title: Calcium hydroxide suppresses Porphyromonas endodontalis lipopolysaccharide-induced bone destruction.
abstract: Porphyromonas endodontalis and its main virulence factor, lipopolysaccharide (LPS), are associated with the development of periapical diseases and alveolar bone loss. Calcium hydroxide is commonly used for endodontic therapy. However, the effects of calcium hydroxide on the virulence of P. endodontalis LPS and the mechanism of P. endodontalis LPS-induced bone destruction are not clear. Calcium hydroxide rescued the P. endodontalis LPS-suppressed viability of MC3T3-E1 cells and activity of nuclear factor-κB (NF-κB) in these cells, resulting in the reduced expression of interleukin-6 and tumor necrosis factor-α. In addition, calcium hydroxide inhibited P. endodontalis LPS-induced osteoclastogenesis by decreasing the activities of NF-κB, p38, and ERK1/2 and the expression of nuclear factor of activated T-cell cytoplasmic 1 in RAW264.7 cells. Calcium hydroxide also rescued the P. endodontalis LPS-induced osteoclastogenesis and bone destruction in mouse calvaria. Taken together, our present results indicate that calcium hydroxide suppressed bone destruction by attenuating the virulence of P. endodontalis LPS on bone cells.
authors.affiliation: Department of Endodontics, School of Stomatology, China Medical University, Shenyang 110002, China.
authors.forename: J
authors.initials: J
authors.lastname: Guo
authors.forename: D
authors.initials: D
authors.lastname: Yang
authors.forename: H
authors.initials: H
authors.lastname: Okamura
authors.forename: J
authors.initials: J
authors.lastname: Teramachi
authors.forename: K
authors.initials: K
authors.lastname: Ochiai
authors.forename: L
authors.initials: L
authors.lastname: Qiu
authors.forename: T
authors.initials: T
authors.lastname: Haneji
mesh_terms: D016475:3T3 Cells; D000135:Acid Phosphatase / Q000032:analysis; D000818:Animals; D015415:Biomarkers / Q000032:analysis; D001862:Bone Resorption / Q000517:prevention & control; D002126:Calcium Hydroxide / Q000494:pharmacology*; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D048049:Extracellular Signal-Regulated MAP Kinases / Q000187:drug effects; D015850:Interleukin-6 / Q000032:analysis; D007527:Isoenzymes / Q000032:analysis; D008070:Lipopolysaccharides / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D051379:Mice; D048052:Mitogen-Activated Protein Kinase 3 / Q000187:drug effects; D016328:NF-kappa B / Q000187:drug effects; D050778:NFATC Transcription Factors / Q000187:drug effects; D010006:Osteoblasts / Q000187:drug effects*; D010010:Osteoclasts / Q000187:drug effects*; D045202:Porphyromonas endodontalis / Q000187:drug effects* / Q000472:pathogenicity; D012388:Root Canal Irrigants / Q000494:pharmacology*; D012886:Skull / Q000187:drug effects; D000071681:Tartrate-Resistant Acid Phosphatase; D014409:Tumor Necrosis Factor-alpha / Q000187:drug effects; D055114:X-Ray Microtomography; D048051:p38 Mitogen-Activated Protein Kinases / Q000187:drug effects
chemical_list: D015415:Biomarkers; D015850:Interleukin-6; D007527:Isoenzymes; D008070:Lipopolysaccharides; D016328:NF-kappa B; D050778:NFATC Transcription Factors; C494005:Nfatc1 protein, mouse; D012388:Root Canal Irrigants; D014409:Tumor Necrosis Factor-alpha; D048049:Extracellular Signal-Regulated MAP Kinases; D048052:Mitogen-Activated Protein Kinase 3; D048051:p38 Mitogen-Activated Protein Kinases; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase; D002126:Calcium Hydroxide
keywords: bone resorption; interleukin-6; nuclear factor of activated T-cell cytoplasmic 1; osteoblasts; osteoclasts; tumor necrosis factor-α