Cartilage defect location and stiffness predispose the tibiofemoral joint to aberrant loading conditions during stance phase of gait

OBJECTIVES: The current study quantified the influence of cartilage defect location on the tibiofemoral load distribution during gait. Furthermore, changes in local mechanical stiffness representative for matrix damage or bone ingrowth were investigated. This may provide insights in the mechanical factors contributing to cartilage degeneration in the presence of an articular cartilage defect. METHODS: The load distribution following cartilage defects was calculated using a musculoskeletal model that included tibiofemoral and patellofemoral joints with 6 degrees-of-freedom. Circular cartilage defects of 100 mm(2) were created at different locations in the tibiofemoral contact geometry. By assigning different mechanical properties to these defect locations, softening and hardening of the tissue were evaluated. RESULTS: Results indicate that cartilage defects located at the load-bearing area only affect the load distribution of the involved compartment. Cartilage defects in the central part of the tibia plateau and anterior-central part of the medial femoral condyle present the largest influence on load distribution. Softening at the defect location results in overloading, i.e., increased contact pressure and compressive strains, of the surrounding tissue. In contrast, inside the defect, the contact pressure decreases and the compressive strain increases. Hardening at the defect location presents the opposite results in load distribution compared to softening. Sensitivity analysis reveals that the surrounding contact pressure, contact force and compressive strain alter significantly when the elastic modulus is below 7 MPa or above 18 MPa. CONCLUSION: Alterations in local mechanical behavior within the high load bearing area resulted in aberrant loading conditions, thereby potentially affecting the homeostatic balance not only at the defect but also at the tissue surrounding and opposing the defect. Especially, cartilage softening predisposes the tissue to loads that may contribute to accelerated risk of cartilage degeneration and the initiation or progression towards osteoarthritis of the whole compartment.