肩胛上神经损伤对大鼠肩袖撕裂模型中肌肉和骨骺再生的影响。

IF 1.8 Q2 ORTHOPEDICS
Kenichiro Eshima, Hiroki Ohzono, Masafumi Gotoh, Hisao Shimokobe, Koji Tanaka, Hidehiro Nakamura, Tomonoshin Kanazawa, Takahiro Okawa, Naoto Shiba
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引用次数: 0

摘要

背景:大量肩袖撕裂(rct)并发肌肉萎缩、纤维化和肌内脂肪变性,这与术后肌腱-骨愈合失败和不良临床结果有关。我们在大鼠模型中评估了有或没有肩胛上神经(SN)损伤的大撕裂时肌肉和椎体的变化。方法:将62只成年sd - dawley大鼠分为SN损伤组(+)和SN损伤组(-),每组31只,分别由肌腱(冈上肌[SSP]/冈下肌[ISP])和神经切除组和仅肌腱切除组组成。术后4周、8周和12周进行肌肉重量测量、组织学评估和生物力学测试。术后8周采用块面成像进行超微结构分析。结果:与对照组和SN损伤(-)组相比,SN损伤(+)组SSP/ISP肌肉出现萎缩,脂肪组织增加,肌肉重量下降。免疫反应性仅在SN损伤(+)组呈阳性。SN损伤(+)组肌原纤维排列不整齐、线粒体肿胀严重程度及脂肪细胞数量均高于SN损伤(-)组。SN损伤(-)组骨-肌腱连接处端部牢固;SN损伤(+)组细胞萎缩变薄,细胞密度降低,纤维软骨未成熟。力学上,SN损伤(+)组的肌腱-骨止点明显弱于对照组和SN损伤(+)组。结论:在临床环境中,在大型随机对照试验中,SN损伤可能导致严重的脂肪改变和术后肌腱愈合的抑制。证据水平:基础研究,对照实验室研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Effect of suprascapular nerve injury on muscle and regenerated enthesis in a rat rotator cuff tear model.

Effect of suprascapular nerve injury on muscle and regenerated enthesis in a rat rotator cuff tear model.

Effect of suprascapular nerve injury on muscle and regenerated enthesis in a rat rotator cuff tear model.

Effect of suprascapular nerve injury on muscle and regenerated enthesis in a rat rotator cuff tear model.

Background: Massive rotator cuff tears (RCTs) are complicated by muscle atrophy, fibrosis, and intramuscular fatty degeneration, which are associated with postoperative tendon-to-bone healing failure and poor clinical outcomes. We evaluated muscle and enthesis changes in large tears with or without suprascapular nerve (SN) injury in a rat model.

Methods: Sixty-two adult Sprague-Dawley rats were divided into SN injury (+) and SN injury (-) groups (n=31 each), comprising tendon (supraspinatus [SSP]/infraspinatus [ISP]) and nerve resection and tendon resection only cases, respectively. Muscle weight measurement, histological evaluation, and biomechanical testing were performed 4, 8, and 12 weeks postoperatively. Ultrastructural analysis with block face imaging was performed 8 weeks postoperatively.

Results: SSP/ISP muscles in the SN injury (+) group appeared atrophic, with increased fatty tissue and decreased muscle weight, compared to those in the control and SN injury (-) groups. Immunoreactivity was only positive in the SN injury (+) group. Myofibril arrangement irregularity and mitochondrial swelling severity, along with number of fatty cells, were higher in the SN injury (+) group than in the SN injury (-) group. The bone-tendon junction enthesis was firm in the SN injury (-) group; this was atrophic and thinner in the SN injury (+) group, with decreased cell density and immature fibrocartilage. Mechanically, the tendon-bone insertion was significantly weaker in the SN injury (+) group than in the control and SN injury (+) groups.

Conclusions: In clinical settings, SN injury may cause severe fatty changes and inhibition of postoperative tendon healing in large RCTs. Level of evidence: Basic research, controlled laboratory study.

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