2226 Gillespie Neuroscience Research Facility, University of California at Irvine, Irvine, CA 92697-4292, USA.
J Bone Joint Surg Am. 2010 Oct 6;92(13):2270-8. doi: 10.2106/JBJS.I.00812.
Detachment of a tendon from its osseous insertion, as can be the case with severe rotator cuff injuries, leads to atrophy of and increased fat in the corresponding muscle. We sought to validate a rotator cuff injury model in the rabbit and to test the hypothesis that tenotomy of a rotator cuff tendon would consistently create muscle atrophy and fatty degeneration analogous to the changes that occur after injury to a nerve innervating the same muscle.
New Zealand white rabbits were divided into three groups: (1) partial rotator cuff tear without retraction of the muscle, (2) complete rotator cuff tear with retraction of the muscle, and (3) nerve transection of the subscapular nerve. Animals were killed at two or six weeks after injury, and the muscles were analyzed for weight, cross-sectional area, myosin fiber-type composition, and fat content. In addition, the subscapular nerve was harvested at two weeks and evaluated for neuronal injury.
At six weeks after injury, the rabbit muscles in the complete tenotomy and nerve transection groups had significant decreases in wet mass and increases in fat content relative to the control groups. Fat accumulation had a similar spatial pattern at six weeks in both the nerve transection and complete tenotomy groups. Such changes were not seen in the partial tenotomy group. No change was found in muscle myosin fiber-type composition. At two weeks after injury, subscapular nerves in the complete tenotomy group showed gross evidence of neuronal injury.
This study establishes the rabbit subscapularis muscle as a valid model to study the muscular changes associated with rotator cuff tears. Our data suggest that the muscular changes associated with complete tenotomy are comparable with those seen with denervation of the muscle and suggest that chronic rotator cuff tears may induce a neurologic injury.
肌腱从其骨附着处分离,如严重肩袖损伤的情况,会导致相应肌肉萎缩和脂肪增加。我们试图验证兔肩袖损伤模型,并验证这样一个假设,即肩袖肌腱的切断将始终导致类似于支配同一肌肉的神经损伤后发生的肌肉萎缩和脂肪变性。
新西兰白兔分为三组:(1)部分肩袖撕裂,肌肉无回缩;(2)完全肩袖撕裂伴肌肉回缩;(3)肩胛下神经切断。损伤后 2 或 6 周处死动物,分析肌肉重量、横截面积、肌球蛋白纤维类型组成和脂肪含量。此外,在 2 周时收获肩胛下神经并评估神经元损伤。
损伤后 6 周,完全切断组和神经切断组的兔肌肉湿重明显下降,脂肪含量明显增加,与对照组相比。在神经切断和完全切断组中,6 周时脂肪堆积的空间模式相似。在部分切断组中未观察到这种变化。肌肉肌球蛋白纤维类型组成无变化。损伤后 2 周,完全切断组的肩胛下神经显示出明显的神经元损伤的大体证据。
本研究确立了兔肩胛下肌作为研究肩袖撕裂相关肌肉变化的有效模型。我们的数据表明,与完全切断相关的肌肉变化与失神经相似,并表明慢性肩袖撕裂可能会引起神经损伤。