Cartilage injuries are increasingly common among Americans, with an estimated 900,000 articular cartilage injuries diagnosed each year. While the natural history of focal cartilage defects is not fully understood, focal cartilage defects may develop due to large forces transmitted through the junction of uncalcified and calcified layers of cartilage. It is believed that cartilage degeneration and defect progression is multifactorial. While there are many important factors in sustaining cartilage health, we aim to examine the effects of the meniscus, loading, articular surface continuity, and local bone geometry.
We first sought to identify how the meniscus influences contact force and area at 10 MPa in the medial and lateral condyles. We created defects in the femoral condyle of 20 porcine knees, and statically loaded that condyle in full extension to 10 MPa. We measured the force required to reach 10 MPa and resultant contact area at 10 MPa. We then performed a two-way analysis of variance and found that the presence of the meniscus and remaining condyle ( p < 0.001 for each) had significant effects on the force required to reach 10 MPa, as well as a significant interaction between the two factors (p = 0.007). These findings suggest that the meniscus should be included in biomechanical testing.
To determine the effects of applied pressure, condyle, and defect on chondrocyte viability, we obtained 96 porcine knees and mounted them in an Instron in full extension. 48 knees were tested on the medial condyle only, and the other 48 were loaded on the lateral condyle. In half of each group of 48, a defect was created. Each of these groups were divided equally into four groups and loaded to either 10, 12, 14, or 16 MPa. The distribution of cell death was measured via live/dead cell assay.
The applied pressure had a significant (p < 0.001) effect on the depth of cell death in samples with no defect. Both pressure level (p < 0.001) and condyle (p = 0.016) had significant effects on the width of cell death. It was found that the depth of cell death was significantly affected by the applied pressure and whether a defect was present or not, (p < 0.001) as well as the interaction between these two factors (p = 0.040).
Our results lead us to the conclusion that the depth and width of chondrocyte death is multifactorial; a function of some combination of whether a defect is present or not, applied pressure, and condyle. Although similarities are present between cell death patterns when cartilage is intact or a defect is present, we believe we have identified different mechanisms of cartilage death and degeneration. In fully intact cartilage, chondrocyte death is apparent in the deep zone of cartilage at 14 and 16 MPa. In samples with defects in the articular surface, chondrocyte death is present in the cartilage deep zone, as well as at the surface surrounding the defect, and the edges of the defect.