title: Involvement of interleukin‑23 induced by Porphyromonas endodontalis lipopolysaccharide in osteoclastogenesis.
abstract: Periapical lesions are characterized by the destruction of periapical bone, and occur as a result of local inflammatory responses to root canal infection by microorganisms including Porphyromonas endodontalis (P. endodontalis). P. endodontalis and its primary virulence factor, lipopolysaccharide (LPS), are associated with the development of periapical lesions and alveolar bone loss. Interleukin‑23 (IL‑23) is critical in the initiation and progression of periodontal disease via effects on peripheral bone metabolism. The present study investigated the expression of IL‑23 in tissue where a periapical lesion was present, and the effect of P. endodontalis LPS on the expression of IL‑23 in periodontal ligament (PDL) cells. Reverse transcription‑ quantitative polymerase chain reaction and immunohistochemistry revealed increased levels of IL‑23 expression in tissue with periapical lesions compared with healthy PDL tissue. Treatment with P. endodontalis LPS increased the expression of IL‑23 in the SH‑9 human PDL cell line. BAY11‑7082, a nuclear factor κB inhibitor, suppressed P. endodontalis LPS‑induced IL‑23 expression in SH‑9 cells. Treatment of RAW264.7 cells with conditioned medium from P. endodontalis LPS‑treated SH‑9 cells promoted osteoclastogenesis. By contrast, RAW264.7 cells treated with conditioned medium from IL‑23‑knockdown SH‑9 cells underwent reduced levels of osteoclastogenesis. The results of the present study indicated that the expression of IL‑23 in PDL cells induced by P. endodontalis LPS treatment may be involved in the progression of periapical lesions via stimulation of the osteoclastogenesis process.
authors.affiliation: Department of Endodontics, School of Stomatology, China Medical University, Shenyang, Liaoning 110002, P.R. China.
authors.forename: Nan
authors.initials: N
authors.lastname: Ma
authors.affiliation: Department of Endodontics, School of Stomatology, China Medical University, Shenyang, Liaoning 110002, P.R. China.
authors.forename: Di
authors.initials: D
authors.lastname: Yang
authors.affiliation: Department of Histology and Oral Histology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima 770‑8504, Japan.
authors.forename: Hirohiko
authors.initials: H
authors.lastname: Okamura
authors.affiliation: Department of Histology and Oral Histology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima 770‑8504, Japan.
authors.forename: Jumpei
authors.initials: J
authors.lastname: Teramachi
authors.affiliation: Department of Pediatric Dentistry, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima 770‑8504, Japan.
authors.forename: Tomokazu
authors.initials: T
authors.lastname: Hasegawa
authors.affiliation: Department of Endodontics, School of Stomatology, China Medical University, Shenyang, Liaoning 110002, P.R. China.
authors.forename: Lihong
authors.initials: L
authors.lastname: Qiu
authors.affiliation: Department of Histology and Oral Histology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima 770‑8504, Japan.
authors.forename: Tatsuji
authors.initials: T
authors.lastname: Haneji
mesh_terms: D000818:Animals; D002867:Chromones / Q000494:pharmacology; D006801:Humans; D007150:Immunohistochemistry; D053759:Interleukin-23 / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000633:toxicity*; D051379:Mice; D009025:Morpholines / Q000494:pharmacology; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000378:metabolism; D050778:NFATC Transcription Factors / Q000378:metabolism; D009570:Nitriles / Q000494:pharmacology; D010006:Osteoblasts / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D010012:Osteogenesis / Q000187:drug effects*; D010518:Periodontitis / Q000175:diagnosis / Q000378:metabolism / Q000473:pathology; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D000081082:Phosphoinositide-3 Kinase Inhibitors; D045202:Porphyromonas endodontalis / Q000378:metabolism*; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D053245:RANK Ligand / Q000494:pharmacology; D000067996:RAW 264.7 Cells; D034622:RNA Interference; D034741:RNA, Small Interfering / Q000378:metabolism; D013450:Sulfones / Q000494:pharmacology
chemical_list: D002867:Chromones; D053759:Interleukin-23; D008070:Lipopolysaccharides; D009025:Morpholines; D016328:NF-kappa B; D050778:NFATC Transcription Factors; D009570:Nitriles; D019869:Phosphatidylinositol 3-Kinases; D000081082:Phosphoinositide-3 Kinase Inhibitors; D016760:Proto-Oncogene Proteins c-fos; D053245:RANK Ligand; D034741:RNA, Small Interfering; D013450:Sulfones; C434003:3-(4-methylphenylsulfonyl)-2-propenenitrile; C494005:Nfatc1 protein, mouse; C085911:2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one