In normal cartilage, there is a balance of repair and degradation of the cartilage matrix components. The chondrocytes are solely responsible for this function, and are influenced by signals stemming from cytokines, growth factors, and mechanical stimuli in a complex interrelationship. For example, the presence of proinflammatory cytokines, such as IL1, stimulates the production of MMPs by the chondrocyte. In OA, there is a change in this normal metabolic balance, with an increase in the catabolic processes relative to the rate of synthesis of matrix components. The end result is that the rate of repair is insufficient to maintain the normal integrity of the matrix. When the changes in the cartilage structure have progressed to the point of affecting its physical characteristics, such as causing a decrease in cartilage resilience, then joint loads lead to further damage to the cartilage. At this stage, biomechanical factors become the most prominent cause of further damage.
Slide 3: "Increase in the Catabolic Processes in Osteoarthritic Cartilage " 400 x 300 pixels 22kb freehand 3dStudio Max.
Slide 4: "Abnormal Balance in Cartilage Repair and Degradation " 400 x 300 pixels 22kb freehand 3dStudio Max.
Thus, the evolution of the OA disease process occurs in three stages. In Stage I, there is an abnormally excessive proteolytic breakdown of the cartilage matrix. In Stage II, fibrillation and erosions of cartilage liberates these breakdown products into the synovial fluid. In Stage III, synovial cells take up these cartilage breakdown products, causing a chronic synovial inflammatory reaction and the ongoing production of proinflammatory cytokines. These cytokines then diffuse back to the cartilage to negatively impact the chondrocyte. By this stage, the chondrocyte has become increasingly sensitized to these proinflammatory cytokines because of an increased number of cytokine cell receptors.
Slide 5: " The Joint and it's Cartilage Components " 400 x 300 pixels 41kb freehand 3dStudio Max
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