Osteonecrosis of the jaw (ONJ) is associated with the use of
bisphosphonates (BPs),
denosumab, and antiangiogenic drugs; however, the pathophysiology of medication-related ONJ (MRONJ) remains unknown. Recent advances in
therapies for diseases that affect bone remodeling have led to the development of agents that inhibit the
receptor activator of nuclear factor-kappa B ligand (RANKL). One such inhibitor is
denosumab, a highly specific, fully human
immunoglobulin G2
monoclonal antibody against RANKL. We report a case of ONJ that developed following dental extraction in a patient treated for metastatic
colorectal cancer with
denosumab. At the first medical examination at our hospital, her clinical presentation was indistinguishable from stage 2 MRONJ, classified according to the 2014 American Academy of
Oral Medicine position paper. Discontinuation of
denosumab was directed by her oncologist, and we prescribed oral
antibiotics and irrigated the exposed area of bone. Seven months after
denosumab cessation, the sequestrum of the anterior part of the mandible was naturally shed and the site was healed.
Denosumab and BPs have significantly different mechanisms of action. The effects of
denosumab on bone turnover are more rapid and reversible than those of BPs. Discontinuation of
denosumab may be effective in the management of
denosumab-related ONJ, depending on the primary
tumor control.