Biomechanical Characterization of a Model of Noninvasive, Traumatic Anterior Cruciate Ligament Injury in the Rat.

Abstract

The onset of post-traumatic osteoarthritis (PTOA) remains prevalent following traumatic joint injury such as anterior cruciate ligament (ACL) rupture, and animal models are important for studying the pathomechanisms of PTOA. Noninvasive ACL injury using the tibial compression model in the rat has not been characterized, and it may represent a more clinically relevant model than the common surgical ACL transection model. This study employed four loading profiles to induce ACL injury, in which motion capture analysis was performed, followed by quantitative joint laxity testing. High-speed, high-displacement loading repeatedly induces complete ACL injury, which causes significant increases in anterior-posterior and varus laxity. No loading protocol induced valgus laxity. Tibial internal rotation and anterior subluxation occurs up to the point of ACL failure, after which the tibia rotates externally as it subluxes over the femoral condyles. High displacement was more determinative of ACL injury compared to high speed. Low-speed protocols induced ACL avulsion from the femoral footprint whereas high-speed protocols caused either midsubstance rupture, avulsion, or a combination injury of avulsion and midsubstance rupture. This repeatable, noninvasive ACL injury protocol can be utilized in studies assessing PTOA or ACL reconstruction in the rat.