Fracture healing is a postnatal regenerative process that mirrors embryonic skeletal development. It involves several phases, including an initial anabolic phase with tissue volume increase and stem cell recruitment, followed by a catabolic phase with tissue remodeling. Immune processes, including innate and adaptive immunity, play a crucial role in fracture healing. Environmental factors such as injury extent, fixation, and vascular tissues also influence healing. Therapeutic strategies, including biophysical and biological interventions, have been tested in animal models and clinical trials. These include electromagnetic fields, low-intensity pulsed ultrasonography, and recombinant human bone morphogenetic proteins (BMPs), parathyroid hormone (PTH), and growth factors like fibroblast growth factor-2 (FGF-2) and platelet-derived growth factors (PDGFs). These therapies aim to enhance bone repair by promoting cartilage formation, bone formation, and tissue remodeling. Stem cell origins and their differentiation into cartilage or bone cells are influenced by injury extent and mechanical strain. The stability of fixation and immobilization also affects the balance between cartilage and bone formation. The mechanisms of fracture healing involve various signaling pathways, including BMPs, FGF-2, hedgehog proteins, PTH, and Wnt signaling. Therapies targeting these pathways have shown promise in enhancing fracture healing. However, challenges remain in optimizing treatment outcomes, particularly in patients with comorbidities such as diabetes or systemic lupus erythematosus. Future research should focus on understanding the interactions between different biological processes and developing targeted therapies to improve fracture healing.Fracture healing is a postnatal regenerative process that mirrors embryonic skeletal development. It involves several phases, including an initial anabolic phase with tissue volume increase and stem cell recruitment, followed by a catabolic phase with tissue remodeling. Immune processes, including innate and adaptive immunity, play a crucial role in fracture healing. Environmental factors such as injury extent, fixation, and vascular tissues also influence healing. Therapeutic strategies, including biophysical and biological interventions, have been tested in animal models and clinical trials. These include electromagnetic fields, low-intensity pulsed ultrasonography, and recombinant human bone morphogenetic proteins (BMPs), parathyroid hormone (PTH), and growth factors like fibroblast growth factor-2 (FGF-2) and platelet-derived growth factors (PDGFs). These therapies aim to enhance bone repair by promoting cartilage formation, bone formation, and tissue remodeling. Stem cell origins and their differentiation into cartilage or bone cells are influenced by injury extent and mechanical strain. The stability of fixation and immobilization also affects the balance between cartilage and bone formation. The mechanisms of fracture healing involve various signaling pathways, including BMPs, FGF-2, hedgehog proteins, PTH, and Wnt signaling. Therapies targeting these pathways have shown promise in enhancing fracture healing. However, challenges remain in optimizing treatment outcomes, particularly in patients with comorbidities such as diabetes or systemic lupus erythematosus. Future research should focus on understanding the interactions between different biological processes and developing targeted therapies to improve fracture healing.