The Role of the Anterolateral Structures and the ACL in Controlling Laxity of the Intact and ACL-Deficient Knee

Abstract

Background: Anterolateral rotatory instability (ALRI) may result from combined anterior cruciate ligament (ACL) and lateral extra-articular lesions, but the roles of the anterolateral structures remain controversial. Purpose: To determine the contribution of each anterolateral structure and the ACL in restraining simulated clinical laxity in both the intact and ACL-deficient knee. Study Design: Controlled laboratory study. Methods: A total of 16 knees were tested using a 6 degrees of freedom robot with a universal force-moment sensor. The system automatically defined the path of unloaded flexion/extension. At different flexion angles, anterior-posterior, internal-external, and internal rotational laxity in response to a simulated pivot shift were tested. Eight ACL-intact and 8 ACL-deficient knees were tested. The kinematics of the intact/deficient knee was replayed after transecting/resecting each structure of interest; therefore, the decrease in force/torque reflected the contribution of the transected/resected structure in restraining laxity. Data were analyzed using repeated-measures analyses of variance and paired t tests. Results: For anterior translation, the intact ACL was clearly the primary restraint. The iliotibial tract (ITT) resisted 31% ± 6% of the drawer force with the ACL cut at 30° of flexion; the anterolateral ligament (ALL) and anterolateral capsule resisted 4%. For internal rotation, the superficial layer of the ITT significantly restrained internal rotation at higher flexion angles: 56% ± 20% and 56% ± 16% at 90° for the ACL-intact and ACL-deficient groups, respectively. The deep layer of the ITT restrained internal rotation at lower flexion angles, with 26% ± 9% and 33% ± 12% at 30° for the ACL-intact and ACL-deficient groups, respectively. The other anterolateral structures provided no significant contribution. During the pivot-shift test, the ITT provided 72% ± 14% of the restraint at 45° for the ACL-deficient group. The ACL and other anterolateral structures made only a small contribution in restraining the pivot shift. Conclusion: The ALL and anterolateral capsule had a minor role in restraining internal rotation; the ITT was the primary restraint at 30° to 90° of flexion. Clinical Relevance: The ITT showed large contributions in restraining anterior subluxation of the lateral tibial plateau and tibial internal rotation, which constitute pathological laxity in ALRI. In cases with ALRI, an ITT injury should be suspected and kept in mind if an extra-articular procedure is performed.