Osteonecrosis of the jaw is a severe bone disease (osteonecrosis) that affects the jaws (the maxilla and the mandible). Various forms of ONJ have been described over the last 160 years, and a number of causes have been suggested in the literature. Osteonecrosis of the jaw associated with bisphosphonate therapy, which is required by some cancer treatment regimens, has been identified and defined as a pathological entity (bisphosphonate-associated osteonecrosis of the jaw) since 2003. The possible risk from lower oral doses of bisphosphonates, taken by patients to prevent or treat osteoporosis, remains uncertain.

Treatment options have been explored; however, severe cases of ONJ still require surgical removal of the affected bone. A thorough history and assessment of pre-existing systemic problems and possible sites of dental infection are required to help prevent the condition, especially if bisphosphonate therapy is considered

The definitive symptom of ONJ is the exposure of mandibular or maxillary bone through lesions in the gingiva that do not heal. Pain, inflammation of the surrounding soft tissue, secondary infection or drainage may or may not be present. The development of lesions is most frequent after invasive dental procedures, such as extractions, and is also known to occur spontaneously. There may be no symptoms for weeks or months, until lesions with exposed bone appear. Lesions are more common on the mandible than the maxilla.

Post radiation maxillary bone osteonecrosis is something that is found more in the lower jaw (mandible) rather than the maxilla (upper jaw) this is because there are many more blood vessels in the upper jaw.

The symptoms of this are very similar to the symptoms of medication-related osteonecrosis of the jaw (MRONJ). Patients are in a lot of pain, the area may swell up, bone may be seen and fractures may take place. The patients may also have a dry mouth and find it difficult to keep their mouth clean. A patient that has osteonecrosis may also be susceptible to bacterial and fungal infections.

The osteoblasts, which form the bone tissue, are destroyed due to the radiation with increased activity of osteoclasts. This condition cannot be treated by antibiotics as there is no blood supply to the bone, making it difficult for the antibiotics to reach the potential infection.

This condition makes eating and drinking very difficult and surgical management removing the necrotic bone improves circulation and decreases microorganisms. Other factors such as toxicants can adversely impact bone cells. Infections, chronic or acute, can affect blood flow by inducing platelet activation and aggregation, contributing to a localized state of excess coagulability (hypercoagulability) that may contribute to clot formation (thrombosis), a known cause of bone infarct and ischemia. Exogenous estrogens, also called hormonal disruptors, have been linked with an increased tendency to clot (thrombophilia) and impaired bone healing.

Heavy metals such as lead and cadmium have been implicated in osteoporosis. Cadmium and lead promotes the synthesis of plasminogen activator inhibitor-1 (PAI-1) which is the major inhibitor of fibrinolysis (the mechanism by which the body breaks down clots) and shown to be a cause of hypo fibrinolysis. Persistent blood clots can lead to congestive blood flow (hyperaemia) in bone marrow, impaired blood flow and ischemia in bone tissue resulting in lack of oxygen (hypoxia), bone cell damage and eventual cell death (apoptosis). Of significance is the fact that the average concentration of cadmium in human bones in the 20th century has increased to about 10 times above the pre-industrial level.

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Sarah eve

Editorial Assistant

Journal of Oral Hygiene and Health