One of the major challenges in rheumatology remains the induction of osteochondral repair in synovial joints. Remarkable progress has been made in controlling the inflammatory pathways of chronic synovitis and tissue damage in rheumatoid arthritis and spondyloarthropathy. Here, we provide an overview of the current knowledge on the mechanisms involved in osteochondral repair in degenerative joint diseases, as well as in immune mediated inflammatory arthritides, with special emphasis on tumor necrosis factor alpha and IL-1.Homeostasis of articular cartilage and subchondral bone are essential for maintaining the integrity of osteochondral structures within synovial joints. This is achieved by the regulation of a delicate balance between anabolic and catabolic signals. In articular cartilage one cell type, the chondrocyte, is responsible for regulation of homeostasis. In bone, however, two distinct cell types, osteoblasts and osteoclasts, are responsible for anabolic and catabolic pathways, respectively. In inflammatory joint disorders, this tight regulation is profoundly dysregulated, with tumor necrosis factor alpha acting as an important catalyst of a disturbed homeostasis, together with IL-1. Targeting these cytokines may restore the intrinsic repair capacity of osteochondral structures.To restore catabolic cytokine balances appears to be a suitable strategy to promote osteochondral repair.