| Objective As a systemic bone disease characterized by reduced bone mass and disrupted bone microstructure, osteoporosis (OP) seriously affects public health. Mineral elements such as copper, phosphorus, aluminum, boron, and iron play critical roles in its occurrence and development, but their mechanisms and clinical applications still require in-depth study. This study aims to systematically clarify the regulatory mechanisms of these mineral elements in OP and provide new insights for OP prevention and treatment. Methods Relevant literature on trace elements and OP in databases such as PubMed and CNKI over the past decade was retrieved. The effects of copper, phosphorus, aluminum, boron, and iron on bone metabolism were analyzed from the dimensions of basic mechanisms, animal experiments, and clinical studies. Their dose-effect relationships and signaling pathway regulatory mechanisms were summarized. Results Copper deficiency reduced osteoblast activity (bone mineral density decreased by 20%-30%, P<0.01). Excess copper induced apoptosis. Its composites promoted bone healing through the Wnt pathway. Phosphorus metabolism imbalance affected bone remodeling. Black phosphorus material showed potential for bone repair. Aluminum exposure triggered bone resorption by disrupting calcium-phosphorus homeostasis (bone mineralization rate decreased by 35%, P<0.01). Boron supplementation increased bone mineral. Boron-composite nano-hydroxyapatite had a significant effect on bone formation. Iron deficiency or excess interfered with the balance between osteogenesis and osteogenesis through molecules such as ferritin and SMAD4. Iron death related genes were expected to become new therapeutic targets. Conclusion These mineral elements affect bone metabolism through multiple pathways. Future research should focus on the safe dosage, individual differences, and molecular targets to promote precision prevention and treatment strategies for OP. |