File Download
There are no files associated with this item.
Links for fulltext
(May Require Subscription)
- Scopus: eid_2-s2.0-69849107147
- PMID: 19492634
- WOS: WOS:000266980100002
- Find via
Supplementary
- Citations:
- Appears in Collections:
Article: Role of fibroblast populations in peri-implantitis
Title | Role of fibroblast populations in peri-implantitis |
---|---|
Authors | |
Keywords | Peri-implantitis Multiprotein arrays Host response Fibroblast heterogeneity |
Issue Date | 2009 |
Citation | International Journal of Oral and Maxillofacial Implants, 2009, v. 24, n. 2, p. 197-204 How to Cite? |
Abstract | Purpose: 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 Identifier | http://hdl.handle.net/10722/199986 |
ISSN | 2023 Impact Factor: 1.7 2023 SCImago Journal Rankings: 0.702 |
ISI Accession Number ID |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Bordin, Sandra | - |
dc.contributor.author | Flemmig, Thomas Frank | - |
dc.contributor.author | Verardi, Simone | - |
dc.date.accessioned | 2014-07-26T23:11:00Z | - |
dc.date.available | 2014-07-26T23:11:00Z | - |
dc.date.issued | 2009 | - |
dc.identifier.citation | International Journal of Oral and Maxillofacial Implants, 2009, v. 24, n. 2, p. 197-204 | - |
dc.identifier.issn | 0882-2786 | - |
dc.identifier.uri | http://hdl.handle.net/10722/199986 | - |
dc.description.abstract | Purpose: 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.language | eng | - |
dc.relation.ispartof | International Journal of Oral and Maxillofacial Implants | - |
dc.subject | Peri-implantitis | - |
dc.subject | Multiprotein arrays | - |
dc.subject | Host response | - |
dc.subject | Fibroblast heterogeneity | - |
dc.title | Role of fibroblast populations in peri-implantitis | - |
dc.type | Article | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.pmid | 19492634 | - |
dc.identifier.scopus | eid_2-s2.0-69849107147 | - |
dc.identifier.volume | 24 | - |
dc.identifier.issue | 2 | - |
dc.identifier.spage | 197 | - |
dc.identifier.epage | 204 | - |
dc.identifier.isi | WOS:000266980100002 | - |
dc.identifier.issnl | 0882-2786 | - |