EARLY EVOLVING JOINT DEGENERATION BY CARTILAGE TRAUMA IS PRIMARILY MECHANICALLY CONTROLLED

Purpose: Disturbance of joint homeostasis, due to several risk factors, can result in osteoarthritis. Both mechanical and inflammatory processes can add to the disease. To what extent both processes contribute during the onset of osteoarthritis after a cartilage trauma is unknown. This study evaluates whether local cartilage damage leads to focally confined or more generalized cartilage damage with synovial inflammation in the early development of joint tissue degeneration in an experimental goat model. Methods: In nine female milk goats’ cartilage damage was surgically induced on the weight bearing area of exclusively the medial-femoral-condyle of the right knee joint. The other tibio-femoral compartments; lateral-femoral-condyle and lateral- and medial-tibial-plateaus, were left untouched. The contralateral left knee joint of each knee joint serves as in intra-animal control. Twenty weeks post-surgery changes in cartilage matrix integrity in each of the four compartments, medial and lateral synovial tissue inflammation, and synovial fluid IL-1 and TNF were evaluated. The Utrecht University Committee for Experiments on Animals approved the study according to Dutch Law. Results: In the experimental medial-femoral-condyles significant macroscopic (+225%; p<0.001) and histologic (+225%; p<0.001) cartilage damage was observed. Also the articulating cartilage of the experimental medial-tibial-plateaus was significantly more damaged (+43% macroscopically and +82% histologically; both p<0.05). This was further supported by the decreased proteoglycan content of the cartilage in both compartments (experimental medial-femoral-condyle −12% and medial-tibial-plateau −7% compared to control, both p<0.04). No differences were seen between the lateral compartments of experimental and contralateral control joints. Synovial tissue inflammation was mild and only macroscopically (not histologically) significantly increased in the experimental medial compartment. Synovial fluid IL-1 level was not significantly increased in the experimental and contralateral control joints, and TNF was overall beneath the detection limit. Conclusions: The present study shows clearly that local damage is a trigger for development of osteoarthritis, which in early onset seems primarily mechanically driven. Joint homeostasis is disturbed, indicated by mild synovial inflammation. However, this did not lead to generalized osteoarthritis in the given time period.