Abstract
18628 Background: Intravenous bisphosphonates are the current standard of care for the treatment of hypercalcemia of malignancy and for the prevention of skeletal complications associated with bone metastases. Generally, the i.v. administration of bisphosphonates is well tolerated. Recently, retrospective case studies have reported an association between long-term bisphosphonate therapy and osteonecrosis of the jaws. Methods: We reviewed data for 12 patients referred to either an oral and maxillofacial surgeon or an oral medicine specialist for the management of clinically apparent chronic oral osteonecrosis of unknown etiology. All had received therapy cancer-related simultaneously with bisphosphonate management. Results: Typical presenting symptoms were pain and exposed bone at the site of a previous tooth extraction. In most patients, lesions initially occurred after dental extraction or other odontostomatological procedures, and 5 had a spontaneous event. Biopsy of the involved area showed the presence of necrotic lacunae, with infiltration of lymphocytes and histiocytes. In 9 cases, histological or cytological diagnosis of suspicious osteomyelitis was done. There was no observed correlation of the intraoral lesions with myelosuppression secondary to antineoplastic therapy. Conclusions: Based on these patients’ respective histories, clinical presentations, and responses to surgical and antibiotic treatments, it appears that the pathogenesis of this osteonecrotic process is most consistent with localized vascular insufficiency. In our opinion, the mechanism by which bisphosphonates could compromise bone vascularity may be related to its effect on the osteoclasts. The potent bisphosphonate mediated inhibition of osteoclast function serves to decrease bone resorption and inhibit normal bone turnover remodeling, resulting in microdamage accumulation and a reduction in some mechanical properties of bone. No significant financial relationships to disclose.
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