Quantitative Investigation of Tibiofemoral Cartilage Early Degeneration After ACL Reconstruction: An Integrated Biomechanical and Longitudinal MRI Analysis

Background: Anterior cruciate ligament reconstruction (ACLR) restores stability but is often followed by early cartilage degeneration. The contribution of altered dynamic contact pressure during gait to this degeneration remains poorly understood. Purpose: To investigate the biomechanical mechanisms underlying early cartilage degeneration after ACLR, with a focus on dynamic contact pressure distribution during gait. Study Design: Controlled laboratory study. Methods: In a 3-year longitudinal magnetic resonance imaging (MRI) study of patients with ACLR (n = 30), cartilage thickness of the tibial plateau was quantitatively assessed using deep-learning-based 3-dimensional segmentation techniques. In parallel, cadaveric knees (n = 8) were tested under intact, ACL-deficient, and ACL-reconstructed conditions using a 6 degree-of-freedom robotic simulator replicating gait cycles. Tibiofemoral contact pressure and pressure center trajectories were recorded using pressure-sensitive film. Results: Quantitative MRI analyses revealed significant cartilage thinning in the posterior tibial subregion 3 years after ACLR. On the medial plateau, the central medial tibia, internal medial tibia, and posterior medial tibia subregions exhibited mean reductions of 10% ( P = .027), 21% ( P = .019), and 13% ( P = .041), respectively. On the lateral plateau, significant decreases were observed in central lateral tibia (9%; P = .031), posterior lateral tibia (14%; P = .029), and external lateral tibia (15%; P = .035). In robotic gait simulations, the reconstructed knees exhibited persistent posterior displacement of the whole-gait-cycle contact center of stress on both tibial plateaus (residual shifts: medial, 5.29 mm; lateral, 4.73 mm; both P < .05). Additionally, the contact area was significantly enlarged in early stance (2%-12% gait cycle) and terminal swing (75%-100%), especially in the medial compartment. Conclusion: ACLR-induced pressure center displacement coincides with focal posterior cartilage degeneration, forming a spatiotemporal mechanical-pathological chain. This work highlights the potential of dynamic loading biomarkers for early osteoarthritis risk stratification and targeted mechanical intervention. Clinical Relevance: Persistent shifts in tibiofemoral pressure centers after ACLR coincide with focal cartilage thinning, suggesting a mechanical pathway to post-ACLR osteoarthritis. Identifying such dynamic loading biomarkers may guide early risk stratification and targeted interventions in sports medicine.