In order to develop a pathophysiologically relevant in vitro model for OA which reflects the complexity of the disease characterised by a vicious circle of cartilage degeneration accompanied by synovial inflammation and remodelling of the subchondral bone, we established an osteochondral-synovial membrane explant co-culture and induced OA-like changes by adding IL1β and TNFα to the culture medium to induce inflammation and creating a partial thickness cartilage defect to simulate this common sequela of mechanical cartilage injury. The gene discussed is TNF; the disease is inflammation.