Bone is a dynamic organ. Normal, healthy bone is composed primarily of lamellar bone (Fig. 5.2). Osteoblasts lay down unmineralized osteoid in layers, or lamellae. Osteoblasts surrounded by bone are called osteocytes, and they reside within spaces called lacunae. The osteocytes communicate with each other via cytoplasmic processes called canaliculi. Osteoclasts are responsible for breaking down the bone by a process of resorption. Together the osteocytes, osteoblasts, and osteoclasts remodel the bone in response to mechanical forces, calcium and phosphate levels, as well as other hormones and cytokines.

When an infection breeches the periosteum and reaches cortical bone, osteoclastic resorption occurs causing scalloping of the cortical surface (Fig. 5.3). Pathogens and neutrophils gain access to the medullary canal via Haversian systems in the cortical bone (Fig. 5.4) and the host response of osteoclastic bone resorption continues. Because a bone is virtually a closed system, the edema from the inflammatory response increases the intramedullary pressure, impairing the blood supply further. Microscopic bone necrosis is evident after approximately 48 h (Fig. 5.5) [19]. Left untreated or partially treated, the process becomes chronic and gross necrosis may become evident. The term sequestrum refers to an area of segmental osteonecrosis which has become separate from the adjacent viable bone and may be identifiable in imaging studies [16]. As bone necrosis continues, the inflammatory activity stimulates the production of osteoblastic new woven bone formation between the periosteum and cortex (Fig. 5.6), termed the involucrum, which encases the sequestrum and strengthens the bone in the damaged area, much like a fracture callus.

The key histologic features of acute osteomyelitis are neutrophils in close association with necrotic bone, and osteoclastic activity with bone scalloping. Bone necrosis is recognized by the absence of osteocytes within lacunae (Fig. 5.7). Other histologic features may also be present such as marrow edema, marrow necrosis, and intravascular thrombi (Fig. 5.8). As the inflammatory process continues, osteoblasts produce woven bone to rebutress trabeculae of necrotic lamellar bone in a reparative process referred to as creeping substitution. Septic arthritis is characterized by acute inflammation involving the joint capsule, synovium, or damaging the articular cartilage (Figs. 5.9 and 5.10).