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Local application of alendronate controls bone formation and β-tricalcium phosphate resorption induced by recombinant human bone morphogenetic protein-2.

07:00 EST 8th November 2019 | BioPortfolio

Summary of "Local application of alendronate controls bone formation and β-tricalcium phosphate resorption induced by recombinant human bone morphogenetic protein-2."

This study examined the ability of local alendronate (ALN) administration to control β-tricalcium phosphate (β-TCP) resorption as well as the induction of bone formation by recombinant human bone morphogenetic protein-2 (rhBMP-2). A 15-mm critical-sized bone defect was created in the diaphysis of rabbit ulnae. Nine female rabbits (4 to 5 months-old) were divided into 3 groups. Group 1 (n = 6 ulnae) animals received implants consisting of β-TCP granules and 25 μg of rhBMP-2 in 6.5% collagen gel. Group 2 (6 ulnae) and Group 3 (6 ulnae) animals received the same implants, but with 10 M and 10 M ALN-treated TCP granules, respectively. Two weeks post-surgery, tartrate-resistant acid phosphatase-positive cell counts, new bone formation, and residual β-TCP were evaluated. This study showed that a high dose of ALN strongly reduced osteoclastic resorption of β-TCP induced by rhBMP-2, resulting in decreased bone formation. In contrast, a low dose of ALN slightly reduced the bone resorptive effect but increased bone formation. These results suggest that osteoclast-mediated resorption plays an important role in bone formation and a coupling-like phenomenon could occur in the β-TCP-implanted area, and that administration of a low dose of ALN may solve clinical bone resorptive problems induced by rhBMP-2. This article is protected by copyright. All rights reserved.

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This article was published in the following journal.

Name: Journal of biomedical materials research. Part A
ISSN: 1552-4965
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