Re-stabilization of joint instability may suppress inflammatory cytokines, thereby delaying the progression of OA. Joint instability is a substantial contributor to cartilage degeneration.

Objective Abnormal joint movement is associated with osteoarthritis (OA). Previous studies using the controlling abnormal joint movement (CAJM) model of OA reported delayed cartilage degeneration; however, none of them focused on gait performance and the localization of matrix metalloproteinase 13 (MMP13) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in chondrocytes. Therefore, we aimed to investigate the effect of controlling abnormal joint movement on gait performance and the localization of MMP13 and TIMP-1, using kinematic and histological analyses. Design Rats were assigned to 2 groups: anterior cruciate ligament transection (ACL-T) group and CAJM group ( n = 5/group); contralateral hind limbs of ACL-T rats were designated as intact. After 1, 2, and 4 weeks, step length was analyzed, and after 2, 4, and 8 weeks, Safranin O-Fast Green staining and immunohistochemical staining for MMP13 and TIMP-1 were performed. Results Step length did not differ significantly between the groups. However, degeneration of articular cartilage was higher in the ACL-T group than in the intact group ( P < 0.05). There was no significant difference in the CAJM group at all time points. Immunohistochemical analysis of the MMP13/TIMP-1 relationship revealed a significant increase in the expression ratio of MMP13 after 4 weeks in the ACL-T group compared to the CAJM group ( P < 0.05). Conclusions Controlling abnormal joint movement may reduce mechanical stress owing to kinematic elements of small articulation including joint instability and delayed cartilage degeneration, despite the lack of kinematic change in step length.

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.

Objective: Abnormal joint instability contributes to cartilage damage and osteophyte formation. We investigated whether controlling joint instability inhibited chronic synovial membrane inflammation and delayed osteophyte formation and examined the role of transforming growth factor-beta (TGF-b) signaling in the associated mechanism. Design: Rats (n ¼ 94) underwent anterior cruciate ligament (ACL) transection. Anterior tibial instability was either controlled (CAM group) or allowed to continue (SHAM group). At 2, 4, and 8 weeks after surgery, radiologic, histopathologic, immunohistochemical, immunofluorescent, and enzyme-linked immunosorbent assay examinations were performed to evaluate osteophyte formation and TGF-b signaling.Results: Joint instability increased cartilage degeneration score and osteophyte formation, and cell hyperplasia and proliferation and synovial thickening were observed in the synovial membrane. Major findings were increased TGF-b expression and Smad2/3 following TGF-b phosphorylation in synovial membarene, articular cartilage, and the posterior tibial growth plate (TGF-b expression using ELISA: 4 weeks; P ¼ 0.009, 95% CI [260.1e1340.0]) (p-Smad2/3 expression density: 4 weeks; P ¼ 0.024, 95% CI [1.67e18.27], 8 weeks; P ¼ 0.034, 95% CI [1.25e25.34]). However, bone morphogenetic protein (BMP)-2 and Smad1/5/8 levels were not difference between the SHAM model and the CAM model. Conclusions: This study showed that the difference between anterior tibial instability caused a change in the expression level of TGF in the posterior tibia and synovial membrane, and the reaction might be consequently involved in osteophyte formation.

The objective of the current study was to evaluate the reliability and validity of the Japanese version of the Mini-Balance Evaluation Systems Test (J-Mini-BESTest) in patients with subacute stroke. Methods: Eighteen patients who had suffered a first hemiplegic stroke (mean age, 59.1 ± 27.0 years) and had been admitted to convalescent rehabilitation wards were enrolled. The J-Mini-BESTest, the Berg Balance Scale (BBS), and the functional reach test (FRT) were used to assess balance. Four physical therapists (PTs) observed and scored the J-Mini-BESTest while another PT conducted the test. The interrater reliability of the J-Mini-BESTest was assessed using intraclass correlation coefficients (ICC[2,1]) for the total and section scores, and kappa statistics for each item. Internal consistency of the five raters was assessed using Cronbach's alpha. Concurrent validity of the J-Mini-BESTest was assessed against the BBS and FRT using Spearman's correlation coefficients. Results: The ICC[2,1] of the total and section scores were 0.90 (95% confidence interval: 0.81-0.95) and 0.63-0.85, respectively. Cronbach's alphas were 0.80-0.87. The kappa statistics were 0.47-1.00. The scores of the J-Mini-BESTest were significantly correlated with those of the BBS (rho=0.66, p=0.006) but not with those of the FRT (rho=-0.36, p= 0.189). Conclusion: The J-Mini-BESTest showed excellent inter-rater reliability and internal consistency. Although the J-Mini-BESTest was not correlated with the FRT, it was significantly correlated with the BBS. The J-Mini-BESTest is a reliable and valid tool for evaluating dynamic balance in patients with subacute stroke.