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

Abstract

ObjectivesThe 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.MethodsThe 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 mm2 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.ResultsResults 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.ConclusionAlterations 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.

Effects of in vivo cyclic compressive loading on the distribution of local Col2 and superficial lubricin in rat knee cartilage

“…Moreover, we did not record the activities of rats after loading that may have influenced the progression of lubricin self‐healing, which may have contributed to the large variation in the data (Figure 5D). Third, in the current study, we assessed only the cartilage lesion on the lateral femur condyle, which is not the main part of cartilage loaded during walking 47 . Considering that cartilage heterogeneity could affect the results of injury assessment, cartilage damage on the other contact surface should be examined in the future.…”

“…Third, in the current study, we assessed only the cartilage lesion on the lateral femur condyle, which is not the main part of cartilage loaded during walking. 47 Considering that cartilage heterogeneity could affect the results of injury assessment, cartilage damage on the other contact surface should be examined in the future. Finally, we failed to compare the current model to any surgery-induced model.…”

Development of a Knee Joint CT-FEM Model in Load Response of the Stance Phase During Walking Using Muscle Exertion, Motion Analysis, and Ground Reaction Force Data

“…We constructed a CT-FEM in the LR phase during walking using gait analysis and musculoskeletal modeling with joint components as the material characteristics. Although the results of the CT-FEM analysis of the knee in static posture have been previously reported [37][38][39][40], there are no reports of accurate model methods based on gait data. In this study, the reproduction of the walk is reliable.…”

Clinical Application of the Basic Science of Articular Cartilage Pathology and Treatment

“…[7][8][9] Lesions in areas of high-load bearing behave differently from those in areas exposed to primarily shear loads. 10 Compressive strains can increase between 50 and 100%, depending on defect size and location. 11 Regardless of location of the defect within the joint, the general cascade of events follows a similar pathway of cell phenotype alterations, necrosis, and/or apoptosis; proteoglycan and collagen disruption, alteration and loss; inflammation; degradation; and remodeling regardless of etiology.…”