Experimental osteoporosis induced by ovariectomy and vitamin D deficiency does not markedly affect fracture healing in rats
Background The question of whether fracture healing and mechanical properties of the callus are influenced by osteoporosis (OP) is still not settled. We therefore studied this issue in vitamin D-depleted ovariectomized (OVX) rats, an OP model previously shown to induce weakening of the femoral neck,...
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Veröffentlicht in: | Acta orthopaedica 2007-01, Vol.78 (3), p.393-403 |
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Zusammenfassung: | Background The question of whether fracture healing and mechanical properties of the callus are influenced by osteoporosis (OP) is still not settled. We therefore studied this issue in vitamin D-depleted ovariectomized (OVX) rats, an OP model previously shown to induce weakening of the femoral neck, and thus thought to be closer to the human condition than the classic OVX rat model.
Methods 72 female Wistar rats were randomized into two groups: ovariectomy and vitamin D-deficient diet (Ovx-D group) or sham operation and normal rat chow (Sham group). After 12 weeks, a closed tibial midshaft fracture was performed on the right side and fixed with an intramedullary nail. Bone loss and callus formation were monitored with DXA; serum levels of estradiol and vitamin D3 were measured and histomorphometric analyses were performed. Mechanical properties of callus, tibia, femoral shaft, and femoral neck were examined in 3-point cantilever bending 6 weeks after fracture.
Results The Ovx-D group showed reduced BMD in the spine and femoral neck, and reduced trabecular bone volume in the femoral head. There were no differences in BMD and mechanical properties of callus between the groups. Except for reduced stiffness of the right femoral neck in the Ovx-D group (p = 0.02), no differences in the mechanical strength of long bones were detected.
Interpretation Our results suggest that the systemic effects of estrogen and vitamin D deficiency are not crucial for fracture healing or mechanical properties of the callus. |
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ISSN: | 1745-3674 1745-3682 |
DOI: | 10.1080/17453670710013988 |