Altered Fluid Pressurization and Fibril Loading in ACL-Deficient Knee Tissues

Anterior cruciate ligament (ACL) deficiency alters knee joint mechanics and may accelerate cartilage degeneration. However, the intra-tissue mechanical consequences of ACL deficiency remain difficult to quantify experimentally because interstitial fluid pressure and collagen fibril stresses cannot be measured in vivo. In this study, a subject-specific fibril-reinforced poromechanical finite element model of the human tibiofemoral joint was used to investigate solid–fluid interactions in ACL-intact and ACL-deficient conditions. The MRI-based geometry incorporated anisotropic collagen fibril networks and Darcy-type interstitial fluid flow to capture the coupled poromechanical response of cartilage and menisci under physiological loading. Ramp compression and posterior drawer creep forces representing single-leg stance were applied to evaluate the time-dependent mechanical behavior of the joint. The results showed that ACL deficiency increased interstitial fluid pressure by up to 19% in the lateral tibial cartilage and 13% in the lateral femoral condyle, while collagen fibril tensile stress increased by 22% in the lateral femoral cartilage and by 5% in the medial meniscus. Although the overall stress distributions were similar between intact and ACL-deficient knees, localized increases in fluid pressurization and fibril loading were observed in load-bearing regions. These findings suggest that ACL deficiency modifies the internal poromechanical environment of cartilaginous tissues and may contribute to degeneration under repetitive physiological loading.