Interleukin-33 could play an important role in the pathogenesis of periodontitis

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dc.contributor.authorKoseoglu, S.
dc.contributor.authorHatipoglu, M.
dc.contributor.authorSaglam, M.
dc.contributor.authorEnhos, S.
dc.contributor.authorEsen, H. H.
dc.date.accessioned2024-02-23T14:24:31Z
dc.date.available2024-02-23T14:24:31Z
dc.date.issued2015
dc.departmentNEÜen_US
dc.description.abstractBackground and ObjectiveInterleukin-33 (IL-33) controls T-helper type 2 (Th2) cytokines and the development of mast cells. This study aimed to investigate the expression of IL-33 and its association with RANKL and osteoprotegerin (OPG) in periodontal health and experimental periodontitis. Material and MethodsEighteen Wistar rats were assigned to two study groups of nine animals each: ligature only (LO) and nonligated (NL). Silk sutures were placed subgingivally, surrounding the right lower first molars. The animals were killed on day 11 after ligature placement, and the alveolar bone loss at the first molars was determined histometrically. Periodontal tissues were examined histopathologically to evaluate the differences between the groups. The expression of IL-33, RANKL and OPG was detected immunohistochemically. ResultsThe LO group showed significantly greater alveolar bone loss compared with the NL group (p<0.05). The numbers of osteoclasts, osteoblasts and inflammatory cells were significantly higher in the LO group compared with the NL group (p<0.05). Osteoblastic activity was significantly lower in the LO group than in the NL group (p<0.05). There was significantly higher expression of IL-33 and RANKL and a greater number of OPG-positive cells in the LO group (p<0.05). IL-33 expression showed a positive correlation with RANKL expression and with the number of mast cells (p<0.05). ConclusionThe experimental periodontitis group exhibited increased expression of IL-33 and RANKL compared with the healthy group. Additionally, there was a positive correlation between these expressions. According to these results, IL-33 could be associated with the pathogenesis of periodontal disease.en_US
dc.identifier.doi10.1111/jre.12235
dc.identifier.endpage534en_US
dc.identifier.issn0022-3484
dc.identifier.issn1600-0765
dc.identifier.issue4en_US
dc.identifier.pmid25266494en_US
dc.identifier.scopus2-s2.0-84935712851en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage525en_US
dc.identifier.urihttps://doi.org/10.1111/jre.12235
dc.identifier.urihttps://hdl.handle.net/20.500.12452/13989
dc.identifier.volume50en_US
dc.identifier.wosWOS:000357696900013en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofJournal Of Periodontal Researchen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAlveolar Bone Lossen_US
dc.subjectInterleukin-33en_US
dc.subjectOsteoprotegerinen_US
dc.subjectPeriodontal Diseaseen_US
dc.subjectRankl Proteinen_US
dc.subjectRaten_US
dc.titleInterleukin-33 could play an important role in the pathogenesis of periodontitisen_US
dc.typeArticleen_US

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