The braking force to Control the Abnormal Tibial Translation Affects the Spontaneous Healing Response for Complete Ruptured Anterior Cruciate Ligament in Mice Model

Author:

Saito RikuORCID,Nakayama KazukiORCID,Usami YunaORCID,Enomoto SaayaORCID,Nogi KoyoORCID,Kokubun TakanoriORCID

Abstract

AbstractThe anterior cruciate ligament (ACL) has been considered to not heal spontaneously after complete injury due to its unique intra-articular environment. However, several clinical and animal studies have reported that ruptured ACL could heal spontaneously by controlling abnormal joint movement. On the other hand, heled ACL has lower collagen maturity and mechanical properties than intact ACL. Appropriate mechanical stress on the ligament could promote spontaneous healing, whereas excessive mechanical stress probably inhibits the healing response. We investigated the effect of braking force to control anterior tibial translation (ATT) on the healing response of the ACL using two different controlled anterior tibial translation (CATT) models. Male and female C57BL/6 mice were ruptured ACL and randomly classified to CATT with 3-0 nylon suture (3-0 CATT) group, CATT with 4-0 nylon suture (4-0 CATT) group, ACL-rupture (ACL-R) group. We evaluated magnitude of ATT, success rate of the ACL healing, collagen maturity and mechanical property immediately after injury, at 4– and 8-weeks post-injury. 3-0 CATT group had better braking force of ATT than 4-0 CATT group immediately after injury and showed higher success rate than 4-0 CATT group females at 4 and 8 weeks. In contrast, collagen maturation and mechanical strength of the healed ACL showed no difference between 3-0 CATT and 4-0 CATT groups. Our results suggested that firm ATT braking immediately after injury is necessary for successful healing of the injured ACL. On the other hand, increased ATT in the early phase was insufficient to improve mechanical strength and collagen maturation, and future studies is needed to elucidate the optimal timing of mechanical stress.Study Design: A controlled laboratory study.

Publisher

Cold Spring Harbor Laboratory

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