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Osteomyelitis of the jaws was relatively common before the era of antibiotic therapy and preventive and restorative dentistry. Today, osteomyelitis of the facial bones is a rare condition osteomyelitis, jaw bone infection. Osteomyelitis represents an inflammation of the medullary cavity, Haversian system, and adjacent cortex of bone. In full-blown cases, there is necrosis of bone and deposition of calcium. The mandible is more commonly involved than the maxilla.

In a review of 141 cases of jaw osteomyelitis in Nigeria, Adekeye and Cornah found odontogenic infections to be the cause of 38% of mandibular and 25% of maxillary involvement. Similarly, Balm et al found odontogenic sources to be the most common cause of mandibular osteomyelitis. Koorbusch et al found an even distribution in cases of osteomyelitis caused by trauma and by odontogenic infections (36% each), with osteoradionecrosis.

Clinically, patients present with facial swelling, localized pain and tenderness, low-grade fever, draining sinus tracts, suppuration, dental loss, and sequestrum (ie, necrotic bone fragment) formation. New bone and oral mucosa will occasionally regenerate beneath the sequestra, probably because of activation of periosteal osteoblasts.

Predisposing factors found to contribute to the development of osteomyelitis include viral fevers (eg, measles), malnutrition, malaria, anemia, and tobacco. Treatment goals include reversal of any predisposing conditions, long-term antibiotic therapy.

Since most of the infections are polymicrobial oral flora (primarily facultative streptococci, Bacteroides spp, Peptostreptococcus, and Peptococcus), antibiotic treatment includes penicillin, metronidazole, and clindamycin. Operative interventions such as sequestrectomy, decortication, removal of nonviable bone (ie, mandibulectomy or maxillectomy), dental extractions, and fracture fixation.

Immediate oral-maxillofacial surgery consultation is recommended. Hyperbaric oxygen may be a useful adjunctive treatment by increasing the oxygen tension in minimally vascularized tissue beds and by stimulating revascularization and collagen formation.

Of all the dural venous sinuses, the cavernous sinuses are most often affected by thrombosis. The two cavernous sinuses are situated on either side of the sella turcica and are connected by the intercavernous sinuses. Within the lateral wall of the sinuses run cranial nerves (CN) III, IV, V1, and V2. The internal carotid artery and CN VI course through the center of the sinuses. Septa within the sinuses are believed to increase the likelihood of embolic entrapment.

Septic thrombi of the cavernous sinuses most often result from infections of the midface, with Staphylococcus aureus being the predominant pathogen. Other primary foci of infection include paranasal sinusitis (primarily sphenoid) and otitis media. In approximately 10% of patients with cavernous sinus thrombosis (CST), the source appears to be odontogenic.

Sterile CST has been associated with polycythemia, sickle cell disease, paroxysmal nocturnal hemoglobinuria, contraceptive use, dehydration, compressive brain tumors or aneurysms, and pregnancy. Occasionally, no predisposing condition is evident.

Patients with CST often present with headache, unilateral retro-orbital pain, periorbital edema, fever, proptosis, chemosis, ptosis, mental status changes, and meningismus. An isolated sixth nerve palsy may be seen, since CN VI is the only CN that runs through the interior of the cavernous sinus. Bilateral signs occur as the thrombophlebitis traverses the intercavernous.

The differential diagnosis includes orbital cellulitis, orbital tumors, ethmoiditis, carotid-cavernous sinus fistulas, exophthalmic goiter, the dural shunt syndrome (ie, vascular communications exist between the small meningeal arteries and cerebral veins.