Td92, an outer membrane protein of Treponema denticola, induces osteoclastogenesis via prostaglandin-E2-mediated RANKL/osteoprotegerin regulation

M. Kim, H. K. Jun, B. K. Choi, JeongHeon Cha, Y. J. Yoo

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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-E2 (PGE2) in osteoblasts were estimated by ELISA.Results: Td92 induced osteoclast formation in the co-cultures. In the osteoblasts, RANKL and PGE2 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 PGE2 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 PGE2-dependent mechanism.

Original languageEnglish
Pages (from-to)772-779
Number of pages8
JournalJournal of Periodontal Research
Volume45
Issue number6
DOIs
Publication statusPublished - 2010 Dec 1

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Treponema denticola
Osteoprotegerin
Osteoclasts
Dinoprostone
Osteogenesis
Membrane Proteins
Osteoblasts
Alveolar Bone Loss
Bone Resorption
Indomethacin
Prostaglandin Antagonists
Periodontium
Periodontitis
Coculture Techniques
Skull
Bone Marrow Cells
Chronic Disease
Enzyme-Linked Immunosorbent Assay
Staining and Labeling
Bone and Bones

All Science Journal Classification (ASJC) codes

  • Periodontics

Cite this

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title = "Td92, an outer membrane protein of Treponema denticola, induces osteoclastogenesis via prostaglandin-E2-mediated RANKL/osteoprotegerin regulation",
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-E2 (PGE2) in osteoblasts were estimated by ELISA.Results: Td92 induced osteoclast formation in the co-cultures. In the osteoblasts, RANKL and PGE2 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 PGE2 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 PGE2-dependent mechanism.",
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Td92, an outer membrane protein of Treponema denticola, induces osteoclastogenesis via prostaglandin-E2-mediated RANKL/osteoprotegerin regulation. / Kim, M.; Jun, H. K.; Choi, B. K.; Cha, JeongHeon; Yoo, Y. J.

In: Journal of Periodontal Research, Vol. 45, No. 6, 01.12.2010, p. 772-779.

Research output: Contribution to journalArticle

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T1 - Td92, an outer membrane protein of Treponema denticola, induces osteoclastogenesis via prostaglandin-E2-mediated RANKL/osteoprotegerin regulation

AU - Kim, M.

AU - Jun, H. K.

AU - Choi, B. K.

AU - Cha, JeongHeon

AU - Yoo, Y. J.

PY - 2010/12/1

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N2 - 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-E2 (PGE2) in osteoblasts were estimated by ELISA.Results: Td92 induced osteoclast formation in the co-cultures. In the osteoblasts, RANKL and PGE2 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 PGE2 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 PGE2-dependent mechanism.

AB - 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-E2 (PGE2) in osteoblasts were estimated by ELISA.Results: Td92 induced osteoclast formation in the co-cultures. In the osteoblasts, RANKL and PGE2 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 PGE2 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 PGE2-dependent mechanism.

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