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Mitigating osteonecrosis of the jaw (ONJ) through preventive dental care and understanding of risk factors

Wan JT1Sheeley DM1Somerman MJ1,2Lee JS1.

Bone Res. 2020 Mar 11;8:14. doi: 10.1038/s41413-020-0088-1. eCollection 2020.


It is well established that alterations in phosphate metabolism have a profound effect on hard and soft tissues of the oral cavity. The present-day clinical form of osteonecrosis of the jaw (ONJ) was preceded by phosphorus necrosis of the jaw, ca. 1860. The subsequent removal of yellow phosphorus from matches in the early 20th century saw a parallel decline in «phossy jaw» until the early 2000s, when similar reports of unusual jaw bone necrosis began to appear in the literature describing jaw necrosis in patients undergoing chemotherapy and concomitant steroid and bisphosphonate treatment. Today, the potential side effect of ONJ associated with medications that block osteoclast activity (antiresorptive) is well known, though the mechanism remains unclear and the management and outcomes are often unsatisfactory. Much of the existing literature has focused on the continuing concerns of appropriate use of bisphosphonates and other antiresorptive medications, the incomplete or underdeveloped research on ONJ, and the use of drugs with anabolic potential for treatment of osteoporosis. While recognizing that ONJ is a rare occurrence and ONJ-associated medications play an important role in fracture risk reduction in osteoporotic patients, evidence to date suggests that health care providers can lower the risk further by dental evaluations and care prior to initiating antiresorptive therapies and by monitoring dental health during and after treatment. This review describes the current clinical management guidelines for ONJ, the critical role of dental-medical management in mitigating risks, and the current understanding of the effects of predominantly osteoclast-modulating drugs on bone homeostasis.


 MRONJ is a rare but potentially devastating side effect of antiresorptive therapy. The unique physiology of craniofacial bones appears to contribute to the increased concentration of BP in this location versus other skeletal tissues and is dependent upon administration route and dosing. In vitro experiments at the cellular level complement these clinical observations and have revealed part of the mechanism. The etiology is complex and remains unclear, and may involve the immune, nervous, skeletal, and vascular systems, coupled with one’s microbiome. The risk for MRONJ is multifactorial and the vast majority of cases include trauma or injury to the jaw bones, particularly dentoalveolar surgery. Oral infection and inflammation and medical comorbidities are significant risk factors for ONJ and are key contributors to initiation and progression of the disease. Through dental evaluations and management of the patient by the health care provider team before drug therapy, during, and long term, the risk of developing ONJ can be reduced significantly thereby increasing patient compliance and improving clinical outcomes.