Abstract
PURPOSE: Quantifying the effects of anterior cruciate ligament (ACL) deficiency on knee joint laxity is fundamental for understanding the outcomes of its reconstruction techniques. The general aim of this study was to determine intra-operatively the main modifications in knee laxity before and after standard isolated intra-articular and additional extra-articular anterolateral reinforcement. Our main hypothesis was that laxity abnormalities, particularly axial rotation, can still result from these ACL reconstruction techniques. METHODS: Thirty-two patients with primary ACL deficiency were analysed by a navigation system immediately before and after each of the two reconstructions. Laxity measurements in terms of knee translations and rotations were taken during the anteroposterior drawer test, with internal-external rotation at 20° and 90° of flexion, and varus-valgus and pivot-shift tests. All these laxity measures were also taken originally from the contralateral healthy knee. RESULTS: With respect to the contralateral healthy knee, in the ACL-deficient knee significantly increased laxity (expressed in %) was found in the medial compared with that of the lateral compartment, respectively, 115 and 68 % in the drawer test at 20° flexion, and 55 and 46 % at 90° flexion. In the medial compartment, a significant 35 % increment was also observed for the coupled tibial anteroposterior translation during axial knee rotation at 20° of flexion. After isolated intra-articular reconstruction, normal values of anteroposterior laxity were found restored in the pivot-shift and drawer tests in the lateral compartment, but not fully in the medial compartment. After the reinforcement, laxity in the medial compartment was also found restored in the axial rotation test at 20° flexion. CONCLUSION: In ACL reconstruction, with respect to the contralateral knee, intra-articular plus additional anterolateral reinforcement procedures do not restore normal joint laxity. This combined procedure over-constrained the lateral compartment, while excessive laxity still persists at the medial one. LEVEL OF EVIDENCE: III.