Prostaglandin E2 is a main mediator in receptor activator of nuclear factor-κB ligand-dependent osteoclastogenesis induced by Porphyromonas gingivalis, treponema denticola, and treponema socranskii

Bong Kyu Choi, Sun Young Moon, Jeong Heon Cha, Kih Wan Kim, Yun Jung Yoo

Research output: Contribution to journalArticle

45 Citations (Scopus)

Abstract

Background: Periodontitis is an inflammatory disease that often leads to destruction of alveolar bone; a number of bacteria in subgingival plaque are associated with bone destruction in periodontitis. To understand the mechanism of how periodontopathogens induce osteoclastogenesis, we determined which mediators are involved in the osteoclastogenesis. Methods: We investigated effects of sonicates from three periodontopathic bacteria, Porphyromonas gingivalis, Treponema denticola, and Treponema socranskii, on osteoclast formation in a co-culture system of mouse calvaria-derived osteoblasts and bone marrow cells. The osteoclast formation was determined by tartrate resistant acid phosphatase (TRAP) staining. The expression of the receptor activator of nuclear factor-κ B ligand (RANKL), prostaglandin E2 (PGE2) and osteoprotegerin (OPG) in mouse calvaria-derived osteoblasts was determined by immunoassay. Results: Each bacterial sonicate induced the osteoclast formation in the co-culture system. These bacterial sonicates increased the expression of RANKL and PGE2, and decreased the expression of OPG in osteoblasts. The addition of OPG, an inhibitor of RANKL, in the co-culture completely suppressed the osteoclastogenesis that was stimulated by each bacterial sonicate. Indomethacin, which is an inhibitor of PGE2 synthesis, reduced more than 88% of the osteoclast formation induced by each bacterial sonicate. Indomethacin inhibited more than 80% of RANKL expression in osteoblasts induced by T. denticola and T. socranskii, and 59% by P. gingivalis. Indomethacin completely recovered the depression of OPG expression in osteoblasts by T. denticola and T. socranskii to the level of the untreated osteoblasts. Indomethacin recovered the reduction of OPG expression by P. gingivalis to 67%. Conclusion: These findings suggest that the osteoclastogenesis by P. gingivalis, T. denticola, and T. socranskii is mediated by a RANKL-dependent pathway and that PGE2 is a main factor in the pathway by the enhancing of RANKL expression and the depression of osteoprotegerin, a RANKL inhibitor.

Original languageEnglish
Pages (from-to)813-820
Number of pages8
JournalJournal of Periodontology
Volume76
Issue number5
DOIs
Publication statusPublished - 2005 May 1

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Treponema denticola
Treponema
Osteoprotegerin
Porphyromonas gingivalis
Cytoplasmic and Nuclear Receptors
Osteoblasts
Dinoprostone
Osteogenesis
Osteoclasts
Ligands
Indomethacin
Coculture Techniques
Periodontitis
Skull
Bacteria
Bone and Bones
Immunoassay
Bone Marrow Cells
Staining and Labeling

All Science Journal Classification (ASJC) codes

  • Periodontics

Cite this

@article{be3ced7599f04cbbbf9012ee3bfb6d6a,
title = "Prostaglandin E2 is a main mediator in receptor activator of nuclear factor-κB ligand-dependent osteoclastogenesis induced by Porphyromonas gingivalis, treponema denticola, and treponema socranskii",
abstract = "Background: Periodontitis is an inflammatory disease that often leads to destruction of alveolar bone; a number of bacteria in subgingival plaque are associated with bone destruction in periodontitis. To understand the mechanism of how periodontopathogens induce osteoclastogenesis, we determined which mediators are involved in the osteoclastogenesis. Methods: We investigated effects of sonicates from three periodontopathic bacteria, Porphyromonas gingivalis, Treponema denticola, and Treponema socranskii, on osteoclast formation in a co-culture system of mouse calvaria-derived osteoblasts and bone marrow cells. The osteoclast formation was determined by tartrate resistant acid phosphatase (TRAP) staining. The expression of the receptor activator of nuclear factor-κ B ligand (RANKL), prostaglandin E2 (PGE2) and osteoprotegerin (OPG) in mouse calvaria-derived osteoblasts was determined by immunoassay. Results: Each bacterial sonicate induced the osteoclast formation in the co-culture system. These bacterial sonicates increased the expression of RANKL and PGE2, and decreased the expression of OPG in osteoblasts. The addition of OPG, an inhibitor of RANKL, in the co-culture completely suppressed the osteoclastogenesis that was stimulated by each bacterial sonicate. Indomethacin, which is an inhibitor of PGE2 synthesis, reduced more than 88{\%} of the osteoclast formation induced by each bacterial sonicate. Indomethacin inhibited more than 80{\%} of RANKL expression in osteoblasts induced by T. denticola and T. socranskii, and 59{\%} by P. gingivalis. Indomethacin completely recovered the depression of OPG expression in osteoblasts by T. denticola and T. socranskii to the level of the untreated osteoblasts. Indomethacin recovered the reduction of OPG expression by P. gingivalis to 67{\%}. Conclusion: These findings suggest that the osteoclastogenesis by P. gingivalis, T. denticola, and T. socranskii is mediated by a RANKL-dependent pathway and that PGE2 is a main factor in the pathway by the enhancing of RANKL expression and the depression of osteoprotegerin, a RANKL inhibitor.",
author = "Choi, {Bong Kyu} and Moon, {Sun Young} and Cha, {Jeong Heon} and Kim, {Kih Wan} and Yoo, {Yun Jung}",
year = "2005",
month = "5",
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language = "English",
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pages = "813--820",
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Prostaglandin E2 is a main mediator in receptor activator of nuclear factor-κB ligand-dependent osteoclastogenesis induced by Porphyromonas gingivalis, treponema denticola, and treponema socranskii. / Choi, Bong Kyu; Moon, Sun Young; Cha, Jeong Heon; Kim, Kih Wan; Yoo, Yun Jung.

