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Article: Systemic inflammation linking chronic periodontitis to cognitive decline

TitleSystemic inflammation linking chronic periodontitis to cognitive decline
Authors
KeywordsAlzheimer’s disease
BBB permeability
Cognitive dysfunctions
Neuroinflammation
Periodontitis
Systemic inflammation
Issue Date2019
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ybrbi
Citation
Brain, Behavior, and Immunity, 2019, v. 81, p. 63-73 How to Cite?
AbstractPersistent inflammation in the systemic immune system can impose detrimental effects on the central nervous system (CNS). Neuroinflammation might be a result of this to accelerate the progressive deterioration of neuronal functions during aging. In this regard, controlling inflammation through delaying and/or preventing chronic inflammatory diseases may be a potential strategy to prevent or modify the progression of Alzheimer’s Disease (AD). Periodontitis is a chronic inflammatory disease of the oral cavity that is common among the elderly, especially for those who have decline in cognitive functions. While epidemiological findings support the association of chronic periodontitis and cognitive decline, whether they have causal relationship remains unclear. Nonetheless, the possibility that periodontopathogens, systemic immune cells and inflammatory cytokines could reach the CNS should not be overlooked. The impacts of periodontitis on CNS homeostasis and inflammation as a pathophysiological factor concerning the association between periodontitis and AD will be discussed in this review. Future work should elucidate the pathological pathways involved in periodontitis-induced cerebral infections and inflammation, and define the role of the latter in AD progression.
Persistent Identifierhttp://hdl.handle.net/10722/276238
ISSN
2019 Impact Factor: 6.633
2015 SCImago Journal Rankings: 2.884

 

DC FieldValueLanguage
dc.contributor.authorWang, RPH-
dc.contributor.authorHo, YS-
dc.contributor.authorLeung, WK-
dc.contributor.authorGoto, T-
dc.contributor.authorChang, RCC-
dc.date.accessioned2019-09-10T02:58:48Z-
dc.date.available2019-09-10T02:58:48Z-
dc.date.issued2019-
dc.identifier.citationBrain, Behavior, and Immunity, 2019, v. 81, p. 63-73-
dc.identifier.issn0889-1591-
dc.identifier.urihttp://hdl.handle.net/10722/276238-
dc.description.abstractPersistent inflammation in the systemic immune system can impose detrimental effects on the central nervous system (CNS). Neuroinflammation might be a result of this to accelerate the progressive deterioration of neuronal functions during aging. In this regard, controlling inflammation through delaying and/or preventing chronic inflammatory diseases may be a potential strategy to prevent or modify the progression of Alzheimer’s Disease (AD). Periodontitis is a chronic inflammatory disease of the oral cavity that is common among the elderly, especially for those who have decline in cognitive functions. While epidemiological findings support the association of chronic periodontitis and cognitive decline, whether they have causal relationship remains unclear. Nonetheless, the possibility that periodontopathogens, systemic immune cells and inflammatory cytokines could reach the CNS should not be overlooked. The impacts of periodontitis on CNS homeostasis and inflammation as a pathophysiological factor concerning the association between periodontitis and AD will be discussed in this review. Future work should elucidate the pathological pathways involved in periodontitis-induced cerebral infections and inflammation, and define the role of the latter in AD progression.-
dc.languageeng-
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ybrbi-
dc.relation.ispartofBrain, Behavior, and Immunity-
dc.subjectAlzheimer’s disease-
dc.subjectBBB permeability-
dc.subjectCognitive dysfunctions-
dc.subjectNeuroinflammation-
dc.subjectPeriodontitis-
dc.subjectSystemic inflammation-
dc.titleSystemic inflammation linking chronic periodontitis to cognitive decline-
dc.typeArticle-
dc.identifier.emailHo, YS: janiceys@hku.hk-
dc.identifier.emailLeung, WK: ewkleung@hkucc.hku.hk-
dc.identifier.emailChang, RCC: rccchang@hku.hk-
dc.identifier.authorityLeung, WK=rp00019-
dc.identifier.authorityChang, RCC=rp00470-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.bbi.2019.07.002-
dc.identifier.pmid31279681-
dc.identifier.scopuseid_2-s2.0-85069652616-
dc.identifier.hkuros304159-
dc.identifier.volume81-
dc.identifier.spage63-
dc.identifier.epage73-
dc.publisher.placeUnited States-

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