[Avascular necrosis of the jaw bone after bisphosphonate therapy]

Bisphosphonates have an antiosteolytic effect by the inhibition of osteoclastic action. Although the exact mode of action is not completely understood, major progress on both the cellular and molecular levels has been made in recent years. Bisphosphonates alleviate pain and reduce complications, such as pathologic fractures, or hypercalcemia. Dental and periodontal research has shown great interest in clinical applications of bisphosphonates' antiosteolytic and antiosteoclastic traits, since they can be applied to counteract bone loss in chronic periodontitis. Investigations have associated avascular necrosis events in the jawbones with bisphosphonate therapy. Maxillary and mandibular osteonecrotic foci accompanied by pain, inconvenience and purulent exudates were incidentally found in patients who were taking pamidronate (Aredia), zolendronate (Zometa) and even alendronate (Fosalan). Our institutional database search over the past year yielded ten patients who were admitted to the Oral and Maxillofacial Surgery Unit at the Tel Aviv Sourasky Medical Center, due to an osteonecrotic bone lesion coupled with a prior history of bisphosphonate therapy. All these patients also had a recent dental extraction. They were all treated according to the osteomyelitis protocol, and their response to therapy varied from several weeks to many months, with some cases requiring repeat surgical intervention (curettage or sequestrectomy). This article strives to alert on the possible linkage between drug therapy using bisphosphonates and the serious event of avascular jawbone necrosis. The important role of the oral surgeon in following up on this group of patients should not be underestimated.