Biomechanical Evaluation of Anterolateral Ligament Repair Augmented with Internal Brace

Injuries to the anterolateral ligament (ALL) of the knee are commonly associated with anterior cruciate ligament (ACL) ruptures. Biomechanical studies have demonstrated conflicting results with regard to the role of the ALL in limiting tibial internal rotation. Clinically, residual pivot shift following ACL reconstruction has been reported to occur up to 25% and has been correlated with poor outcomes. As such, surgical techniques have been developed to enhance rotational stability. Recent biomechanical studies have demonstrated restoration of internal rotational control following ALL reconstruction. The purpose of our study was to understand the biomechanical effects of ACL reconstruction with an ALL internal brace augmentation. We hypothesized that (1) sectioning of the ALL while preserving other lateral extra-articular structures would lead to significant internal rotation laxity and gap formation and (2) ALL repair with internal brace augmentation would lead to reduction in internal rotation instability and gap formation. In total, 10 fresh-frozen cadaveric knees were thawed and biomechanically tested in internal rotation for 10 cycles of normal physiologic torque in the intact, ACL-deficient, ACL/ALL-deficient, ACL-reconstructed, and ALL-repaired conditions. Each condition was tested at 30, 60, and 90 degrees of flexion. Following the final ALL-repaired condition, specimens were additionally subjected to a final internal rotation to failure at 1 degree at the last-tested degree of flexion. Kinematic measurements of angle and linear gap between the femur and tibia were calculated in addition to torsional stiffness and failure torque. As hypothesized, ALL repair with internal brace augmentation significantly reduced internal rotation angular motion and gap formation at flexion angles greater than 30 degrees. Additionally, ALL sectioning produced nonsignificant increases in internal rotation laxity and gap formation compared with ACL-deficient and ACL-reconstructed states, which did not support our other hypothesis.