ECTS2013 Poster Presentations Bone development/growth and fracture repair (40 abstracts)
Metaphyseal fracture healing in a sheep model of low turnover osteoporosis induced by hypothalamic–pituitary disconnection
Ronny Bindl 1 , Ralf Oheim 2 , Pia Pogoda 2 , Frank Timo Beil 2 , Katharina Gruchenberg 1 , Sandra Reitmaier 1 , Tim Wehner 1 , Enrico Calcia 3 , Peter Radermacher 3 , Lutz Claes 1 , Michael Amling 2 & Anita Ignatius 1
1Institute of Orthopaedic Research and Biomechanics, Center of Musculoskeletal Research, University of Ulm, Ulm, Germany; 2Department of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; 3Division of Pathophysiology and Process Development in Anesthesia, Department of Anesthesia, University Medical School, Ulm, Germany.
We recently established a large animal model of osteoporosis in sheep using hypothalamic–pituitary disconnection (HPD). As central regulation is important for bone metabolism, HPD-sheep developed severe osteoporosis because of low bone turnover. In this study we investigated metaphyseal fracture healing in HPD-sheep. To elucidate potential pathomechanisms, we included a treatment group receiving thyroxine (T4) and 17β-estradiol. Because clinically osteoporotic fractures often occur in the bone metaphysis, HPD-sheep and healthy controls received an osteotomy in the distal femoral condyle. Half of the HPD-sheep were systemically treated with T4 and 17β-estradiol during the healing period. Fracture healing was evaluated after 8 weeks using pQCT, μCT and histomorphometrical analysis. Bone mineral density (BMD) and bone volume/total volume (BV/TV) were significantly reduced by 32 and 34%, respectively, in the osteotomy gap of the HPD-sheep compared to healthy sheep. Histomorphometry also revealed a decreased amount of newly formed bone (−30%) and some remaining cartilage in the HPD-group. T4 and 17β-estradiol substitution completely rescued bone healing in the HPD-sheep.
In summary we found disturbed metaphyseal bone healing in a sheep model of low turnover osteoporosis induced by HPD. This was confirmed by a decreased amount of newly formed bone in the osteotomy gap of HPD-sheep compared to healthy sheep. The mechanisms being responsible for the low turnover osteoporosis in the HPD-sheep are not yet fully clarified. In this pilot study we demonstrated that the substitution of the thyroid hormone T4 and the estrogen 17β-estradiol nearly completely abolished the deleterious effect of HPD on fracture healing indicating that the deficiency of these hormones play an important role in the pathomechanisms of disturbed fracture healing in the HPD sheep.
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Bone Abstracts
ISSN 2052-1219 (online)
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