Editorial: Medication-related osteonecrosis of the jaw (MRONJ): Bisphosphonates, antiresorptives, and antiangiogenic agents. What next?

Abstract

From a recent recommendation of the special committee on medication-related osteonecrosis of the jaws of the American Association of Oral and Maxillofacial Surgeons (AAOMS) 1 came the name change: bisphosphonate-related osteonecrosis of the jaw (BRONJ) or antiresorptive agent-related osteonecrosis of the jaw (ARONJ) to medication-related osteonecrosis of the jaw (MRONJ). Various drug groups that promote the osteonecrosis of the jaw include intravenous bisphosphonates, oral bisphosphonates, RANK ligand inhibitors, and angiogenesis inhibitors. There is a variety of local factors that influence the effect of these medications; often for the worse. These factors include dentoalveolar surgery, anatomical factors, and concomitant oral disease, as well as less confirmed risk factors such as sex, age, steroid therapy, smoking, and anemia in cancer patients. 2 It has been noted that the prevalence of MRONJ is more in cancer patients receiving antiresorptive therapies compared to those receiving treatment for osteoporosis alone. The common oral bisphosphonates used 1 are alendronate sodium, risedronate sodium, and ibandronate sodium. The common intravenous bisphonates used are ibandronate, pamidronate disodium, and zoledronate. Denosumab (Xgeva® and Prolia®) is a new group of medication that is essentially a humanized monoclonal antibody administered subcutaneously. Other antiangiogenic agents include sunitinib and sorafenib (tyrosine kinase inhibitors); bevacizumab, another humanized monoclonal antibody; and last but not the least, sirolimus, a mammalian target of rapamycin pathway that is given to patients who are at risk of developing organ rejection secondary to renal transplant. 1