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BACKGROUNDrnOsteonecrosis of the jaw (ONJ) is classically considered a disruption of vascular supply or avascular necrosis with exposure of the jaw bones. It can be caused by radiation, high-dose steroid therapy, and medications that disrupt vascular supply or bone tover in the jaws.1-2 Malignancies of, or metastatic disease to, the jaw can also result in osteonecrosis and subsequent exposure of the jaw bones. In the last 20 years, more drug therapies have been introduced to treat both osteoporosis and malignancies with skeletal-related events by slowing bone tover through antiresorptive functions, i.e., targeting the osteoclasts with bisphosphonates (BPs) and RANK ligand (RANKL) inhibitors. Some examples of drugs used to treat osteoporosis, osteopenia, genetic disorders of mineralized tissues, and cancer-mediated bone effects include alendronate (ALN), zoledronate (ZOL), and denosumab (DNB) (a RANKL inhibitor).3-4 Table 1 lists pharma-ceutical agents including trade names associated with medication-related ONJ (MRONJ) and their primary use, oncologic or osteoporotic, based on their mode of action. Evidence demon-strates a reduction in risk of vertebral and hip fragility fractures in osteoporotic patients taking such drugs. However, while rare, these agents may cause atypical femur fractures.