Abstract

Osteomyelitis may manifest itself in acute, subacute, or chronic forms. Chronic osteomyelitis will result in variable sclerosis and deformity of the affected bone. After the age of 50, the majority of the blood supply to the mandible comes from the overlying periosteum and attached musculature, due to age and atherosclerosis-related involution of the inferior alveolar artery. With an infection of the bone, the subsequent inflammatory response will elevate this overlying periosteum, leading to a loss of the nourishing vasculature, vascular thrombosis, and bone necrosis, resulting occasionally in formation of sequestra. These become areas that are more resistant to systemic antibiotic therapy due to lack of the normal Haversian canals that are blocked by scar tissue, inflammatory exudate, and necrotic bone. At this point, not only systemic antibiotic therapy, but also surgical debridement maybe required to remove the affected bone and prevent disease propagation to adjacent areas. The relative hypoxia seen in infected bone will impair leukocyte bacterial killing, and impede fibroblastic collagen production that is required to support angiogenesis. Thus, it is not surprising that the concomitant use of hyperbaric oxygen therapy maybe beneficial in cases refractory to medical management alone or in patients with a severely compromised immune response. Generally, 20 dives (2.8–3.0 at 100% oxygen for 90 minutes) are administered preoperatively, followed by 20 dives after the debridement of necrotic tissue.