ObjectiveTo review and summarize the role of helper T cell (Th) in the pathogenesis of osteoarthritis (OA) and research progress of Th cell-related treatment for OA.MethodsThe domestic and foreign literature in recent years was reviewed. The role of Th cells [Th1, Th2, Th9, Th17, Th22, and follicular helper T cell (Tfh)] and related cytokines in the pathogenesis of OA and the latest research progress of treatment were summarized.ResultsTh cells play an important role in the pathogenesis of OA. Th1, Th9, and Th17 cells are more important than Th2, Th22, and Tfh cells in the pathogenesis of OA. Cytokines such as tumor necrosis factor α and interleukin 17 can cause damage to articular cartilage significantly.ConclusionAt present, the role of Th cells in the pathogenesis of OA has been played in the spotlight. The specific mechanism has not been clear. Regulating the Th cell-associated cytokines, intracellular and extracellular signals, and cellular metabolism is a potential method for prevention and treatment of OA.
Objective To summarize the research progress on the role of macrophage-mediated osteoimmune in osteonecrosis of the femoral head (ONFH) and its mechanisms. Methods Recent studies on the role and mechanism of macrophage-mediated osteoimmune in ONFH at home and abroad were extensively reviewed. The classification and function of macrophages were summarized, the osteoimmune regulation of macrophages on chronic inflammation in ONFH was summarized, and the pathophysiological mechanism of osteonecrosis was expounded from the perspective of osteoimmune, which provided new ideas for the treatment of ONFH. Results Macrophages are important immune cells involved in inflammatory response, which can differentiate into classically activated type (M1) and alternatively activated type (M2), and play specific functions to participate in and regulate the physiological and pathological processes of the body. Studies have shown that bone immune imbalance mediated by macrophages can cause local chronic inflammation and lead to the occurrence and development of ONFH. Therefore, regulating macrophage polarization is a potential ONFH treatment strategy. In chronic inflammatory microenvironment, inhibiting macrophage polarization to M1 can promote local inflammatory dissipation and effectively delay the progression of ONFH; regulating macrophage polarization to M2 can build a local osteoimmune microenvironment conducive to bone repair, which is helpful to necrotic tissue regeneration and repair to a certain extent. Conclusion At present, it has been confirmed that macrophage-mediated chronic inflammatory immune microenvironment is an important mechanism for the occurrence and development of ONFH. It is necessary to study the subtypes of immune cells in ONFH, the interaction between immune cells and macrophages, and the interaction between various immune cells and macrophages, which is beneficial to the development of potential therapeutic methods for ONFH.