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Mineral trioxide aggregate solution inhibits osteoclast differentiation through the maintenance of osteoprotegerin expression in osteoblasts
Author(s) -
Hashiguchi Daisuke,
Fukushima Hidefumi,
Nakamura Midori,
Morikawa Kazumasa,
Yasuda Hisataka,
Udagawa Nobuyuki,
Maki Kenshi,
Jimi Eijiro
Publication year - 2011
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.32990
Subject(s) - rankl , osteoprotegerin , osteoclast , mineral trioxide aggregate , activator (genetics) , osteoblast , materials science , in vitro , microbiology and biotechnology , receptor , cancer research , medicine , chemistry , biochemistry , biology , dentistry
Mineral trioxide aggregate (MTA) is a therapeutic, endodontic repair material that is reported to exhibit calcified tissue‐conductive activity. The aim of this study was to investigate whether MTA may prevent osteoclast differentiation in vitro . MTA solution, but not other commonly used retrofilling materials, such as Dycal, Super‐EBA, or intermediate restorative material (IRM) solution, dose‐dependently inhibited osteoclastogenesis in cocultures of mouse bone marrow cells (BMCs) with primary osteoblast cells (POBs) induced by 1α,25‐dihydroxyvitamin D 3 [1α,25(OH) 2 D 3 ]. Exogenous CaCl 2 medium supplementation did not inhibit osteoclastogenesis in cocultures. Furthermore, MTA solution did not affect receptor activator of NF‐κB ligand (RANKL)‐induced osteoclastogenesis, suggesting that POBs are targets of MTA. MTA solution suppressed the 1α,25(OH) 2 D 3 ‐induced reduction of osteoprotegerin (OPG) mRNA and protein production without changing RANKL expression in POBs. Consistent with this result, MTA solution did not inhibit osteoclastogenesis in cocultures of BMCs and POBs from OPG‐deficient mice. Therefore, the maintenance of OPG expression in POBs appears to be critical for the inhibitory effect of MTA solution on osteoclast differentiation. © 2010 Wiley Periodicals, Inc. J Biomed Mater Res Part A:, 2011.