title: Porphyromonas gingivalis is associated with protease-activated receptor-2 upregulation in chronic periodontitis.
abstract: BACKGROUND
  We previously reported a higher expression of protease-activated receptor-2 (PAR(2)) together with higher interleukin (IL)-1α, IL-6, IL-8, and tumor necrosis factor-α levels, total proteolytic activity, Porphyromonas gingivalis (Pg) prevalence, and neutrophil-protease 3 messenger RNA (mRNA) expression in patients with chronic periodontitis compared to healthy control patients. The aim of the present study is to expand this observation by considering the site level according to the presence of Pg.
  
  
  METHODS
  Microbiologic and gingival crevicular fluid samples were collected from patients with chronic periodontitis. Pg presence was evaluated by polymerase chain reaction and PAR(2) mRNA expression was evaluated by reverse-transcription polymerase chain reaction. Total proteolytic activity in the crevicular fluid was analyzed by using a specific substrate benzoylarginine nitroanilide, and the proinflammatory mediators IL-1α, IL-6, IL-8, and tumor necrosis factor-α were analyzed by enzyme-linked immunosorbent assay.
  
  
  RESULTS
  In Pg-positive periodontal sites, the mean probing depth and clinical attachment level, the prevalence of bleeding on probing sites, and crevicular fluid volume were higher (P <0.05) compared to Pg-negative sites. In addition, with the exception of IL-8, all other inflammatory mediators were positively (P <0.05) associated with Pg presence. Pg presence was also positively associated with a higher proteolytic activity (P = 0.0037) and higher PAR(2) mRNA expression (P = 0.0271).
  
  
  CONCLUSIONS
  We conclude that in chronic periodontitis, periodontal pockets presenting Pg show an upregulation of PAR(2) gene expression, and higher proinflammatory profile associated with advanced clinical destruction, therefore suggesting that Pg plays a pivotal role on PAR(2)-mediated periodontal inflammation in humans.
authors.affiliation: Department of Periodontology, University of Taubaté, São Paulo, Brazil.
authors.forename: José Américo G
authors.initials: JA
authors.lastname: Fagundes
authors.forename: Letícia D
authors.initials: LD
authors.lastname: Monoo
authors.forename: Vanessa Tubero
authors.initials: VT
authors.lastname: Euzébio Alves
authors.forename: Cláudio Mendes
authors.initials: CM
authors.lastname: Pannuti
authors.forename: Sheila Cavalca
authors.initials: SC
authors.lastname: Cortelli
authors.forename: José Roberto
authors.initials: JR
authors.lastname: Cortelli
authors.forename: Marinella
authors.initials: M
authors.lastname: Holzhausen
mesh_terms: D000328:Adult; D055113:Chronic Periodontitis / Q000276:immunology / Q000378:metabolism / Q000382:microbiology*; D015169:Colony Count, Microbial; D005260:Female; D005883:Gingival Crevicular Fluid / Q000276:immunology / Q000378:metabolism / Q000382:microbiology*; D054884:Host-Pathogen Interactions / Q000276:immunology*; D006801:Humans; D007378:Interleukins / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D016966:Porphyromonas gingivalis / Q000502:physiology*; D044464:Receptor, PAR-2 / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D007378:Interleukins; D044464:Receptor, PAR-2; D014409:Tumor Necrosis Factor-alpha