title: Mineral trioxide aggregate solution inhibits osteoclast differentiation through the maintenance of osteoprotegerin expression in osteoblasts.
abstract: 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.
authors.affiliation: Division of Molecular Signaling and Biochemistry, Department of Biosciences, Kyushu Dental College, 2-6-1 Manazuru, Kokurakita-ku, Kitakyushu, Fukuoka 803-8580, Japan.
authors.forename: Daisuke
authors.initials: D
authors.lastname: Hashiguchi
authors.forename: Hidefumi
authors.initials: H
authors.lastname: Fukushima
authors.forename: Midori
authors.initials: M
authors.lastname: Nakamura
authors.forename: Kazumasa
authors.initials: K
authors.lastname: Morikawa
authors.forename: Hisataka
authors.initials: H
authors.lastname: Yasuda
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Udagawa
authors.forename: Kenshi
authors.initials: K
authors.lastname: Maki
authors.forename: Eijiro
authors.initials: E
authors.lastname: Jimi
mesh_terms: D017607:Aluminum Compounds / Q000494:pharmacology*; D000818:Animals; D001854:Bone Marrow Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D002117:Calcitriol / Q000494:pharmacology; D002122:Calcium Chloride / Q000494:pharmacology; D017610:Calcium Compounds / Q000494:pharmacology*; D002454:Cell Differentiation / Q000187:drug effects*; D018920:Coculture Techniques; D004338:Drug Combinations; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D051379:Mice; D010006:Osteoblasts / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism*; D010010:Osteoclasts / Q000166:cytology* / Q000187:drug effects* / Q000378:metabolism; D010012:Osteogenesis / Q000187:drug effects; D053244:Osteoprotegerin / Q000235:genetics / Q000378:metabolism*; D010087:Oxides / Q000494:pharmacology*; D053245:RANK Ligand / Q000494:pharmacology; D017640:Silicates / Q000494:pharmacology*; D012996:Solutions
chemical_list: D017607:Aluminum Compounds; D017610:Calcium Compounds; D004338:Drug Combinations; D053244:Osteoprotegerin; D010087:Oxides; D053245:RANK Ligand; D017640:Silicates; D012996:Solutions; C086631:mineral trioxide aggregate; D002117:Calcitriol; D002122:Calcium Chloride