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It is unclear whether vascular endothelial growth factor (VEGF) can initiate osteoarthritis (OA) in the temporomandibular joint (TMJ). In this study we evaluated the effects of intra-articular injection of exogenous VEGF in the TMJ in mice on the early stage. Forty-eight male Sprague-Dawley mice were equally divided into 3 groups. In the vegf group, the mice received an injection of VEGF solution (50 μL) in the TMJ once a week over a period of 4 weeks. In the sham group, the mice received an injection of saline (50 μL). The control group did not receive any injection. Four mice from each group were sacrificed at 1, 2, 4, and 8 weeks. Gradual prominent cartilage degeneration was observed in the vegf group. Additionally, this group showed higher expressions of metalloproteinase (MMP)-9, MMP-13, receptor activator of nuclear factor-kappa-B ligand (RANKL), and a higher number of apoptotic chondrocytes and VEGF receptor 2 (VEGFR2)-positive chondrocytes. Micro-computed tomography (CT) revealed prominent subchondral bone resorption in the vegf group, with a high number of osteoclasts in the subchondral bone. In vitro study demonstrated that VEGF can promote osteoclast differentiation. In conclusion, our study found that VEGF can initiate TMJ OA by destroying cartilage and subchondral bone.