OM may occur by direct inoculation of pathogens into the bone (through surgery or injury), by spread of an adjacent area of infection or by seeding of the infection from a non adjacent site via the blood supply (hematogenous spread). Unlike OM of the long bones, hematogenous OM in the bones of the<unk>  is rare. OM of the<unk>  is mainly caused by spread of adjacent odontogenic infection. The second most common cause is trauma, including traumatic fracture and usually following a compound fracture (i.e. one that communicates with the mouth or the external environment). In OM of the long bones, a single invading pathogenic micro-organism is usually found (commonly staphylococci spp.). The mandible is affected more commonly than the maxilla. This is thought to be related to the differences in blood supply between the mandible and the maxilla. The maxilla has a better blood supply, and has thin cortical plates and less medullary spaces. These factors mean that infections of the maxilla are not readily confined to the bone, and readily dissipate edema and pus into the surrounding soft tissues and the paranasal air sinuses. OM of the maxilla may rarely occur during an uncontrolled infection of the middle ear or in infants who have sustained birth injury due to forceps. The mandible in contrast has a relatively poor blood supply, which deteriorates with increasing age. The cortical plates are thick and there is a medullary cavity. The sites of the mandible most commonly affected by OM are (decreasing order of frequency) the body, the symphysis, the angle, the ramus and finally the condyle. The mandible's blood supply is primarily via the inferior alveolar artery, and secondarily via the periosteum. Compromise of this supply is a critical factor in the development of OM in the mandible. Most periapical and periodontal infections are isolated by the body which produces a protective pyogenic membrane or abscess wall to keep the area of infection localized. Micro-organisms which are sufficiently virulent may destroy this barrier. Factors which may contribute to this are decreased host resistance, surgery or repeated movement of fracture segments, as may occur with an untreated fracture. Mechanical trauma burnishes the bone, causing ischemia by crushing blood vessels and seeds micro-organisms into the tissues. The events preceding OM are acute inflammatory changes such as hyperemia, increased capillary permeability and infiltration of granulocytes. Proteolytic enzymes are released, and thrombus formation in the blood vessels and tissue necrosis occur. Pus accumulates in the medullary spaces of the bone, which increases the pressure and leads to collapse of the blood vessels, venous stasis and ischemia. Pus may also spread to the sub-periosteal layer, dissecting it away from the surface of the bone and further reducing the blood supply. The inferior alveolar neurovascular bundle is compressed within the mandible, causing anesthesia or paresthesia in the distribution of the mental nerve. Pus may drain via sinuses on the skin and in the mouth, and these may in time become lined with epithelium, when they are termed fistulas. Chronic OM is characterized by a degree of healing which takes place as a lesser degree of inflammation is present. Granulation tissue and new blood vessels form, and fragments of necrotic bone (sequestra) are separated from vital bone. Small sections of necrotic bone may be resorbed completely, and larger segments may become surrounded by granulation tissue and new bone (an involucrum). Sequestra may also be revascularized by new blood vessels, cause no symptoms or become chronically infected. Sometimes the involucrum is penetrated by channels (cloacae) through which pus drains to the skin or mouth. OM of the<unk>  often occurs in the presence of one or more predisposing factors. These factors are related to compromised vascular perfusion locally, regionally or systemically, causes of immunocompromise and poor wound healing. Specific examples include familial hypercoagulation, diabetes, autoimmune diseases, Agranulocytosis, leukemia, severe anemia, syphilis, chemotherapy, corticosteroid therapy, sickle cell disease, acquired immunodeficiency syndrome, old age, malnutrition, smoking and alcohol consumption, radiotherapy, osteoporosis, Paget's disease of bone, fibrous dysplasia, bone malignancy and causes of bone necrosis such as Bismuth, Mercury or arsenic. Poor compliance or access to health care is also a risk factor. Rarely, OM of the<unk>  may be a complication of trigeminal herpes zoster.
Osteomyelitis of the jaws
Cysts of the jaws
Osteonecrosis of the jaw
Metastatic tumor of jaws
Hemifacial hypertrophy
Dental abscess
Melanocytic oral lesion
Onycholysis