This study investigated the effects of treadmill walking during remobilization on range of motion (ROM) and histopathology in rat knee joints, which were immobilized for 3 wk in a flexed position. After fixator removal, rats were divided into a no-intervention (RM) group and a group forced to walk on a treadmill daily at 12 m/min for 60 min (WALK group). Passive knee extension ROMs were measured before (m-ROM) and after (a-ROM) knee flexor myotomy on the first and last day of a 7-day remobilization period, with m-ROM mainly reflecting myogenic factors and a-ROM reflecting arthrogenic factors. Knee joints were histologically analyzed and gene expression of inflammatory or fibrosis-related mediators in the posterior joint capsule were examined. m-ROM and a-ROM restrictions were established after immobilization. m-ROM significantly increased following the remobilization period both in RM and WALK groups compared with that of immobilized (IM) group. Conversely, a-ROM decreased following the remobilization period in both RM and WALK groups compared with that of IM group. Importantly, a-ROM was smaller in the WALK group than the RM group. Remobilization without intervention induced inflammatory and fibrotic reactions in the posterior joint capsule after 1 and 7 days. Treadmill walking promoted these reactions and also increased the expression of fibrosis-related TGF-β1 and collagen type I and III genes. While free movement after immobilization improved myogenic contracture, arthrogenic contracture worsened. Treadmill walking further aggravated arthrogenic contracture through amplified inflammatory and fibrotic reactions. Thus active exercise immediately after immobilization may not improve immobilization-induced joint contracture. NEW & NOTEWORTHY In clinical practice, it is widely accepted that facilitation of joint movements is effective in improving immobilization-induced joint contracture. However, whether active exercises improve arthrogenic contracture is not known. In this study, we revealed that treadmill walking further promoted remobilization-induced progression of arthrogenic contracture. To our knowledge, this is the first study demonstrating no favorable effect of active exercise on immobilization-induced arthrogenic contracture.

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Objective The process of anterior cruciate ligament (ACL) injury-induced meniscal tear formation is not fully understood. Clinical studies have shown that ACL reconstruction (ACLR) reduces the development of secondary meniscal tears, but it is difficult to gain insight into the protective effects of ACLR from clinical studies alone. Using rat ACL transection (ACLT) and ACLR models, we aimed to reveal (1) the formation process of meniscal tears secondary to ACLT and (2) the protective effects of ACLR on secondary meniscal tears. Design ACLT surgery alone or with ACLR was performed on the knees of rats. Histomorphological and histopathological changes were examined in the posteromedial region of the meniscus in intact rats and in rats that received ACLT or ACLR up to 12 weeks postsurgery. In addition, anterior-posterior joint laxity was measured using the universal testing machine to evaluate the effects of ACLT and ACLR on joint laxity. Results AAnterior-posterior laxity was significantly increased by ACLT compared to the intact knee. This ACLT-induced joint laxity was partially but significantly reduced by ACLR. Meniscal proliferation and hyaline cartilage–like tissue formation were detected in the medial meniscus at 4 weeks post-ACLT. At 12 weeks post-ACLT, hyaline cartilage–like tissue was replaced by ossicles and meniscal tears were observed. These ACLT-induced abnormalities were attenuated by ACLR. Conclusions Our results suggest that ACLT-induced joint laxity induces secondary medial meniscal tears through meniscal proliferation and ossicle formation via endochondral ossification. Joint re-stabilization by ACLR suppresses meniscal proliferation and ossicle formation and consequently prevents secondary meniscal tears.

Knee joint contracture is often induced by anterior cruciate ligament reconstruction (ACLR). However, the temporal and spatial arthrofibrotic changes following inflammatory events, which occur in parallel with the formation of joint contractures after ACLR, are unknown. This study aimed to reveal: (a) time-dependent changes in myogenic and arthrogenic contractures; and (b) the process of arthrofibrosis development after ACLR. ACLR was performed on knees of rats unilaterally. Passive ranges of motions (ROMs) before and after myotomy, as well as inflammatory and fibrotic reactions, were examined before and after the surgery at various periods up to 56 days. Both ROMs before and after myotomy exhibited their lowest value on day 7 and increased thereafter in a time-dependent manner; nevertheless,