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.
Objective To review the research progress of mitochondrial dynamics mediated by optic atrophy 1 (OPA1) in skeletal system diseases. MethodsThe literatures about OPA1-mediated mitochondrial dynamics in recent years were reviewed, and the bioactive ingredients and drugs for the treatment of skeletal system diseases were summarized, which provided a new idea for the treatment of osteoarthritis. Results OPA1 is a key factor involved in mitochondrial dynamics and energetics and in maintaining the stability of the mitochondrial genome. Accumulating evidence indicates that OPA1-mediated mitochondrial dynamics plays an important role in the regulation of skeletal system diseases such as osteoarthritis, osteoporosis, and osteosarcoma. Conclusion OPA1-mediated mitochondrial dynamics provides an important theoretical basis for the prevention and treatment of skeletal system diseases.
Artificial intelligence (AI) technologies, encompassing virtual reality, augmented reality and adaptive learning platforms, offer immersive and personalised opportunities for undergraduate orthopaedic education. However, their adoption is hindered by limited faculty acceptance, data privacy and ethical risks, and disparities in educational resources. This study examines the opportunities and challenges of AI integration in orthopaedic teaching and proposes strategies including systematic AI training, strengthened data protection, resource sharing, and blended learning models. These measures aim to enhance the quality of learning for students and educators while fostering innovation and progress in medical education.
Objective To review the research progress on lactylation modification in the pathogenesis of osteoarthritis (OA). Methods Relevant studies published in recent years on lactate metabolism and lactylation modification in OA were retrieved and analyzed, summarizing the molecular mechanisms of lactylation and its regulatory roles in different cells and pathological processes. Results Lactate, as the major metabolic product of glycolysis, not only participates in energy metabolism but also plays a crucial role in OA progression through lactylation modification. Lactate-driven histone and non-histone lactylation regulate gene transcription and cellular functions, contributing to chondrocyte metabolic reprogramming, extracellular matrix (ECM) synthesis and degradation, cell proliferation and apoptosis, as well as ferroptosis. In fibroblast-like synoviocytes, lactylation modification promotes cellular senescence and the release of inflammatory factors; in immune cells, lactylation regulates inflammatory responses by influencing macrophage polarization and intercellular communication. Overall, lactylation modification exhibits a dual effect in OA: it aggravates ECM degradation and inflammation on the one hand, but under specific microenvironments, it also promotes repair and regeneration. However, the site-specificity, cell-type heterogeneity, and cross-talk of lactylation with other epigenetic modifications remain to be further clarified. Conclusion Lactylation modification provides a novel perspective for understanding the metabolic and epigenetic mechanisms of OA and may serve as a potential biomarker and therapeutic target. Future studies combining multi-omics approaches to map the global lactylation landscape, together with small-molecule inhibitors, epigenetic editing tools, and regenerative medicine strategies, may enable precise regulation of lactylation, offering new strategies to delay or even reverse OA progression.