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Periodontal disease and bisphosphonates induce osteonecrosis of the jaws in the rat
Author(s) -
Aghaloo Tara L,
Kang Ben,
Sung Eric C,
Shoff Michael,
Ronconi Matthew,
Gotcher Jack E,
Bezouglaia Olga,
Dry Sarah M,
Tetradis Sotirios
Publication year - 2011
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1002/jbmr.379
Subject(s) - medicine , osteonecrosis of the jaw , zoledronic acid , dental alveolus , periodontitis , osteoporosis , dentistry , bone mineral , pathology , bisphosphonate
Bisphosphonates (BPs) are medications used commonly to treat primary and metastatic bone cancer, as well as osteoporosis. Although BPs improve bone mineral density, reduce fracture risk, and reduce hypercalcemia of malignancy, some patients develop BP‐related osteonecrosis of the jaws (BRONJ). This devastating complication is defined as clinically exposed bone in the maxillofacial region for more than 8 weeks. Despite an increasing number of BRONJ cases since first reported, the disease pathophysiology remains largely unknown. Since published studies suggest a significant role for dental disease in the pathophysiology of BRONJ, we developed a BRONJ animal model where aggressive periodontal disease is induced by ligature placement around the crown of the right maxillary first molar in the presence of vehicle (veh) or zoledronic acid (ZA), a potent BP. Ligature placement induced significant alveolar bone loss, which was attenuated by ZA treatment. Osteonecrosis was observed associated with ligature‐induced periodontitis in the ZA‐treated group. This was seen as sequestration and extensive periosteal alveolar bone formation on micro–computed tomography (µCT) in the ligated site of BP‐treated animals. Histologic examination confirmed these findings, seen as necrotic bone with diffuse loss of osteocytes and empty lacunae, rimming of the necrotic bone by squamous epithelium and inflammation, and exposure to the oral cavity. Importantly, the rat lesions were strikingly similar to those of BRONJ patients. Our data suggest that dental disease and potent BP therapy are sufficient for BRONJ development in the rat. © 2011 American Society for Bone and Mineral Research

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