Osteoarthritis (0A) is a degradative disease affecting both the articular cartilage and the underlying bone, with the final stages being loss of cartilage leading to bone on bone contact and pain. OA may cost society $54 billion annually in treatment and lost workdays. Excessive or abnormal loading has been implicated in initiating this joint degradation. Early signs of OA include fissuring, softening and increased permeability of the articular cartilage, chondrocyte death, and increased thickening of the underlying subchondral bone.

To better understand the mechanisms of mechanically induced changes to joint tissues our laboratory has developed an in vivo animal model that involves impacting the patellofemoral joint of Giant Flemish rabbits. At 12 months post-impact the retropatellar cartilage is fissured and softened and the subchondral plate is thickened. A computational model of the rabbit patella suggests that impact-induced shear stresses were associated with acute fissuring and chronic softening of the cartilage and thickening of the underlying bone. To better control mechanical loading, studies on cultured explanted cartilage have shown that a single severe impact can result in acute matrix damage (fissures) and chondrocyte death. Impact interfaces, impact orientation, and impact duration are all important parameters that could influence the state of stress and strain in joint tissues and therefore have an effect on both acute and chronic damages to the tissues. Impact modeling of articular cartilage needs to take into account the well documented non-linear stiffening and time-dependent effect of cartilage.

The overall aims of this dissertation were threefold First, to use the established animal model to examine the influence of impact interface, impact direction, and impact duration on chronic alterations in joint tissues. Second, use a cartilage explant system to examine the influence of impact duration on matrix damage and cell death, and attempt to correlate the state of stress and strain in the tissue and cells with these damages. Third, determine a method to estimate the non-linear viscoelastic material properties of cartilage from in situ indentation testing for the modeling of impact experiments.

This study found that distributing the impact load resulted in shear stresses being decreased in the bone, but not the cartilage. As predicted there were chronic alterations in the cartilage, but no thickening of the bone. Impacting the joint centrally compared to slightly medial resulted in shear stresses being increased in the bone and decreased in the cartilage. As expected there were no chronic changes in the cartilage, however, there was also no thickening of the bone. An increase in normal bone stresses in the central impacts could have helped protect the bone. Impacting at a higher rate of loading resulted in more damage compared to a lower rate of loading in both the animal and explant models. Modeling of the explant suggested that depth-dependent material properties are needed and matrix damage was associated with high shear stresses while cell death corresponded to high cell strains. Finally, in situ indentation testing was used to estimate the hyperviscoelastic material properties of cartilage, which were able to predict experimental unconfined compression tests on cartilage. Future studies will be able to use these material properties of cartilage for more appropriate modeling of impact scenarios.