Bone fractures disrupt the cortical and cancellous architecture, triggering a complex healing cascade. The initial inflammatory phase (days 1-7) involves hematoma formation at the fracture site as disrupted periosteal and endosteal blood vessels hemorrhage. Platelet aggregation and fibrin clot formation create a scaffold while macrophages and neutrophils remove debris. The reparative phase involves mesenchymal stem cell differentiation into chondroblasts forming soft callus (fibrocartilage) at 2-3 weeks, followed by osteoblastic ossification creating hard callus (woven bone) at 3-12 weeks. The remodeling phase, lasting months to years, involves osteoclastic resorption of excessive callus and osteoblastic deposition of lamellar bone along stress lines per Wolff's law. Open fractures carry high infection risk because the fracture communicates with the external environment, allowing bacterial contamination of exposed bone and soft tissue. Pathologic fractures occur through weakened bone from metastatic disease, osteoporosis, or other bone-destroying processes.