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dc.contributor.authorVAN DYKE, Thomas E.
dc.contributor.authorCekici, ALİ
dc.contributor.authorKANTARCI, Alpdogan
dc.contributor.authorHASTURK, Hatice
dc.date.accessioned2021-03-04T09:00:40Z
dc.date.available2021-03-04T09:00:40Z
dc.date.issued2014
dc.identifier.citationCekici A., KANTARCI A., HASTURK H., VAN DYKE T. E. , "Inflammatory and immune pathways in the pathogenesis of periodontal disease", PERIODONTOLOGY 2000, cilt.64, sa.1, ss.57-80, 2014
dc.identifier.issn0906-6713
dc.identifier.otherav_663c27bd-cbb7-4e5f-9b88-ff03f3090a59
dc.identifier.othervv_1032021
dc.identifier.urihttp://hdl.handle.net/20.500.12627/71006
dc.identifier.urihttps://doi.org/10.1111/prd.12002
dc.description.abstractThe pathogenesis of periodontitis involves a complex immune/inflammatory cascade that is initiated by the bacteria of the oral biofilm that forms naturally on the teeth. The susceptibility to periodontitis appears to be determined by the host response; specifically, the magnitude of the inflammatory response and the differential activation of immune pathways. The purpose of this review was to delineate our current knowledge of the host response in periodontitis. The role of innate immunity, the failure of acute inflammation to resolve (thus becoming chronic), the cytokine pathways that regulate the activation of acquired immunity and the cells and products of the immune system are considered. New information relating to regulation of both inflammation and the immune response will be reviewed in the context of susceptibility to, and perhaps control of, periodontitis.
dc.language.isoeng
dc.subjectDiş Hekimliği
dc.subjectTıp
dc.subjectSağlık Bilimleri
dc.subjectKlinik Tıp (MED)
dc.subjectKlinik Tıp
dc.subjectDİŞ HEKİMLİĞİ, ORAL CERRAHİ VE TIP
dc.titleInflammatory and immune pathways in the pathogenesis of periodontal disease
dc.typeMakale
dc.relation.journalPERIODONTOLOGY 2000
dc.contributor.department, ,
dc.identifier.volume64
dc.identifier.issue1
dc.identifier.startpage57
dc.identifier.endpage80
dc.contributor.firstauthorID75488


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