Expression Of Matrix Metalloproteinase And Collagen In Rat Articular Cartilage After Trauma

ObjectTo make the rat animal models of articular cartilage defects and investigate pathomechanism of articular cartilage degeneration after trauma by analyzing the expression changes of matrix metalloproteinase (MMP) and collagen in cartilage tissue.MethodsForty eight SD female rats were used in this experiment. These rats were randomly divided into A, B and C group. Group A(n=18): a full-thickness cylindrical osteochondral defect of 3.0mm diameter and 3.0mm depth was created in both condyles of femur. Group B(n=18): several partial-thickness articular cartilage defects of 0.3mm depth 0.3 mm Width in both condyles of femur. Group C(n=12) is the opposite as pseudo operative control. The rats were sacrificed at 4,8,12 weeks. Each femoral condyle were evaluated histologically by HE stain and toluidine blue (TB) stain analyses and immunohistochemically by immunohistochemical analyses of collagen I, collagen II, MMP-2, MMP-3 and MMP-9.ResultsIn group A, after 4 W defect in a small amount of new organization generation, 8 W and 12 W can be seen filled with fibrous tissue. At the three time points, type I collagen immunohistochemical staining of the extracellular matrix in repair tissue is positive while type II collagen immunohistochemical staining is negative. Articular cartilage of MMP-2, MMP-3, MMP-9 expression increased (compared with C There was a significant difference, P <0.05). In group B, surface cartilage defect 8 W and 4 W no signs of repair were found. 12 W visible trace filled with fibrous tissue, in which type I collagen immunohistochemical staining is positive while type II collagen immunohistochemical staining is negative. Articular cartilage at three time points of MMP-2, MMP-3, MMP-9 expression were increased (compared with C There was a significant difference, P <0.05).Group C three time points were normal articular cartilage, collagen type I immunohistochemical staining negative, collagen type II positive immunohistochemical staining, MMP-2, MMP-3, MMP-9 expression low, no morphological abnormal change.ConclusionsRats osteochondral defect can be repaired by mesenchymal cells in fibers form, repair organizations unable to restore normal articular surface of the formation, the non- hyaline cartilage tissue. As the surface of articular cartilage defects not penetrate subchondral bone plate, seamless mesenchymal cells participation, it is hard to achieve self-healing. With the passage of time around the cartilage defect thinning, a different degree of degeneration. Through surgical methods can establish osteochondral defect and surface cartilage defect in the rat knee joint cartilage, which can be used to study transplantation method of repair of cartilage defects. Mechanical injury can lead to articular cartilage extracellular matrix composition changed, the loss of their original biological characteristics. Matnx degradation (MMP-3) and gelatinase (MMP-2, 9) in the injury of cartilage tissue increased, so that the degradation of extracellular matrix increase as a result of articular cartilage degeneration important factors.