In: Journal of Periodontology, Vol. 76, No. 5, 01.05.2005, p. 813-820.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Prostaglandin E2 is a main mediator in receptor activator of nuclear factor-κB ligand-dependent osteoclastogenesis induced by Porphyromonas gingivalis, treponema denticola, and treponema socranskii

AU - Choi, Bong Kyu

AU - Moon, Sun Young

AU - Cha, Jeong Heon

AU - Kim, Kih Wan

AU - Yoo, Yun Jung

PY - 2005/5/1

Y1 - 2005/5/1

N2 - Background: Periodontitis is an inflammatory disease that often leads to destruction of alveolar bone; a number of bacteria in subgingival plaque are associated with bone destruction in periodontitis. To understand the mechanism of how periodontopathogens induce osteoclastogenesis, we determined which mediators are involved in the osteoclastogenesis. Methods: We investigated effects of sonicates from three periodontopathic bacteria, Porphyromonas gingivalis, Treponema denticola, and Treponema socranskii, on osteoclast formation in a co-culture system of mouse calvaria-derived osteoblasts and bone marrow cells. The osteoclast formation was determined by tartrate resistant acid phosphatase (TRAP) staining. The expression of the receptor activator of nuclear factor-κ B ligand (RANKL), prostaglandin E2 (PGE2) and osteoprotegerin (OPG) in mouse calvaria-derived osteoblasts was determined by immunoassay. Results: Each bacterial sonicate induced the osteoclast formation in the co-culture system. These bacterial sonicates increased the expression of RANKL and PGE2, and decreased the expression of OPG in osteoblasts. The addition of OPG, an inhibitor of RANKL, in the co-culture completely suppressed the osteoclastogenesis that was stimulated by each bacterial sonicate. Indomethacin, which is an inhibitor of PGE2 synthesis, reduced more than 88% of the osteoclast formation induced by each bacterial sonicate. Indomethacin inhibited more than 80% of RANKL expression in osteoblasts induced by T. denticola and T. socranskii, and 59% by P. gingivalis. Indomethacin completely recovered the depression of OPG expression in osteoblasts by T. denticola and T. socranskii to the level of the untreated osteoblasts. Indomethacin recovered the reduction of OPG expression by P. gingivalis to 67%. Conclusion: These findings suggest that the osteoclastogenesis by P. gingivalis, T. denticola, and T. socranskii is mediated by a RANKL-dependent pathway and that PGE2 is a main factor in the pathway by the enhancing of RANKL expression and the depression of osteoprotegerin, a RANKL inhibitor.

AB - Background: Periodontitis is an inflammatory disease that often leads to destruction of alveolar bone; a number of bacteria in subgingival plaque are associated with bone destruction in periodontitis. To understand the mechanism of how periodontopathogens induce osteoclastogenesis, we determined which mediators are involved in the osteoclastogenesis. Methods: We investigated effects of sonicates from three periodontopathic bacteria, Porphyromonas gingivalis, Treponema denticola, and Treponema socranskii, on osteoclast formation in a co-culture system of mouse calvaria-derived osteoblasts and bone marrow cells. The osteoclast formation was determined by tartrate resistant acid phosphatase (TRAP) staining. The expression of the receptor activator of nuclear factor-κ B ligand (RANKL), prostaglandin E2 (PGE2) and osteoprotegerin (OPG) in mouse calvaria-derived osteoblasts was determined by immunoassay. Results: Each bacterial sonicate induced the osteoclast formation in the co-culture system. These bacterial sonicates increased the expression of RANKL and PGE2, and decreased the expression of OPG in osteoblasts. The addition of OPG, an inhibitor of RANKL, in the co-culture completely suppressed the osteoclastogenesis that was stimulated by each bacterial sonicate. Indomethacin, which is an inhibitor of PGE2 synthesis, reduced more than 88% of the osteoclast formation induced by each bacterial sonicate. Indomethacin inhibited more than 80% of RANKL expression in osteoblasts induced by T. denticola and T. socranskii, and 59% by P. gingivalis. Indomethacin completely recovered the depression of OPG expression in osteoblasts by T. denticola and T. socranskii to the level of the untreated osteoblasts. Indomethacin recovered the reduction of OPG expression by P. gingivalis to 67%. Conclusion: These findings suggest that the osteoclastogenesis by P. gingivalis, T. denticola, and T. socranskii is mediated by a RANKL-dependent pathway and that PGE2 is a main factor in the pathway by the enhancing of RANKL expression and the depression of osteoprotegerin, a RANKL inhibitor.

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U2 - 10.1902/jop.2005.76.5.813

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JO - Journal of Periodontology

JF - Journal of Periodontology

SN - 0022-3492

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