肱二头肌隧道炎症的分子特征

IF 1.2 Q3 SPORT SCIENCES
A. Campbell, Samuel A. Taylor, E. O’Dea, Mary E. Shorey, R. Warren, S. O’Brien
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引用次数: 0

摘要

关节外二头肌疾病的病理生理学尚不完全清楚。本研究的目的是评估二头肌关节外肌腱及其限制隧道3个独立解剖区内炎症、降解和伤害性的分子证据。从11名疑似二头肌-阴唇复合体疾病患者的肱二头肌隧道中进行关节镜活检,这些患者正在接受三角肌下二头肌移植到联合肌腱。分析组织中各种炎症介质的mRNA表达,包括白介素-6、白介素-1β、转化生长因子β(TGF-β)、基质金属蛋白酶-13和P物质前体。将关节外组织与关节内肌腱(内部对照)进行比较,以确定表达的折叠变化。与关节内肌腱相比,关节外二头肌腱和滑膜中上述介质的水平增加,显著增加TGF-β(P=.012)。在有二头肌腱长头腱病临床病史以及滑膜炎、撕裂和松动体关节镜检查结果的患者中,关节外肌腱中的促炎性和退行性细胞因子上调。在临床上明显的二头肌复合体疾病患者的二头肌腱关节外长头及其约束性纤维骨二头肌隧道内发现了与伤害相关的炎症细胞因子、退行性介质和疼痛分子。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A molecular characterization of inflammation in the bicipital tunnel
The pathophysiology of extra‐articular biceps disease is not fully understood. The purpose of the study was to assess molecular evidence of inflammation, degradation, and nociception within the 3 separate anatomic zones of the extra‐articular biceps tendon and its confining tunnel. Arthroscopic biopsies were taken from the bicipital tunnel from 11 patients with suspected biceps‐labrum complex disease undergoing subdeltoid biceps transfer to the conjoint tendon. Tissue was analyzed for mRNA expression of various inflammatory mediators including interleukin‐6, interleukin‐1β, transforming growth factor‐β (TGF‐β), matrix metalloproteinase‐13, and substance P precursor. Extra‐articular tissue was compared with intra‐articular tendon (internal control) to determine fold change in expression. Compared to intra‐articular tendon, extra‐articular biceps tendon and synovium have increased levels of these aforementioned mediators, significantly TGF‐β (P = .012). In patients with clinical history of long head of the biceps tendon tendinopathy as well as arthroscopic findings of synovitis, tear, and loose bodies, pro‐inflammatory and degenerative cytokines were upregulated in the extra‐articular tendon. Inflammatory cytokines, degenerative mediators, and pain molecules associated with nociception were found within both the extra‐articular long head of biceps tendon and its constraining fibro‐osseous bicipital tunnel in patients with clinically evident biceps‐labral complex disease.
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