Background

Biomechanical studies of ACL reconstruction in-vitro are based on ACL transection instead of a realistic injury trauma and therefore resulting laxities might have been underestimated, because the surrounding soft tissues remain undamaged. Injury models that would give realistic injury patterns have not been used when studying ACL reconstruction in the past. The patterns of bone bruises post-ACL rupture in vivo are known, and that work has established and provided clinical validation of the injury kinematics reproduced in the current study.

Purpose

To replicate an ACL injury in-vitro and compare the laxity with an isolated ACL transection injury pre and post ACL reconstruction.

Hypothesis

That a simulated ACL injury would cause more laxity than isolated ACL transection.
Study design: Controlled laboratory study.

Methods

Nine paired knees were ‘ACL injured’ or ‘ACL transected’ in each pair. For ACL injury, knees were mounted in a rig which imposed tibial anterior translation at 1000 mm/min to rupture the ACL at 22.5° flexion, 5° internal rotation and 710N joint compressive force, replicating data published on clinical bone bruise locations. In contralateral knees, the ACL was transected arthroscopically at mid-substance. Both groups had ACL reconstruction with BTB graft. Native, ACL-deficient, and reconstructed laxities were measured in a kinematics rig from 0°-100° flexion with optical tracking: anterior tibial translation (ATT), internal rotation (IR), anterolateral (ATT+IR), and pivot-shift (PS:IR+valgus). Data were compared by repeated-measures ANOVA with post-testing,

Results

The ACL ruptured at 26±5mm ATT and 1550±620N force, with an audible spring-back tibiofemoral impact, with 5o valgus. ACL injury and transection increased ATT (p<0.001). ACL injury caused greater ATT than ACL transection, by 1.4(0.4-2.2)mm; p=0.033. IR increased significantly in ACL injured knees between 0°-30° and ACL transection knees from 0°-20° flexion. The ATT during the (AT+IR) maneuver was increased by ACL injury between 0°-80° and 0°-60° after ACL transection. Residual laxity persisted post-ACL reconstruction in ACL injured knees from 0°-40° and 0°-20° in the ACL transection knees. ACL deficiency increased both ATT and IR in the PS test (p<0.001). The PS-ATT increased significantly at 0°-20° after ACL transection and 0°-50° after ACL injury, and this persisted across 0°-20° and 0°-40° post ACL reconstruction.

Conclusion

This study developed an ACL injury model in-vitro that replicated clinical ACL injury as evidenced by bone bruise patterns. ACL injury caused larger increases of laxity than ACL transection, likely due to damage to adjacent tissues; these differences often persisted after ACL reconstruction.
Clinical relevance: This in-vitro model created more realistic ACL injuries than surgical transection, facilitating future evaluation of ACL reconstruction techniques.
What this study adds to existing knowledge: This study developed a reliable in-vitro ACL injury mechanism based on imaging of clinical cases. The ACL injury caused greater knee laxities than transecting the ACL. Knees with an ‘ACL injury’ had a wider persistence of residual laxity post-ACL reconstruction than did knees where the ACL had been transected. This may be a more demanding and realistic testbed for future evaluations of novel ACL and similar ligament reconstruction procedures.