进行实验。通过对膝关节伸肌进行股神经刺激来产生髌股关节负荷。通过切除股内侧肌来造成膝关节伸肌失衡。使用富士压力敏感膜记录在膝关节角度为30°、60°和90°时,最大和次最大匹配力收缩时的接触面积、形状和压力。

结果

在切除股内侧肌前后,对于匹配力收缩的所有负荷条件,髌股峰值压力、平均压力、接触面积和接触形状均相同。

解读

我们得出结论,股内侧肌无力不会导致髌股接触压力的变化。由于兔子和人类的肌肉和膝关节几何结构相似,我们对股内侧肌无力作为髌骨轨迹异常和髌股关节疼痛原因的观点提出质疑。

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