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Type H vessels-a bridge connecting subchondral bone remodelling and articular cartilage degeneration in
Yuan Liu1, Hui-Qi Xie2, Bin Shen1
1Orthopedics Research Institute, Department of Orthopedics, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Recent studies have shed light on the cellular and molecular mechanisms that link subchondral bone remodelling and angiogenesis in knee osteoarthritis (OA). Type H vessels are a newly identified bone blood vessel characterized by high expression of CD31 and endomucin that are coupled with osteogenesis. Factors including mechanical loading, TGF-β1, platelet-derived growth factor type BB, the osteoprotegerin-RANK ligand-RANK system, osteopontin, mechanistic target of rapamycin, VEGF, stromal cell-derived factor l and prostaglandin E2 participate in the formation of type H vessels in osteoarthritic subchondral bone. In this review, we summarize the current understanding of type H vessels in knee OA, as well as the signalling pathways involved and potential therapeutic medicines. In future, the pathogenesis of knee OA could be further clarified by connecting type H vessels and the design of new disease-modifying osteoarthritis drugs. However, further experiments are needed to determine the upstream signals regulating type H vessel formation in osteoarthritic subchondral bone.
Recent studies have shed light on the cellular and molecular mechanisms that link subchondral bone remodelling and angiogenesis in knee osteoarthritis (OA). Type H vessels are a newly identified bone blood vessel characterized by high expression of CD31 and endomucin that are coupled with osteogenesis. Factors including mechanical loading, TGF-β1, platelet-derived growth factor type BB, the osteoprotegerin-RANK ligand-RANK system, osteopontin, mechanistic target of rapamycin, VEGF, stromal cell-derived factor l and prostaglandin E2 participate in the formation of type H vessels in osteoarthritic subchondral bone. In this review, we summarize the current understanding of type H vessels in knee OA, as well as the signalling pathways involved and potential therapeutic medicines. In future, the pathogenesis of knee OA could be further clarified by connecting type H vessels and the design of new disease-modifying osteoarthritis drugs. However, further experiments are needed to determine the upstream signals regulating type H vessel formation in osteoarthritic subchondral bone.
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