Parathyroid hormone and bisphosphonate have opposite effects on stress fracture repair |
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| Authors: | Ashley V Sloan Joseph R Martin Shuo Li Jiliang Li |
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| Institution: | 1. United States (US) Army Research Institute of Environmental Medicine, Military Nutrition Division, Natick, MA 01760, USA;2. Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA 70808, USA;3. Initial Military Training Center of Excellence, Fort Eustis, VA 23604, USA;1. Biomedical Life and Health Sciences Research Centre, Nottingham Trent University, Clifton Lane, Nottingham NG11 8NS, UK;2. Department of Occupational Medicine, Headquarters Army Recruiting and Training Division, UK;3. Canadian Sport Institute-Pacific, Victoria, British Columbia, Canada;4. Cardiff School of Sport, Cardiff Metropolitan University, Cardiff, Wales, UK;5. Norwich Medical School, University of East Anglia, UK;1. Department for BioMedical Research (DBMR), University of Bern, Bern, Switzerland;2. Graduate School of Cellular and Biomedical Sciences, University of Bern, Bern, Switzerland;1. School of Marine and Atmospheric Sciences, Stony Brook University, Stony Brook, NY, USA;2. Department of Pathology and Microbiology, Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, PE, Canada |
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| Abstract: | This study was aimed to investigate the effects of Parathyroid hormone (PTH) and alendronate (ALN) on stress fracture repair. Stress fractures were induced in the ulnae of female adult rats. Animals were treated daily with vehicle, PTH (40 µg/kg) or alendronate (2 µg/kg), respectively. Bone mineral content (BMC) and bone mineral density (BMD) of bilateral ulnae were measured at two, four and eight weeks following induction of stress fracture. Histology at the ulna midshaft was undertaken at 2 and 4 weeks and mechanical testing was done at 8 weeks after stress fracture. PTH increased BMC significantly by 7% at 4 weeks and BMD and BMC significantly by 10% and 7% at 8 weeks compared to the control. Alendronate did not change BMD or BMC in comparison with the control. PTH significantly stimulated bone formation by 114% at 2 weeks, increased intracortical resorption area by 23% at 4 weeks, and enhanced the ultimate force of the affected ulnae by 15% at 8 weeks compared to the control. Alendronate significantly suppressed bone formation rate by 44% compared to the control at 4 weeks. These data indicate that PTH may accelerate intracortical bone remodeling induced by microdamage and alendronate may delay intracortical bone remodeling during stress fracture repair in rats. This study suggests that PTH may be used to facilitate stress fracture repair whereas bisphosphonates may delay tissue level repair of stress fractures. |
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