Show simple item record

dc.contributor.authorPetcu, Eugen Bogdan
dc.contributor.authorKocher, Thomas
dc.contributor.authorKuhr, Alexander
dc.contributor.authorBuga, Ana-Maria
dc.contributor.authorKloeting, Ingrid
dc.contributor.authorHerndon, James G
dc.contributor.authorKessler, Christof
dc.contributor.authorPopa-Wagner, Aurel
dc.contributor.editorBenthan Publisher
dc.date.accessioned2017-05-03T15:15:32Z
dc.date.available2017-05-03T15:15:32Z
dc.date.issued2008
dc.date.modified2009-12-03T06:08:22Z
dc.identifier.issn1567-2026
dc.identifier.urihttp://hdl.handle.net/10072/23295
dc.description.abstractStroke is accompanied by a strong inflammatory reaction in the brain. Periodontal disease is a chronic local infection which causes a systemic low grade inflammation. We hypothesized that a mild systemic inflammatory reaction as caused by periodontal disease prior to stroke onset, may exert a neuroprotective effect in a rat model of focal ischemia. To test this hypothesis, marginal periodontitis was induced by ligatures on the second maxillary molars in BB/LL Wistar rats for 3 weeks. Two weeks after periodontitis initiation, focal cerebral ischemia was produced by reversible occlusion of the right middle cerebral artery. After a survival time of 7 days after ischemia, rats were killed and bone loss was determined on the buccal and palatinal surfaces of the defleshed jaw. In addition, markers of systemic inflammation were determined in a different group of laboratory animals at 14 days after the onset of periodontitis. The infarct size and markers of the inflammatory reaction in the brain were determined by immunohistochemistry. We found: (i) rats with ligatures exhibited significantly more periodontal bone loss than the control rats; (ii) the development of periodontitis was associated with an elevated gene expression for several markers of systemic inflammation (interleukin-10, transforming growth factor beta 1, tumor necrosis factor alpha, interleukin-1beta and interferon gamma; (iii) rats with periodontitis and a mild systemic inflammation had a significantly reduced infarct volume and a significant reduction in the number of brain macrophages in the infarcted area. In conclusion we found that mild systemic inflammation elicited prior to stroke onset may have a neuroprotective effect in rats by reducing the infarct volume and tissue destruction by brain macrophages.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.languageEnglish
dc.language.isoeng
dc.publisherBentham Publisher
dc.publisher.placeUSA
dc.publisher.urihttp://www.bentham.org/cnr/contabs/cnr5-4.htm
dc.relation.ispartofstudentpublicationN
dc.relation.ispartofpagefrom214
dc.relation.ispartofpageto223
dc.relation.ispartofissue4
dc.relation.ispartofjournalCurrent Neurovascular Research
dc.relation.ispartofvolume5
dc.rights.retentionY
dc.subject.fieldofresearchCardiovascular medicine and haematology
dc.subject.fieldofresearchNeurosciences
dc.subject.fieldofresearchNeurosciences not elsewhere classified
dc.subject.fieldofresearchcode3201
dc.subject.fieldofresearchcode3209
dc.subject.fieldofresearchcode320999
dc.titleMild systemic inflammation has a neuroprotective effect after stroke in rats
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.facultyGriffith Health, School of Medicine
gro.date.issued2008
gro.hasfulltextNo Full Text
gro.griffith.authorPetcu, Eugen B.
gro.griffith.authorPopa-Wagner, Aurel


Files in this item

FilesSizeFormatView

There are no files associated with this item.

This item appears in the following Collection(s)

  • Journal articles
    Contains articles published by Griffith authors in scholarly journals.

Show simple item record