Bone & joint research · 2026
OX40L in endothelial cells promotes temporomandibular joint subchondral bone angiogenesis and osteoclastogenesis in mice.
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Zheng Yifan, Liu Chufeng, Liao Zhihao, Lin Jiayu, Luo Yuxiao, Yang Xia, Cai Xuepei, Lan Zedong
Аннотация
AIMS: Subchondral vascular proliferation is a substantial pathological manifestation of temporomandibular joint osteoarthritis (TMJOA), yet its underlying mechanisms remain unclear. This study aimed to investigate the role of OX40-OX40L signalling in mediating subchondral angiogenesis and osteoclastogenesis in early stage TMJOA.
METHODS: A unilateral anterior cross-bite (UAC) model was established in mice to induce TMJOA, and the expression of OX40L in subchondral vessels was examined at the early stages of the disease. In vitro, the OX40-OX40L pathway was activated in bone microvascular endothelial cells (BMECs) to assess its effects on cell migration, tube formation, and osteoclast differentiation. An OX40L monoclonal antibody was used during in vivo experiments to block this signalling pathway.
RESULTS: We observed increased expression of OX40L in the subchondral vessels during early TMJOA, accompanied by significant bone destruction. OX40L activation enhanced endothelial cell migration and angiogenesis in vitro, whereas pathway inhibition reversed these effects and reduced osteoclast differentiation. In vivo, OX40L monoclonal antibody effectively alleviated subchondral angiogenesis and osteoclastogenesis.
CONCLUSION: Endothelial OX40L signalling promotes pathological subchondral angiogenesis and osteoclastogenesis in early TMJOA.
METHODS: A unilateral anterior cross-bite (UAC) model was established in mice to induce TMJOA, and the expression of OX40L in subchondral vessels was examined at the early stages of the disease. In vitro, the OX40-OX40L pathway was activated in bone microvascular endothelial cells (BMECs) to assess its effects on cell migration, tube formation, and osteoclast differentiation. An OX40L monoclonal antibody was used during in vivo experiments to block this signalling pathway.
RESULTS: We observed increased expression of OX40L in the subchondral vessels during early TMJOA, accompanied by significant bone destruction. OX40L activation enhanced endothelial cell migration and angiogenesis in vitro, whereas pathway inhibition reversed these effects and reduced osteoclast differentiation. In vivo, OX40L monoclonal antibody effectively alleviated subchondral angiogenesis and osteoclastogenesis.
CONCLUSION: Endothelial OX40L signalling promotes pathological subchondral angiogenesis and osteoclastogenesis in early TMJOA.