Osteomyelitis is classified as acute (developing over days to weeks) or chronic (persisting beyond 6 weeks or recurring after apparent treatment). The distinction is critical because pathophysiology, imaging findings, and management differ significantly between the two forms. In acute osteomyelitis, bacteria reach bone via hematogenous spread (most common in children and vertebral osteomyelitis in adults), contiguous spread from adjacent soft tissue infection (diabetic foot ulcers, decubitus ulcers), or direct inoculation (open fractures, surgical hardware). The most common pathogen across all forms is Staphylococcus aureus, which possesses surface adhesins (MSCRAMMs -- microbial surface components recognizing adhesive matrix molecules) that bind collagen, fibronectin, and bone sialoprotein in the extracellular bone matrix. Once adherent, S. aureus produces biofilm -- a polysaccharide matrix that shields organisms from immune cells and creates antibiotic concentrations 100-1000x lower than in surrounding tissue. The acute inflammatory response recruits neutrophils and macrophages, which release proteolytic enzymes and reactive oxygen species. Within the rigid bony architecture, purulent exudate accumulates and increases intramedullary pressure, compressing nutrient blood vessels within Haversian canals and Volkmann canals. This vascular compromise causes ischemic necrosis of...