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Protease-activated receptor-2 (PAR(2)) in human periodontitis

M Holzhausen1, J R Cortelli, V Araújo da Silva

  • 1Division of Periodontics, Department of Stomatology, School of Dentistry, University of São Paulo, São Paulo, SP, Avenida Prof. Lineu Prestes, 2227, Cidade Universitária, São Paulo-SP, CEP: 05508-000, Brazil. marinella@usp.br

Journal of Dental Research
|June 10, 2010
PubMed

Insights

Protease-activated receptor-2 (PAR(2)) mRNA expression and its activators are elevated in chronic periodontitis. This suggests PAR(2) plays a role in periodontal inflammation, with levels decreasing after treatment.

Area of Science:

  • Oral biology
  • Immunology
  • Periodontology

Background:

  • Protease-activated receptor-2 (PAR(2)) role in human periodontal disease remains unclear.
  • Chronic periodontitis involves complex inflammatory processes and microbial challenges.

Purpose of the Study:

  • Investigate PAR(2) mRNA expression in chronic periodontitis.
  • Determine the relationship between PAR(2) expression and its potential activators.
  • Assess the impact of periodontal treatment on PAR(2) expression.

Main Methods:

  • Collected microbiological and gingival crevicular fluid samples from chronic periodontitis patients and controls.
  • Evaluated the presence of neutrophil serine proteinase 3 (P3) and Porphyromonas gingivalis.
  • Quantified PAR(2) mRNA expression and levels of inflammatory cytokines (IL-1α, IL-6, IL-8, TNF-α).

Main Results:

  • Significantly higher PAR(2) mRNA expression in chronic periodontitis patients compared to controls (p < 0.001).
  • Elevated levels of IL-1α, IL-6, IL-8, TNF-α, proteolytic activity, P. gingivalis, and P3 mRNA in periodontitis patients (p < 0.05).
  • PAR(2) mRNA expression decreased significantly after periodontal treatment (p = 0.0006).

Conclusions:

  • PAR(2) mRNA expression and its activators are elevated in human chronic periodontitis.
  • Findings suggest a potential role for PAR(2) in mediating periodontal inflammation.
  • Periodontal treatment may reduce PAR(2) expression, indicating its involvement in the disease process.

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