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Td92, an outer membrane protein of Treponema denticola, induces osteoclastogenesis via prostaglandin E(2)-mediated RANKL/osteoprotegerin regulation

Authors
 M. Kim  ;  H.-K. Jun  ;  B.-K. Choi  ;  J.-H. Cha  ;  Y.-J. Yoo 
Citation
 JOURNAL OF PERIODONTAL RESEARCH, Vol.45(6) : 772-779, 2010 
Journal Title
 JOURNAL OF PERIODONTAL RESEARCH 
ISSN
 0022-3484 
Issue Date
2010
MeSH
Adhesins, Bacterial/genetics ; Adhesins, Bacterial/pharmacology ; Adhesins, Bacterial/physiology* ; Alveolar Bone Loss/metabolism* ; Alveolar Bone Loss/microbiology ; Animals ; Bone Marrow Cells ; Cells, Cultured ; Coculture Techniques ; Dinoprostone/metabolism* ; Gene Expression Regulation ; Mice ; Mice, Inbred Strains ; Osteoblasts ; Osteoclasts/drug effects ; Osteoclasts/metabolism ; Osteoclasts/physiology* ; Osteoprotegerin/biosynthesis* ; Osteoprotegerin/genetics ; RANK Ligand/biosynthesis* ; RANK Ligand/genetics ; Recombinant Proteins/pharmacology ; Treponema denticola/chemistry* ; Treponema denticola/physiology
Abstract
BACKGROUND AND OBJECTIVE: Periodontitis is a chronic inflammatory disease of the periodontium that causes significant alveolar bone loss. Osteoclasts are bone-resorbing multinucleated cells. Osteoblasts regulate osteoclast differentiation by expression of RANKL and osteoprotegerin (OPG). Td92 is a surface-exposed outer membrane protein of Treponema denticola, a periodontopathogen. Although it has been demonstrated that Td92 acts as a stimulator of various proinflammatory mediators, the role of Td92 in alveolar bone resorption remains unclear. Therefore, in this study, we investigated the role of Td92 in bone resorption. MATERIAL AND METHODS: Mouse bone marrow cells were co-cultured with calvariae-derived osteoblasts in the presence or absence of Td92. Osteoclast formation was assessed by TRAP staining. Expressions of RANKL, osteoprotegerin (OPG) and prostaglandin E(2) (PGE(2) ) in osteoblasts were estimated by ELISA. RESULTS: Td92 induced osteoclast formation in the co-cultures. In the osteoblasts, RANKL and PGE(2) expressions were up-regulated, whereas OPG expression was down-regulated by Td92. The addition of OPG inhibited Td92-induced osteoclast formation. The prostaglandin synthesis inhibitors NS398 and indomethacin were also shown to inhibit Td92-induced osteoclast formation. The effects of Td92 on the expressions of RANKL, OPG and PGE(2) in osteoblasts were blocked by NS398 or indomethacin. CONCLUSION: These results suggest that Td92 promotes osteoclast formation through the regulation of RANKL and OPG production via a PGE(2) -dependent mechanism.
Full Text
http://onlinelibrary.wiley.com/doi/10.1111/j.1600-0765.2010.01298.x/abstract
DOI
10.1111/j.1600-0765.2010.01298.x
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers
Yonsei Authors
Kim, Min Young(김민영)
Yoo, Yun Jung(유윤정) ORCID logo https://orcid.org/0000-0002-0045-9597
Cha, Jung Heon(차정헌) ORCID logo https://orcid.org/0000-0002-9385-2653
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/102142
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