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 Etiology: patient risk factors, poor surgical technique, infection

 Management: antibiotics, surgical debridement, decortication, sequestrectomy, or resection

The incidence of osteomyelitis as a result of third molar extraction is not reported frequently in the literature; however, it is a known complication of postoperative infection, fracture, and/or extractions performed in medically compromised patients. Osteomyelitis is an inflammation of the bone marrow and is most common in the mandible due to its dependence on blood supply from the inferior alveolar artery and periosteum and poorly vascularized thick cortical bone. Since the maxilla has a rich vascular supply from multiple vessels, it is less likely to develop osteomyelitis. The presence of bacteria within the marrow space leads to inflammation and edema with subsequent compression of blood vessels and a decrease in blood supply. This decrease in blood flow results in ischemia, bone necrosis, and proliferation of bacteria. Purulence and bacteria can spread within the marrow via Haversian systems and Volkmann's canals and extend into cortical bone. Once the cortical bone and periosteum are involved, the blood supply is further compromised and perforation of soft tissues can occur resulting in fistula formation. Predisposing factors in the development of osteomyelitis involve suppression of host defenses in some form. Diabetes, alcoholism, malnutrition syndrome, autoimmune disease, radiation therapy, chemotherapy, steroid use, osteopetrosis, and myeloproliferative diseases can contribute to the development of osteomyelitis.

Table 2.1. Types of osteomyelitis

Source: Adapted from Alpert et al. [37].

AcuteContiguous focusProgressiveHematogenous ChronicRecurrent multifocalGarré's proliferative periostitisSuppurative or nonsuppurativeSclerosing

The classification of osteomyelitis offered by Hudson is commonly cited in the literature and includes acute and chronic forms, based upon disease presence for either less than (acute) or greater than (chronic) one month (30 days) [37] (Table 2.1).

Patients with osteomyelitis will often present with complaints of a dull and deep pain, swelling and erythema of overlying tissues, paresthesia of the IAN, trismus, lymphadenopathy, fistula, fever, and malaise [38, 39]. In patients with chronic osteomyelitis, signs of acute infection such as fever are often not present; however, fistulas, both intra‐ and extraorally, are more common. Radiographs typically demonstrate a “moth‐eaten” appearance or the presence of radio‐opaque bony sequestra. CT scanning can assist in the demarcation of lesion extent, although it should be noted that 30–50% demineralization of bone is necessary before radiographic changes [38] (Figure 2.9). In chronic osteomyelitis, there may be radiopacity due to an osteitis‐type reaction and proliferation of bone. Laboratory workup will demonstrate a leukocytosis in acute forms, and elevated erythrocyte sedimentation rate (ESR) and C‐reactive protein (CRP) levels. Further laboratory evaluation of ESR and CRP levels during treatment can assist in assessment of resolution of the disease process. Culture specimens will often yield bacteria traditionally responsible for odontogenic infections, such as Bacteroides, Peptostreptococcus, Fusobacterium, and Streptococcus species. Occasionally, less common odontogenic bacteria are present, including Lactobacillus, Eubacterium, Klebsiella, Acinetobacter, and Pseudomonas aeruginosa . Osteomyelitis of the jaws is different from osteomyelitis of other bones in that staphylococci are usually not the predominant bacteria [38].

The treatment of osteomyelitis involves both surgical and medical management. Treatment of comorbid systemic diseases must be considered along with medical consultation, when appropriate. Empirical systemic antibiotics should be administered while awaiting final culture and sensitivity results. Penicillin/metronidazole or clindamycin are excellent first‐line choices for empirical antibiotics. In chronic cases, sequestrectomy, decortication, and saucerization may be necessary to debride the involved bone to vital, bleeding bone margins to assist in healing acceleration. Removal of the bony cortex with attachment of the periosteum directly on the marrow space assists in blood flow and revascularization. After aggressive bone debridement, bone fixation and stabilization may be needed to prevent a pathological mandible fracture or stabilize an existing fracture. External fixation, rigid internal fixation, or intermaxillary fixation may be used with various fixation schemes, with the specific type dependent upon surgeon preference and degree of success of surgical debridement [38, 39] (Figure 2.10a–i). Other methods of treatment have been proposed, such as local antibiotic administration, with both resorbable and nonresorbable carriers (antibiotic‐impregnated beads) and hyperbaric oxygen (HBO) (controversial). Poly(methyl methacrylate) beads impregnated with gentamicin have been used in orthopedic surgery; however, results can be disappointing due to inadequate local release and subinhibitory antibiotic levels. Also, a second surgery is necessary to remove the beads. HBO has not been demonstrated to have a significant effect on outcome based on the limited available literature [40, 41]. Esterhai et al. studied the use of HBO in 28 patients with chronic refractory osteomyelitis, and this controlled trial concluded that HBO had no effect on length of hospitalization, rate of wound repair, or recurrence of infection [40].

Fig. 2.9. 3D reconstruction of right mandibular osteomyelitis demonstrating a “moth‐eaten” appearance to the bone.