Kaneguchi A1, Ozawa J1, Minamimoto K2
1Hiroshima International University, Department of Rehabilitation, Faculty of Rehabilitation, Higashi-Hiroshima, Japan, 2Hiroshima International University, Major in Medical Engineering and Technology, Graduate School of Medical Technology and Health Welfare Sciences, Higashi-Hiroshima, Japan
Background: Anterior cruciate ligament (ACL) injury is one of the most common injuries in athletes. ACL reconstruction (ACLR) is considered to enable early return to sports, however, ACLR leads to joint contracture as a side effect. Accelerated rehabilitation which is unrestricted joint motion in early postoperative period is widely accepted in a clinical setting but nevertheless, joint contracture is developed after ACLR. Therefore, we consider that factors other than immobilization (reduced joint motion) play a critical role in joint contracture formation following ACLR. In order to verify this hypothesis, development of an animal model of joint contracture induced by ACLR without joint immobilization is required.
Purpose: We aimed 1) to develop a rat model of joint contracture following ACLR; 2) to investigate whether immobilization (reduced joint motion) contributes to the formation of joint contracture following ACLR.
Methods: Eight-week-old Wistar rats were divided into two groups; ACL transection (ACLT; n = 6) and ACL reconstruction groups (ACLR; n = 7). ACL transection and reconstruction were performed in the right knees, and untreated left knees were used as controls. After surgery, rats were allowed to move freely in a cage without any intervention. Active knee range of motion (ROM) and the nociception index of the one-hindlimb standing time ratio (STR) during treadmill locomotion were assessed using three-dimensional locomotion analysis at pre- and post-surgery up to 8 weeks. The knee joint diameter and passive knee extension ROM were also measured at the same time points to assess the inflammation and flexion contracture, respectively.
Results: At 1 week post-surgery, flexion contracture represented by passive ROM reduction was 49° and 21° in ACLR and ACLT groups, respectively. Thereafter, flexion contractures were attenuated in a time-dependent manner and reached 28° and 9° at 8 weeks in ACLR and ACLT groups, respectively. In ACLR group, active ROM during locomotion was also decreased at 1 week (72% of the contralateral side) and recovered to the contralateral side level at 8 weeks. In ACLT group, active ROM was not changed significantly until 8 weeks. STR was transiently decreased in ACLR group at 1 week, but not in ACLT group. Joint diameter in ACLR group was significantly increased between 1 to 8 weeks, while that in ACLT group was not changed until 8 weeks.
Conclusion(s): We could develop a new model of joint contracture induced by ACLR without joint immobilization. Although reduction in active ROM was partial, joint contracture following ACLR developed more rapidly than that following joint immobilization reported in previous studies (30-40° at 1 week). Therefore, reduced joint motion during locomotion would play little if any role in the development of joint contracture following ACLR. Joint contracture was also observed in ACLT group, but it was less than half of ACLR group. Nociception and inflammation after reconstruction surgery might induce severe joint contracture.
Implications: Our rat model will be suitable to examine formation mechanisms and effective therapeutic strategies for ACLR-induced joint contracture. Inhibition of nociception and inflammation may be attractive targets for the formation of ACLR-induced joint contracture.
Keywords: ACL injury, ACL reconstruction, joint contracture
Funding acknowledgements: This study was supported by grants from the Japanese Society of Physio Therapeutics.
Purpose: We aimed 1) to develop a rat model of joint contracture following ACLR; 2) to investigate whether immobilization (reduced joint motion) contributes to the formation of joint contracture following ACLR.
Methods: Eight-week-old Wistar rats were divided into two groups; ACL transection (ACLT; n = 6) and ACL reconstruction groups (ACLR; n = 7). ACL transection and reconstruction were performed in the right knees, and untreated left knees were used as controls. After surgery, rats were allowed to move freely in a cage without any intervention. Active knee range of motion (ROM) and the nociception index of the one-hindlimb standing time ratio (STR) during treadmill locomotion were assessed using three-dimensional locomotion analysis at pre- and post-surgery up to 8 weeks. The knee joint diameter and passive knee extension ROM were also measured at the same time points to assess the inflammation and flexion contracture, respectively.
Results: At 1 week post-surgery, flexion contracture represented by passive ROM reduction was 49° and 21° in ACLR and ACLT groups, respectively. Thereafter, flexion contractures were attenuated in a time-dependent manner and reached 28° and 9° at 8 weeks in ACLR and ACLT groups, respectively. In ACLR group, active ROM during locomotion was also decreased at 1 week (72% of the contralateral side) and recovered to the contralateral side level at 8 weeks. In ACLT group, active ROM was not changed significantly until 8 weeks. STR was transiently decreased in ACLR group at 1 week, but not in ACLT group. Joint diameter in ACLR group was significantly increased between 1 to 8 weeks, while that in ACLT group was not changed until 8 weeks.
Conclusion(s): We could develop a new model of joint contracture induced by ACLR without joint immobilization. Although reduction in active ROM was partial, joint contracture following ACLR developed more rapidly than that following joint immobilization reported in previous studies (30-40° at 1 week). Therefore, reduced joint motion during locomotion would play little if any role in the development of joint contracture following ACLR. Joint contracture was also observed in ACLT group, but it was less than half of ACLR group. Nociception and inflammation after reconstruction surgery might induce severe joint contracture.
Implications: Our rat model will be suitable to examine formation mechanisms and effective therapeutic strategies for ACLR-induced joint contracture. Inhibition of nociception and inflammation may be attractive targets for the formation of ACLR-induced joint contracture.
Keywords: ACL injury, ACL reconstruction, joint contracture
Funding acknowledgements: This study was supported by grants from the Japanese Society of Physio Therapeutics.
Topic: Sport & sports injuries; Musculoskeletal: lower limb; Orthopaedics
Ethics approval required: Yes
Institution: Hiroshima International University
Ethics committee: Animal experimentation committee
Ethics number: AE18-018
All authors, affiliations and abstracts have been published as submitted.
