The in vivo and in vitro experiments performed in this study revealed that SDF-1α was expressed at high levels in subchondral bone in an OA model and that by promoting the proliferation and osteogenic differentiation of BMSCs, SDF-1 hardened subchondral bone and aggravated the progression of OA, providing clinically significant evidence for the pathogenesis of osteoarthritis. This evidence concerns the gene CXCL12 and osteoarthritis.