title: Detection of platelet-activating factor in gingival tissue surrounding failed dental implants.
abstract: BACKGROUND
  Dental implant therapy has entered routine clinical practice. However, the failure rate of implants at 5 years, due to biological factors, is still around 7%. The pathogenesis of implant loss involves a complex network of cells and inflammatory mediators. This study evaluated platelet-activating factor (PAF), a potent phospholipid mediator of inflammation, in soft tissue surrounding failed dental implants versus healthy implants.
  
  
  METHODS
  PAF was estimated on extracted lipids by bioassay on washed rabbit platelets; inflammatory cell populations were assessed semiquantitatively after staining, and microvessel density was evaluated after immunohistochemical staining.
  
  
  RESULTS
  Biologically active PAF was detected in the lipid extracts of samples excised from gingival tissue of patients with failed implants, but not in samples from patients with osseointegrated implants or from healthy edentulous subjects. The amount of PAF detected in failed implants was significantly higher than in healthy implants, suggesting a local production of this mediator.
  
  
  CONCLUSIONS
  The presence of PAF was associated with histopathological findings of local inflammation and increased blood vessel density.
authors.affiliation: Department of Clinical Physiopathology, University of Turin, Italy.
authors.forename: F
authors.initials: F
authors.lastname: Bassi
authors.forename: C
authors.initials: C
authors.lastname: Marchisella
authors.forename: G
authors.initials: G
authors.lastname: Schierano
authors.forename: E
authors.initials: E
authors.lastname: Gasser
authors.forename: G
authors.initials: G
authors.lastname: Montrucchio
authors.forename: G
authors.initials: G
authors.lastname: Valente
authors.forename: G
authors.initials: G
authors.lastname: Camussi
authors.forename: G
authors.initials: G
authors.lastname: Preti
mesh_terms: D000328:Adult; D000368:Aged; D004396:Coloring Agents; D003758:Dental Implantation, Endosseous; D015921:Dental Implants / Q000009:adverse effects; D019232:Dental Restoration Failure; D005260:Female; D005500:Follow-Up Studies; D005881:Gingiva / Q000098:blood supply / Q000737:chemistry* / Q000473:pathology; D005891:Gingivitis / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D018836:Inflammation Mediators / Q000032:analysis; D008055:Lipids / Q000032:analysis; D008214:Lymphocytes / Q000473:pathology; D008264:Macrophages / Q000473:pathology; D008297:Male; D008407:Mast Cells / Q000473:pathology; D008833:Microcirculation / Q000473:pathology; D008875:Middle Aged; D009066:Mouth, Edentulous / Q000378:metabolism; D016348:Osseointegration; D010950:Plasma Cells / Q000473:pathology; D010972:Platelet Activating Factor / Q000032:analysis*; D018709:Statistics, Nonparametric
chemical_list: D004396:Coloring Agents; D015921:Dental Implants; D018836:Inflammation Mediators; D008055:Lipids; D010972:Platelet Activating Factor