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Local application of alendronate controls bone formation and β‐tricalcium phosphate resorption induced by recombinant human bone morphogenetic protein‐2
Author(s) -
Kitasato Seiichiro,
Tanaka Takaaki,
Chazono Masaaki,
Komaki Hirokazu,
Kakuta Atsuhito,
Inagaki Naoya,
Akiyama Shoshi,
Marumo Keishi
Publication year - 2020
Publication title -
journal of biomedical materials research part a
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.849
H-Index - 150
eISSN - 1552-4965
pISSN - 1549-3296
DOI - 10.1002/jbm.a.36833
Subject(s) - bone resorption , resorption , bone formation , bone morphogenetic protein , materials science , bone morphogenetic protein 2 , endocrinology , medicine , chemistry , in vitro , biochemistry , gene
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 −6 M and 10 −3 M ALN‐treated TCP granules, respectively. Two weeks postsurgery, 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.