Osteomyelitis of the jaws: a 50-year perspective

The incidence of osteomyelitis of the jaws has decreased dramatically, except for a few subsets of individuals. This has been due, in no small part, to the availability of bacteriocidal antimicrobial therapy. The pathogenesis of osteomyelitis of the jaws is predominately due to odontogenic microorganisms rather than the classic skin contaminant, Staphylococcus. This causative relationship relegates the classification of osteomyelitis of the bimaxillary skeleton to predominately that of contiguous foci. These may be regionally progressive, secondary to microvascular compromise brought about by inherent flaws in regional anatomic calcified tissue vascular perfusion as well as by inflammatory metaplastic processes. Diagnosis is based on the presence of painful sequestra and suppurative areas of tooth-bearing jaw bone unresponsive to debridement and conservative therapy. This is usually accompanied by regional or systemic compromise of the immune response, microvascular decompensation, or both. Treatment of both acute and chronic forms of the disease, as outlined in Table 5, is successful if surgically supported. Sustained bacteriocidal antibiotic therapy is pertinent, especially in the face of potentially refractory virulent microorganisms and compromised regional vascular penetrance. The use of adjunctive hyperbaric oxygen therapy also may be included in the more refractory forms of osteomyelitis of the jaws to enhance the local and regional immune response of the jaws as well as to produce microvascular neoangiogenesis for reperfusion support. With resolution of infection, hard and soft tissue reconstruction may be necessary to augment the reparative process.