Objective To introduce the research progress on the relationship between gut microbiota dysbiosis and osteoarthritis (OA), focus on the possible mechanism of gut microbiota dysbiosis promoting OA, and propose a new therapeutic direction. Methods The domestic and foreign research literature on the relationship between gut microbiota dysbiosis and OA was reviewed. The role of the former in the occurrence and development of OA and the new ideas for the treatment of OA were summarized. Results The gut microbiota dysbiosis promotes the development of OA mainly in three aspects. First, the gut microbiota dysbiosis destroys intestinal permeability and causes low-grade inflammation, which aggravate OA. Secondly, the gut microbiota dysbiosis promotes the development of OA through metabolic syndrome. Thirdly, the gut microbiota dysbiosis is involved in the development of OA by regulating the metabolism and transport of trace elements. Studies have shown that improving gut microbiota dysbiosis by taking probiotics and transplanting fecal microbiota can reduce systemic inflammation and regulate metabolic balance, thus treating OA. Conclusion Gut microbiota dysbiosis is closely related to the development of OA, and improving gut microbiota dysbiosis can be an important idea for OA treatment.
Objective To summarize the research progress of bioactive scaffolds in the repair and regeneration of osteoporotic bone defects. Methods Recent literature on bioactive scaffolds for the repair of osteoporotic bone defects was reviewed to summarize various types of bioactive scaffolds and their associated repair methods. Results The application of bioactive scaffolds provides a new idea for the repair and regeneration of osteoporotic bone defects. For example, calcium phosphate ceramics scaffolds, hydrogel scaffolds, three-dimensional (3D)-printed biological scaffolds, metal scaffolds, as well as polymer material scaffolds and bone organoids, have all demonstrated good bone repair-promoting effects. However, in the pathological bone microenvironment of osteoporosis, the function of single-material scaffolds to promote bone regeneration is insufficient. Therefore, the design of bioactive scaffolds must consider multiple factors, including material biocompatibility, mechanical properties, bioactivity, bone conductivity, and osteogenic induction. Furthermore, physical and chemical surface modifications, along with advanced biotechnological approaches, can help to improve the osteogenic microenvironment and promote the differentiation of bone cells. ConclusionWith advancements in technology, the synergistic application of 3D bioprinting, bone organoids technologies, and advanced biotechnologies holds promise for providing more efficient bioactive scaffolds for the repair and regeneration of osteoporotic bone defects.
ObjectiveTo review the role of chemokine networks in regulating synovial macrophage heterogeneity during osteoarthritis (OA) pathogenesis. Methods A review of recent literature on the developmental origins of OA synovial macrophages, single-cell transcriptomic characteristics, and chemokine signaling pathways was conducted to systematically summarize the functional phenotypes, immunometabolic mechanisms, and regulatory roles of synovial macrophages in OA. Results OA has been established as a low-grade, chronic inflammatory disease affecting the entire joint. Single-cell and spatial transcriptomic studies have confirmed that synovial macrophages are not a single population but rather a dynamic continuum of different functional states, including steady-state barrier-like, inflammatory amplification, fibrosis-related, and lipid-enriched phenotypes. Chemokine networks play a dual crucial role in this process: on one hand, chemokine gradients guide the migration of peripheral monocytes to the synovium and influence their differentiation; on the other hand, synovial macrophages in different states secrete chemokines, mediating transcellular communication between the synovium, subchondral bone, and peripheral nerves. This process reshapes the microenvironment and amplifies local inflammation and pain signals. Current therapeutic strategies targeting macrophage metabolic reprogramming and chemokine axis blockade show potential clinical applications. Conclusion Re-examining the interaction between synovial macrophages and microenvironment and constructing an integrated perspective of “lineage-state-chemokine network” will help to understand the pathological progression mechanism of OA. In the future, it is expected to provide a theoretical framework and intervention targets for the precise immune regulation of OA and the development of new targeted drugs by accurately analyzing the spatiotemporal evolution of macrophage subsets and their interaction with chemokines.