The article provides a comprehensive overview of the biology of fracture healing, which is a complex process involving multiple anatomical and biochemical events. It begins by explaining that bone healing can occur through either direct intramembranous or indirect endochondral bone formation. Indirect healing, which is more common, involves the recruitment of mesenchymal stem cells (MSCs) to form a primary cartilaginous callus, followed by revascularization and calcification. The acute inflammatory response, involving cytokines like TNF-α and IL-1, plays a crucial role in initiating this process. MSCs are recruited through pathways such as the SDF-1/CXCR-4 axis and HIF-1α, which regulate their homing to the injury site. The formation of the cartilaginous callus is followed by its mineralization and resorption, leading to the generation of a hard bony callus. This process is regulated by factors like VEGF and BMPs, which promote angiogenesis and chondrocyte apoptosis. The final phase involves bone remodeling, where osteoclasts resorb the hard callus and osteoblasts deposit new bone, restoring the mechanical properties of the bone. Direct healing, which requires precise anatomical reduction and stable fixation, involves the direct remodeling of lamellar bone and Haversian canals. The article concludes by highlighting the importance of understanding these processes for developing effective treatments to enhance fracture healing.The article provides a comprehensive overview of the biology of fracture healing, which is a complex process involving multiple anatomical and biochemical events. It begins by explaining that bone healing can occur through either direct intramembranous or indirect endochondral bone formation. Indirect healing, which is more common, involves the recruitment of mesenchymal stem cells (MSCs) to form a primary cartilaginous callus, followed by revascularization and calcification. The acute inflammatory response, involving cytokines like TNF-α and IL-1, plays a crucial role in initiating this process. MSCs are recruited through pathways such as the SDF-1/CXCR-4 axis and HIF-1α, which regulate their homing to the injury site. The formation of the cartilaginous callus is followed by its mineralization and resorption, leading to the generation of a hard bony callus. This process is regulated by factors like VEGF and BMPs, which promote angiogenesis and chondrocyte apoptosis. The final phase involves bone remodeling, where osteoclasts resorb the hard callus and osteoblasts deposit new bone, restoring the mechanical properties of the bone. Direct healing, which requires precise anatomical reduction and stable fixation, involves the direct remodeling of lamellar bone and Haversian canals. The article concludes by highlighting the importance of understanding these processes for developing effective treatments to enhance fracture healing.