Medication-related osteonecrosis of the jaw (MRONJ) is a severe complication that develops in patients receiving antiresorptive or antiangiogenic therapy, most often with bisphosphonates or monoclonal antibodies (denosumab), which are used to treat osteoporosis and hypercalcemia in case of metastatic bone lesions. These drugs affect bone tissue, suppress the osteoclasts activity and, indirectly, osteoblasts, slowing down mineral metabolism in general. Denosumab is a monoclonal antibody against RANKL that blocks the differentiation and activation of osteoclasts. Despite their effectiveness in preventing bone loss, both classes of drugs can cause osteonecrosis of the jaw. The direct mechanisms of osteonecrosis are not completely understood, but it is believed that this process is associated with the suppression of bone remodeling, deterioration of bone trophism, and the microbial-induced inflammation, which is facilitated by the action of antiresorptive drugs. In addition to physical examination and X-ray imaging, various methods based on the effect of fluorescence are used for the precise visualization of necrotic tissue. Osteonecrosis is treated conservatively or surgically, depending on the stage of the disease. Understanding the mechanisms and specific morphological features of MRONJ is necessary to optimize treatment strategy and minimize possible complications.
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Salpagarov et al. (2026) studied this question.
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