Murata Kenji, Kokubun Takanori, Morishita Yuri, Onitsuka Katsuya, Fujiwara Shuhei, Nakajima Aya, Fujino Tsutomu, Takayanagi Kiyomi, Kanemura Naohiko
1 Department of Physical Therapy, School of Health and Social Services, Saitama Prefectural University, Saitama, Japan.
2 Department of Health and Social Services, Course of Health and Social Services, Graduate School of Saitama Prefectural University, Saitama, Japan.
Cartilage. 2018 Oct;9(4):391-401. doi: 10.1177/1947603517700955. Epub 2017 Apr 11.
Objective Osteoarthritis (OA) is induced by accumulated mechanical stress to joints; however, little has been reported regarding the cause among detailed mechanical stress on cartilage degeneration. This study investigated the influence of the control of abnormal joint movement induced by anterior cruciate ligament (ACL) injury in the articular cartilage. Design The animals were divided into 3 experimental groups: CAJM group ( n = 22: controlling abnormal joint movement), ACL-T group ( n = 22: ACL transection or knee anterior instability increased), and INTACT group ( n = 12: no surgery). After 2 and 4 weeks, the knees were harvested for digital microscopic observation, soft X-ray analysis, histological analysis, and synovial membrane molecular evaluation. Results The 4-week OARSI scores showed that cartilage degeneration was significantly inhibited in the CAJM group as compared with the ACL-T group ( P < 0.001). At 4 weeks, the osteophyte formation had also significantly increased in the ACL-T group ( P < 0.001). These results reflected the microscopic scoring and soft X-ray analysis findings at 4 weeks. Real-time synovial membrane polymerase chain reaction analysis for evaluation of the osteophyte formation-associated factors showed that the mRNA expression of BMP-2 and VEGF in the ACL-T group had significantly increased after 2 weeks. Conclusions Typically, abnormal mechanical stress induces osteophyte formation; however, our results demonstrated that CAJM group inhibited osteophyte formation. Therefore, controlling abnormal joint movement may be a beneficial precautionary measure for OA progression in the future.
目的 骨关节炎（OA）是由关节累积的机械应力诱发的；然而，关于软骨退变具体机械应力中的病因报道较少。本研究调查了前交叉韧带（ACL）损伤引起的异常关节运动控制对关节软骨的影响。
设计 将动物分为3个实验组：CAJM组（n = 22：控制异常关节运动）、ACL-T组（n = 22：ACL横断或膝关节前向不稳增加）和完整组（n = 12：未手术）。2周和4周后，取膝关节进行数字显微镜观察、软X线分析、组织学分析和滑膜分子评估。
结果 4周时的OARSI评分显示，与ACL-T组相比，CAJM组软骨退变受到显著抑制（P < 0.001）。4周时，ACL-T组骨赘形成也显著增加（P < 0.001）。这些结果反映了4周时的显微镜评分和软X线分析结果。用于评估骨赘形成相关因子的实时滑膜聚合酶链反应分析表明，ACL-T组2周后BMP-2和VEGF的mRNA表达显著增加。
结论 通常，异常机械应力会诱导骨赘形成；然而，我们的结果表明CAJM组抑制了骨赘形成。因此，控制异常关节运动可能是未来预防OA进展的有益措施。
