Publications

Detailed Information

Bacterial invasion and persistence: critical events in the pathogenesis of periodontitis?

DC Field Value Language
dc.contributor.authorJi, S.-
dc.contributor.authorChoi, Y. S.-
dc.contributor.authorChoi, Y.-
dc.date.accessioned2016-01-26T07:10:25Z-
dc.date.available2016-01-26T07:10:25Z-
dc.date.created2018-11-05-
dc.date.created2018-11-05-
dc.date.issued2015-10-
dc.identifier.citationJournal of Periodontal Research, Vol.50 No.5, pp.570-585-
dc.identifier.issn0022-3484-
dc.identifier.urihttps://hdl.handle.net/10371/95419-
dc.descriptionThis is an open access article under the terms
of the Creative Commons Attribution-
NonCommercial-NoDerivs License, which
permits use and distribution in any medium,
provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
-
dc.description.abstractPeriodontitis is chronic inflammation of the periodontium caused by the host's inflammatory response to plaque biofilm, which destroys tooth-supporting soft and hard tissues. Periodontitis is a complex disease that involves interactions among three main features - microbial challenge, the host immune response, and environmental and genetic risk factors - in its pathogenesis. Although periodontitis has been regarded as the result of hyperimmune or hyperinflammatory responses to plaque bacteria, recent studies indicate that periodontal pathogens are rather poor activators and/or suppressors of the host immune response. This raises the question of how periodontal pathogens cause inflammation. To resolve this issue, in the present review we propose that bacterial invasion into gingival tissue is a key event in the initiation of periodontitis and that the persistence of these bacteria within host tissue results in chronic inflammation. In support of this hypothesis, we present the ways in which microbial, environmental and genetic risk factors contribute to bacterial invasion. It is hoped that the current model will instigate active discussion and new research to complete the puzzle of this complex disease process.-
dc.language영어-
dc.language.isoen-
dc.publisherBlackwell Publishing Inc.-
dc.titleBacterial invasion and persistence: critical events in the pathogenesis of periodontitis?-
dc.typeArticle-
dc.contributor.AlternativeAuthor최영님-
dc.identifier.doi10.1111/jre.12248-
dc.citation.journaltitleJournal of Periodontal Research-
dc.identifier.wosid000360859600002-
dc.identifier.scopusid2-s2.0-84940892332-
dc.description.srndOAIID:oai:osos.snu.ac.kr:snu2014-01/102/0000025661/5-
dc.description.srndADJUST_YN:N-
dc.description.srndEMP_ID:A075701-
dc.description.srndDEPT_CD:852-
dc.description.srndCITE_RATE:2.466-
dc.description.srndDEPT_NM:치의과학과-
dc.description.srndSCOPUS_YN:Y-
dc.description.srndCONFIRM:Y-
dc.citation.endpage585-
dc.citation.number5-
dc.citation.startpage570-
dc.citation.volume50-
dc.description.isOpenAccessN-
dc.contributor.affiliatedAuthorChoi, Y.-
dc.identifier.srnd2014-01/102/0000025661/5-
dc.type.docTypeReview-
dc.description.journalClass1-
dc.subject.keywordPlusGINGIVAL EPITHELIAL-CELLS-
dc.subject.keywordPlusREGULATORY T-CELLS-
dc.subject.keywordPlusEARLY-ONSET PERIODONTITIS-
dc.subject.keywordPlusCHEDIAK-HIGASHI-SYNDROME-
dc.subject.keywordPlusTIGHT-JUNCTION PROTEINS-
dc.subject.keywordPlusPAPILLON-LEFEVRE-SYNDROME-
dc.subject.keywordPlusPORPHYROMONAS-GINGIVALIS-
dc.subject.keywordPlusFUSOBACTERIUM-NUCLEATUM-
dc.subject.keywordPlusTREPONEMA-DENTICOLA-
dc.subject.keywordPlusIN-VITRO-
dc.subject.keywordAuthormicrobiology-
dc.subject.keywordAuthorperiodontal immunology-
dc.subject.keywordAuthorperiodontal pathogens-
dc.subject.keywordAuthorperiodontal risk factor-
Appears in Collections:
Files in This Item:

Altmetrics

Item View & Download Count

  • mendeley

Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.

Share