Osteonecrosis of the jaw
| Osteonecrosis of the jaws | |
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| Osteonecrosis of the jaw of the upper left jaw in a patient diagnosed with chronic venous insufficiency | |
| Classification and external resources | |
| Specialty | rheumatology |
| ICD-10 | M87.1 |
| ICD-9-CM | 733.45 |
| DiseasesDB | 1174 |
| eMedicine | derm/816 |
Osteonecrosis of the jaw (ONJ) 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.
Osteonecrosis of the jaw is classified based on severity, number of lesions, and lesion size. Osteonecrosis of greater severity is given a higher grade, with asymptomatic ONJ designated as grade 1 and severe ONJ as grade 4.
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.
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 ischaemia. Exogenous estrogens, also called hormonal disruptors, have been linked with an increased tendency to clot (thrombophilia) and impaired bone healing.
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