Spontaneous Periodontitis Development in Diabetic Rats Involves an Unrestricted Expression of Inflammatory Cytokines and Tissue Destructive Factors in the Absence of Major Changes in Commensal Oral Microbiota

dc.contributor.authorClaudino, Marcela
dc.contributor.authorGennaro, Gabriela
dc.contributor.authorCestari, Tania Mary
dc.contributor.authorSpadella, César Tadeu [UNESP]
dc.contributor.authorGarlet, Gustavo Pompermaier
dc.contributor.authorAssis, Gerson Francisco
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T13:32:43Z
dc.date.available2014-05-20T13:32:43Z
dc.date.issued2012-01-01
dc.description.abstractDiabetes mellitus is a heterogeneous group of disorders, in which hyperglycemia is a main feature. The objective was to evaluate the involvement of RAGE, inflammatory cytokines, and metalloproteinases in spontaneous periodontitis triggered by diabetes induction. Immunohistochemical procedures for MMP-2, MMP-9, TNF-alpha, IL-1 beta, IL-6, RANKL, and RAGE were performed in rats after 1, 3, 6, 9, and 12 months of diabetes induction. Total DNA was extracted from paraffin-embedded tissues and evaluated by Real-TimePCR for 16S total bacterial load and specific periodontopathogens. Our data did not demonstrate differences in microbiological patterns between groups. In diabetic groups, an increase in RAGE-positive cells was detected at 6, 9, and 12 months, while TNF-alpha-stained cells were more prevalent at 6 and 12 months. In experimental groups, IL-beta-positive cells were increased after 12 months, IL-6 stained cells were increased at 9 and 12 months, and RANKL-positive cells at 9 months. Diabetes resulted in widespread expression of RAGE, followed by expression of proinflammatory mediators, without major alterations in oral microbial profile. The pervasive expression of cytokines suggests that spontaneous periodontitis development may be independent of microbial stimulation and may be triggered by diabetes-driven imbalance of homeostasis.en
dc.description.affiliationSão Paulo Univ FOB USP, Sch Dent Bauru, Dept Biol Sci, BR-17012901 Bauru, SP, Brazil
dc.description.affiliationSão Paulo State Univ UNESP, Sch Med Botucatu, Dept Surg & Orthoped, BR-18618970 Botucatu, SP, Brazil
dc.description.affiliationUnespSão Paulo State Univ UNESP, Sch Med Botucatu, Dept Surg & Orthoped, BR-18618970 Botucatu, SP, Brazil
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipIdFAPESP: 07/07681-2
dc.format.extent10
dc.identifierhttp://dx.doi.org/10.1155/2012/356841
dc.identifier.citationExperimental Diabetes Research. New York: Hindawi Publishing Corporation, p. 10, 2012.
dc.identifier.doi10.1155/2012/356841
dc.identifier.fileWOS000304960800001.pdf
dc.identifier.issn1687-5214
dc.identifier.lattes6223012281302736
dc.identifier.urihttp://hdl.handle.net/11449/11178
dc.identifier.wosWOS:000304960800001
dc.language.isoeng
dc.publisherHindawi Publishing Corporation
dc.relation.ispartofExperimental Diabetes Research
dc.rights.accessRightsAcesso aberto
dc.sourceWeb of Science
dc.titleSpontaneous Periodontitis Development in Diabetic Rats Involves an Unrestricted Expression of Inflammatory Cytokines and Tissue Destructive Factors in the Absence of Major Changes in Commensal Oral Microbiotaen
dc.typeArtigo
dcterms.licensehttp://www.hindawi.com/journals/apm/apc/
dcterms.rightsHolderHindawi Publishing Corporation
unesp.author.lattes6223012281302736
unesp.author.orcid0000-0002-5071-8382[5]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Medicina, Botucatupt

Arquivos

Pacote Original
Agora exibindo 1 - 1 de 1
Carregando...
Imagem de Miniatura
Nome:
WOS000304960800001.pdf
Tamanho:
3.84 MB
Formato:
Adobe Portable Document Format
Licença do Pacote
Agora exibindo 1 - 2 de 2
Nenhuma Miniatura disponível
Nome:
license.txt
Tamanho:
1.71 KB
Formato:
Item-specific license agreed upon to submission
Descrição:
Nenhuma Miniatura disponível
Nome:
license.txt
Tamanho:
1.71 KB
Formato:
Item-specific license agreed upon to submission
Descrição: