Osteoarthritis (OA) affects around 40 million people in Europe. OA causes a heavy socioeconomic burden. There is currently no cure for OA. Also, the development of therapies that can prevent joint damage associated with OA is thus urgently needed. OA is characterized by loss of joint cartilage, pathological change in the bone that lines the cartilage, and mild inflammation of the synovial membrane. The disappearance of cartilage results from an alteration in the functions of chondrocytes, the cells that compose cartilage. Notably, the chondrocytes become hypertrophic. This transformation is currently considered to be critical in the progression of OA. It could be the link between the disappearance of cartilage and its replacement with bone. In OA, the interface between the articular cartilage which is avascular and the bone is characterized by the development of blood vessels (angiogenesis). We believe that these blood vessels play a key role in replacing articular cartilage with bone and that their development is stimulated by hypertrophic chondrocytes. Our preliminary results show that articular chondrocytes rendered hypertrophic in culture acquire angiogenic activity. This property is inhibited by blocking CXCR4 on the surface of endothelial cells, the cells of blood vessels. CXCR4 is the CXCL12 receptor which is produced by hypertrophic chondrocytes. In the TARGET-OA project, we propose that the CXCL12 / CXCR4 axis has a crucial role in the dialogue between hypertrophic chondrocytes and endothelial cells in OA. Our objectives are to define the role of this axis in pathological communication between chondrocytes and endothelial cells and to demonstrate that its targeting has a clinical interest for the treatment of OA.