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Article: Role of fibroblast populations in peri-implantitis

TitleRole of fibroblast populations in peri-implantitis
Authors
KeywordsPeri-implantitis
Multiprotein arrays
Host response
Fibroblast heterogeneity
Issue Date2009
Citation
International Journal of Oral and Maxillofacial Implants, 2009, v. 24, n. 2, p. 197-204 How to Cite?
AbstractPurpose: To understand the contribution of stromal cells, such as granulation tissue fibroblasts, to peri-implantitis with regard to (1) the secretion of constitutive factors promoting migration/survival of infiltrates into osseointegrated sites; and (2) the effect of exogenous infiltrate cytokines on the cells' secretion. Materials and Methods: Fibroblasts were cultured from eight peri-implantitis sites. Multiplexed enzyme-linked immunosorbent assay was used to quantify factors secreted by the cells either unstimulated or stimulated with gamma interferon (IFNγ), interleukin 4 (IL4), or tumor necrosis factor alpha (TNF7alpha;). Controls consisted of fibroblasts cultured from healthy gingival and chronic periodontitis granulation tissues. Results: Peri-implantitis fibroblasts differed significantly from periodontitis fibroblasts in their reduced secretion of the collagen inducer transforming growth factor beta-1 (TGFβl) and tissue inhibitor of metalloproteinase-1. The cells exhibited enhanced secretion of angiogenic factor vascular endothelial growth factor (VEGF) and collagenolytic matrix metalloproteinase 1 (MMP1) compared to both healthy and periodontitis fibroblasts. Fibroblasts from both periodontitis and peri- implantitis sites exhibited a pronounced proinflammatory profile compared to normal gingival fibroblasts with respect to secretion of chemokines IL6, IL8, and monocyte chemoattractant protein 1 (MCP1). Fibroblasts stimulated with TNFa showed increased levels of IL6, IL8, MCP1; neutrophil chemokine growth-related oncogene alpha stimulation with IFNγ increased MCP1; and stimulation with IL4 increased VEGF. Conclusion: The results indicate that peri-implantitis fibroblasts represent a distinct stromal population. The cells might participate in the pathogenesis of peri-implantitis by up- regulating both vascularity and matrix breakdown, thus promoting migration/maintenance of infiltrates into the site. Cytokines produced by infiltrates could enhance the inflammatory nature of the cells in a self-feeding loop. Int J Oral Maxillofac Implants.
Persistent Identifierhttp://hdl.handle.net/10722/199986
ISSN
2015 Impact Factor: 1.859
2015 SCImago Journal Rankings: 0.671
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorBordin, Sandra-
dc.contributor.authorFlemmig, Thomas Frank-
dc.contributor.authorVerardi, Simone-
dc.date.accessioned2014-07-26T23:11:00Z-
dc.date.available2014-07-26T23:11:00Z-
dc.date.issued2009-
dc.identifier.citationInternational Journal of Oral and Maxillofacial Implants, 2009, v. 24, n. 2, p. 197-204-
dc.identifier.issn0882-2786-
dc.identifier.urihttp://hdl.handle.net/10722/199986-
dc.description.abstractPurpose: To understand the contribution of stromal cells, such as granulation tissue fibroblasts, to peri-implantitis with regard to (1) the secretion of constitutive factors promoting migration/survival of infiltrates into osseointegrated sites; and (2) the effect of exogenous infiltrate cytokines on the cells' secretion. Materials and Methods: Fibroblasts were cultured from eight peri-implantitis sites. Multiplexed enzyme-linked immunosorbent assay was used to quantify factors secreted by the cells either unstimulated or stimulated with gamma interferon (IFNγ), interleukin 4 (IL4), or tumor necrosis factor alpha (TNF7alpha;). Controls consisted of fibroblasts cultured from healthy gingival and chronic periodontitis granulation tissues. Results: Peri-implantitis fibroblasts differed significantly from periodontitis fibroblasts in their reduced secretion of the collagen inducer transforming growth factor beta-1 (TGFβl) and tissue inhibitor of metalloproteinase-1. The cells exhibited enhanced secretion of angiogenic factor vascular endothelial growth factor (VEGF) and collagenolytic matrix metalloproteinase 1 (MMP1) compared to both healthy and periodontitis fibroblasts. Fibroblasts from both periodontitis and peri- implantitis sites exhibited a pronounced proinflammatory profile compared to normal gingival fibroblasts with respect to secretion of chemokines IL6, IL8, and monocyte chemoattractant protein 1 (MCP1). Fibroblasts stimulated with TNFa showed increased levels of IL6, IL8, MCP1; neutrophil chemokine growth-related oncogene alpha stimulation with IFNγ increased MCP1; and stimulation with IL4 increased VEGF. Conclusion: The results indicate that peri-implantitis fibroblasts represent a distinct stromal population. The cells might participate in the pathogenesis of peri-implantitis by up- regulating both vascularity and matrix breakdown, thus promoting migration/maintenance of infiltrates into the site. Cytokines produced by infiltrates could enhance the inflammatory nature of the cells in a self-feeding loop. Int J Oral Maxillofac Implants.-
dc.languageeng-
dc.relation.ispartofInternational Journal of Oral and Maxillofacial Implants-
dc.subjectPeri-implantitis-
dc.subjectMultiprotein arrays-
dc.subjectHost response-
dc.subjectFibroblast heterogeneity-
dc.titleRole of fibroblast populations in peri-implantitis-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid19492634-
dc.identifier.scopuseid_2-s2.0-69849107147-
dc.identifier.volume24-
dc.identifier.issue2-
dc.identifier.spage197-
dc.identifier.epage204-
dc.identifier.isiWOS:000266980100002-

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