Vance Michael A
Department of Pharmaceutical Sciences, Butler University, College of Pharmacy and Allied Health Sciences, Indianapolis, Indiana 46208, USA.
Clin Toxicol (Phila). 2007 Oct-Nov;45(7):753-62. doi: 10.1080/15563650701232505.
Recent reports of bisphosphonate-associated jaw osteonecrosis are reminiscent of earlier incidents in which a comparable syndrome was caused by occupational exposure to white phosphorus or radium. Osteonecrosis of the jaw is also caused by an inherited disease: osteopetrosis. This review analyzes the biomedical and social aspects of these four situations associated with jaw osteonecrosis.
Clinical evidence is contradictory but suggests aminobisphosphonates cause rare cases of jaw necrosis. In addition to jaw problems, generalized skeletal defects characterize osteopetrosis and exposure to phosphorus or radium and there is evidence of decreased bone resorption in these conditions and with bisphosphonate therapy.
Bisphosphonate-induced jaw necrosis appears to be an on-target toxicity as the same mechanism, inhibition bone resorption, probably underlies both the therapeutic and adverse effects. Since bisphosphonates are retained for long periods by bone the theoretical potential for skeletal toxicity is increased by using higher doses of potent aminobisphosphonates administered less frequently.
