This review examines a mechanism for the initiation of osteoarthritis after anterior cruciate ligament (ACL) injury by considering the relationship between reported ambulatory changes after ACL injury, cartilage adaptation to load, and the association between cartilage loads during walking and regional variations in cartilage structure and biology. Taken together, these observations suggest that cartilage degeneration after ACL injury could be caused by a kinematic gait change that shifts ambulatory loading applied to cartilage. Such a shift may cause regions of cartilage to become newly loaded, be subjected to altered levels of compression and tension, or become unloaded. The metabolic sensitivity of chondrocytes to such changes in their mechanical environment, combined with the low adaptation potential of mature cartilage, could lead to cartilage degeneration and premature osteoarthritis after ACL injury. This proposed mechanism demonstrates the value of using the ACL injury model to understand the relationship between mechanics and biology, as well as helping to explain the importance of restoring normal ambulatory kinematics after ACL injury to avoid premature osteoarthritis.
We examined the relationship between specific gait changes after anterior cruciate ligament injury and the progression of osteoarthritis at the knee. The study was done using a finite-element model derived from subject specific three-dimensional cartilage volumes created from magnetic resonance images. Cartilage thinning was predicted using an iterative algorithm based on the octahedral shear stress. Simulations were done for a knee with normal alignment and for a knee with an internal tibial rotation offset, as associated with anterior cruciate ligament deficiency. For the healthy knee, the model predicted patterns of cartilage thinning consistent with a previous clinical report of idiopathic osteoarthritis. For the ACL-deficient scenario the model predicted a more rapid rate of cartilage thinning throughout the knee, especially in the medial compartment. The results suggest that the progression of osteoarthritis after anterior cruciate ligament injury is associated with a shift in the normal load bearing regions of the knee joint during normal function due to kinematic changes, and highlight the importance of restoring proper gait during anterior cruciate ligament reconstruction.
Chondrocytes from different regions of the porcine tibial plateau express mRNA for structural proteins at different levels and respond to equivalent in vitro mechanical loading with distinctive changes in gene expression. These regional biological variations appear to be related to the local mechanical environment in the normal joint, and thus may indicate a sensitivity of the joint to conditions that alter joint loading such as anterior cruciate ligament (ACL) injury, meniscectomy, or joint instability.
There is increasing evidence that the regional spatial variations in the biological and mechanical properties of articular cartilage are an important consideration in the pathogenesis of knee osteoarthritis (OA) following kinematic changes at the knee due to joint destabilizing events (such as an anterior cruciate ligament (ACL) injury). Thus, given the sensitivity of chondrocytes to the mechanical environment, understanding the internal mechanical strains in knee articular cartilage under macroscopic loads is an important element in understanding knee OA. The purpose of this study was to test the hypothesis that cartilage from the central and peripheral regions of the tibial plateau has different internal strain distributions under the same applied load. The internal matrix strain distribution for each specimen was measured on osteochondral blocks from the tibial plateau of mature ovine stifle joints. Each specimen was loaded cyclically for 20 min, after which the specimen was cryofixed in its deformed position and freeze fractured. The internal matrix was viewed in a scanning electron microscope (SEM) and internal strains were measured by quantifying the deformation of the collagen fiber network. The peak surface tensile strain, maximum principal strain, and maximum shear strain were compared between the regions. The results demonstrated significantly different internal mechanical strain distributions between the central and peripheral regions of tibial plateau articular cartilage under both the same applied load and same applied nominal strain. These differences in the above strain measures were due to differences in the deformation patterns of the collagen network between the central and peripheral regions. Taken together with previous studies demonstrating differences in the biochemical response of chondrocytes from the central and peripheral regions of the tibial plateau to mechanical load, the differences in collagen network deformation observed in this study help to provide a fundamental basis for understanding the association between altered knee joint kinematics and premature knee OA.
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