title: Induction of osteoclastogenesis and matrix metalloproteinase expression by the lipooligosaccharide of Treponema denticola.
abstract: Alveolar bone destruction is a characteristic feature of periodontitis. Treponema denticola is known to be involved in periodontitis. To elucidate the role of T. denticola in alveolar bone destruction in periodontitis, the effects of lipooligosaccharide (LOS) from T. denticola on osteoclast formation and on expression of osteoclast differentiation factor (ODF) and osteoprotegerin (OPG) mRNAs were examined in a coculture system by using mouse calvaria and bone marrow cells. In addition, the effect of T. denticola LOS on expression of matrix metalloproteinases (MMPs), which are involved in bone resorption, was estimated in mouse calvaria-derived osteoblastic cells. When the mouse calvaria and bone marrow cells were challenged with LOS (0.1 to 10 micro g/ml) for 4 days, the number of tartrate-resistant acid phosphatase-positive multinucleated cells increased in a dose-dependent manner. The expression of ODF mRNA increased, while OPG mRNA expression decreased. Polymyxin B changed the effect of LOS (10 micro g/ml) on ODF and OPG mRNA expression to the control level. LOS (10 micro g/ml) stimulated prostaglandin E(2) (PGE(2)) production in the cocultures. Adding indomethacin, an inhibitor of prostaglandin synthesis, resulted in a reduction in the number of osteoclasts induced by LOS and eliminated the effect of T. denticola LOS on ODF and OPG mRNA expression. T. denticola LOS increased the levels of mRNAs encoding MMP-3, -8, -9, -10, -13, and -14. Expression of one of these mRNAs, MMP-9 mRNA, was significantly induced by T. denticola LOS. These findings suggest that LOS from T. denticola stimulates osteoclastogenesis and MMP expression. Up-regulation of ODF and down-regulation of OPG by a PGE(2)-dependent mechanism were involved in the osteoclastogenesis induced by T. denticola LOS.
authors.affiliation: Department of Oral Biology, College of Dentistry, Brain Korea 21 Project for Medical Sciences, Yonsei University, Seoul, Korea.
authors.forename: Bong-Kyu
authors.initials: BK
authors.lastname: Choi
authors.forename: Hyun Jung
authors.initials: HJ
authors.lastname: Lee
authors.forename: Jung Hwa
authors.initials: JH
authors.lastname: Kang
authors.forename: Gook Jin
authors.initials: GJ
authors.lastname: Jeong
authors.forename: Cheon Ki
authors.initials: CK
authors.lastname: Min
authors.forename: Yun-Jung
authors.initials: YJ
authors.lastname: Yoo
mesh_terms: D016301:Alveolar Bone Loss / Q000382:microbiology; D000818:Animals; D001854:Bone Marrow Cells; D002454:Cell Differentiation / Q000187:drug effects*; D018920:Coculture Techniques; D005786:Gene Expression Regulation; D006023:Glycoproteins / Q000235:genetics / Q000378:metabolism; D006360:Heat-Shock Proteins; D008070:Lipopolysaccharides / Q000378:metabolism / Q000494:pharmacology*; D020782:Matrix Metalloproteinases / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D008813:Mice, Inbred ICR; D010010:Osteoclasts / Q000166:cytology / Q000187:drug effects*; D053244:Osteoprotegerin; D011506:Proteins / Q000235:genetics / Q000378:metabolism; D018160:Receptors, Cytoplasmic and Nuclear / Q000235:genetics / Q000378:metabolism; D018124:Receptors, Tumor Necrosis Factor; D012886:Skull; D014208:Treponema / Q000472:pathogenicity*
chemical_list: D006023:Glycoproteins; D006360:Heat-Shock Proteins; D008070:Lipopolysaccharides; C490109:Odf1 protein, mouse; D053244:Osteoprotegerin; D011506:Proteins; D018160:Receptors, Cytoplasmic and Nuclear; D018124:Receptors, Tumor Necrosis Factor; C506031:Tnfrsf11b protein, mouse; C023023:lipid-linked oligosaccharides; D020782:Matrix Metalloproteinases