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首页> 外文期刊>Journal of orthopaedic research >Nociception contributes to the formation of myogenic contracture in the early phase of adjuvant-induced arthritis in a rat knee
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Nociception contributes to the formation of myogenic contracture in the early phase of adjuvant-induced arthritis in a rat knee

机译：伤害效果有助于在大鼠膝关节中佐剂诱导的关节炎的早期形成肌原挛缩挛缩

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It is unknown how joint contracture is generated in inflamed joints. This study aimed to clarify the role of nociception on the formation of joint contracture secondary to arthritis. Monoarthritis was induced by intra-articular injections of complete Freund's adjuvant (CFA) into rat knees. On day 5 after CFA injection, the passive extension range of motion (ROM) of knee joints were measured, both before and after myotomy of knee flexors, to evaluate the extent of muscular contribution to CFA-induced joint contracture. The steroidal anti-inflammatory drug dexamethasone could prevent ROM restrictions completely, both before and after myotomy. On the other hand, the opioid analgesic drug morphine did not prevent the development of restricted ROM observed after myotomy, while it did before myotomy. This indicates that nociception contributes to joint contracture through alterations in muscular structure (myogenic factors). Next, we tested the hypothesis that nociception-induced reflexive flexor muscle contractions cause myogenic contracture in arthritic joints. To do this, chemical denervation was performed by Botulinum toxin type A (BTX-A) injections into knee flexor muscles, simultaneously with CFA injections into the knee. As expected, BTX-A could alleviate ROM restrictions observed before myotomy. These findings suggest that nociceptive-related muscle contractions play an essential role in the formation of joint contracture. Thus, our study indicates that analgesic management during an early stage of joint arthritis is an essential mean to prevent the formation of joint contracture. (c) 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:1404-1413, 2017.
机译：尚不清楚如何在发炎的关节中产生联合挛缩。本研究旨在阐明Nocieptions对关节炎关节挛缩形成的作用。通过关节内注射完整的弗氏佐剂（CFA）诱导单细胞炎进入大鼠膝盖。在CFA注射后第5天，测量膝关节前后膝关节的动作（ROM）的被动延伸范围（ROM），以评估对CFA诱导的关节挛缩的肌肉贡献程度。甾体抗炎药物地塞米松可以完全防止MyOtomy之前和之后完全限制。另一方面，阿片类药物镇痛药物吗啡没有阻止在肌肌瘤后观察到的限制性rom的发育，而在肌动术前做过。这表明伤害效果通过肌肉结构（肌源性因子）的改变有助于接触挛缩。接下来，我们测试了伤害诱导的反射屈肌收缩导致关节炎关节中肌菌挛缩的假设。为此，通过肉毒杆菌毒素型A（BTX-A）注射到膝关节肌肉中，同时用CFA注射进入膝关节。正如预期的那样，BTX-A可以减轻在肌肌瘤之前观察到的ROM限制。这些研究结果表明，伤害相关的肌肉收缩在联合挛缩的形成中起重要作用。因此，我们的研究表明，在关节炎的早期阶段期间镇痛管理是预防接合挛缩的必然意义。 （c）2016骨科研究会。由Wiley Hearyicals，Inc.J Orthop Res 35：1404-1413,2017出版。

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