Research findings reveal that thermal environments precisely regulate the skeletal system through a triple regulation of "structural morphology-cellular dynamics-molecular mechanisms": At the tissue morphology level, moderate heat exposure can promote increased bone density and longitudinal growth, as well as improved fracture load and yield point, but may negatively affect geometric shape and cortical bone thickness. Continuous high-temperature exposure harms bone structure, manifested as changes in biomechanical characteristics such as decreased toughness and rigidity. At the cellular level, thermal environments directly affect the proliferation/apoptosis balance of osteoblasts and osteoclasts, and by regulating osteocyte network activity and bone marrow mesenchymal stem cell fate decisions, these four cell populations form temperature-dependent metabolic regulatory circuits. At the molecular dimension, heat stress can activate the release of neural factors such as CGRP and NPY, which possess dual regulatory functions promoting both bone formation and resorption; simultaneously achieving coordinated regulation of angiogenesis and fat inhibition through VEGF and TGFβ. The thermal environment-bone regulatory mechanisms revealed in this study have important translational value: they not only provide theoretical basis for biomechanical protection strategies for high-temperature workers and athletes, but also offer innovative entry points for analyzing the pathological mechanisms of heat stroke secondary bone injury and osteoporosis through heat stress-related signaling pathways, while establishing a theoretical foundation for the development of temperature-responsive functionalized biomaterials in bone tissue engineering.
Keywords: bone cells; bone metabolism; bone microenvironment; thermal environment.