Mandibular bone formation rates in aged ovariectomized rats treated with anti-resorptive agents alone and in combination with intermittent parathyroid hormone.
Anti-resorptive agents--including estrogen (E), calcitonin (CT), and bisphosphonates--are established in the treatment of osteoporosis. Intermittent administration of parathyroid hormone (PTH) stimulates bone formation and is a possible therapeutic agent for the restoration of bone mass. The purpose was to determine the effects of the anti-resorptive agents alone and in combination with intermittent PTH on bone formation in the mandible and a long bone in the aged ovariectomized (Ovx) rat. Female rats were ovariectomized or sham-operated. One year later, groups of Ovx rats were treated with E, CT, or the bisphosphonate, Risedronate (NE). Additional groups of Ovx rats were treated with each of these agents in combination with human PTH for 10 weeks. Estrogen treatment suppressed most indices of bone formation in the humerus and mandible, while NE decreased some indices of formation at the endocortical and endosteal surfaces of the mandible and humerus. Increased double-labeled surface and mineral apposition rates were observed only on the mandibular endosteal surfaces following CT treatment. When the anti-resorptive agents were combined with intermittent PTH, most indices of bone formation at all skeletal sites were substantially greater than those of the untreated Ovx controls as well as the E-, CT-, and NE-treated groups, respectively. These results provide additional evidence that established and emerging therapies for osteoporosis affect osseous tissues in the oral cavity, and this may influence the progression of diseases and/or aging changes at this site.
Hunziker
J
J
Department of Radiology, School of Medicine, University of Utah, Salt Lake City 84108-1218, USA.
Wronski
T J
TJ
Miller
S C
SC
D000704:Analysis of Variance; D000818:Animals; D001862:Bone Resorption / Q000473:pathology / Q000517:prevention & control*; D002116:Calcitonin / Q000008:administration & dosage / Q000627:therapeutic use; D002121:Calcium Channel Blockers / Q000008:administration & dosage / Q000627:therapeutic use; D004164:Diphosphonates / Q000008:administration & dosage / Q000627:therapeutic use; D004195:Disease Models, Animal; D018450:Disease Progression; D004338:Drug Combinations; D004967:Estrogens / Q000008:administration & dosage / Q000627:therapeutic use; D012968:Etidronic Acid / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000627:therapeutic use; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006811:Humerus / Q000187:drug effects / Q000473:pathology; D008334:Mandible / Q000187:drug effects* / Q000473:pathology; D008336:Mandibular Diseases / Q000473:pathology / Q000517:prevention & control*; D008903:Minerals / Q000378:metabolism; D010012:Osteogenesis / Q000187:drug effects*; D010024:Osteoporosis / Q000517:prevention & control; D010052:Ovariectomy; D010281:Parathyroid Hormone / Q000008:administration & dosage / Q000627:therapeutic use*; D010521:Periosteum / Q000187:drug effects / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D000068296:Risedronic Acid
D002121:Calcium Channel Blockers; D004164:Diphosphonates; D004338:Drug Combinations; D004967:Estrogens; D008903:Minerals; D010281:Parathyroid Hormone; D002116:Calcitonin; D000068296:Risedronic Acid; D012968:Etidronic Acid