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1 Calcium Research Laboratories, McGill University Health Centre, Montreal, QC, Canada; Division of Geriatric Medicine, McGill University, Montreal, QC, Canada
2 Calcium Research Laboratories, McGill University Health Centre, Montreal, QC, Canada
3 Research Centre, Hopital Saint-Luc, Centre Hospitalier de l' Universite de Montreal, Montreal, QC, Canada
* To whom correspondence should be addressed. E-mail: richard.kremer{at}mcgill.ca.
Recent studies suggest that vitamin D signaling regulates bone formation. However, the overall effect of 1,25 dihydroxyvitamin D3 [1,25(OH)2D3] on bone turnover in vivo is still unclear. In this study our aim was to examine the effect of 1,25(OH)2D3 on bone turnover in SAM-P/6, a hormone-independent mouse model of senile osteoporosis characterized by a decrease in bone formation. Male and female 4 month old SAM-P/6 mice were treated with 1,25(OH)2D3 (18 pmol/24h) or vehicle for a period of 6 weeks and a group of age and sex-matched non-osteoporotic animals was used as control. Bone mineral density (BMD) at the lumbar spine increased rapidly by over 30 ± 5% (P < 0.001) in 1,25(OH)2D3-treated SAM-P/6 animals whereas BMD decreased significantly by 18 ± 2% (P < 0.01) in vehicle-treated SAM-P/6 animals and remained stable in control animals during the same period. Static and dynamic bone histomorphometry indicated that 1,25(OH)2D3 significantly increase bone volume and other parameters of bone quality as well as subperiosteal bone formation rate as compared to vehicle-treated SAM-P/6. However, no effect on trabecular bone formation was observed. This was accompanied by a marked decrease in the number of osteoclasts and eroded surfaces. A significant increase in circulating bone formation markers and a decrease in bone resorption markers was also observed. Finally, bone marrow cells, obtained from 1,25(OH)2D3-treated animals and cultured in the absence of 1,25(OH)2D3, differentiated more intensely into osteoblasts compared to bone marrow stem cells derived from vehicle-treated mice cultured in the same conditions. Taken together these findings demonstrate that 1,25(OH)2D3 acts simultaneously on bone formation and resorption to prevent the development of senile osteoporosis.
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