The 3020insC mutation of the NOD2/CARD15 gene in patients with periodontal disease.

Abstract

The 3020insC mutation of the NOD2/CARD15 gene leads to impaired activation of nuclear factor-kappa B (NF-kappaB) in vitro. As the destruction of periodontal tissue is mediated via activation of NF-kappaB, with subsequent transcription of proinflammatory cytokines, the c-insertion mutation of the NOD2/CARD15 gene might contribute to the proposed genetic background of periodontitis. The present study analysed the frequency of this mutation in 80 patients with chronic periodontal disease and 122 healthy controls. The 3020insC mutation was identified by employing the polymerase chain reaction followed by restriction fragment length polymorphism analysis. The prevalence of the 3020insC mutation of the NOD2/CARD15 protein in patients with periodontitis was 1.9% (three of 160) and that for the control group was 2.0% (five of 244) (P = 0.942). Hence, unlike in Crohn's disease, the 3020insC mutation of the NOD2/CARD15 gene does not seem to influence the pathophysiology of periodontitis.

• Authors: Matthias Folwaczny, Jürgen Glas, Helga-Paula Török, Daniel Mauermann, Christian Folwaczny
• Journal: European journal of oral sciences (Eur J Oral Sci) Vol. 112 Issue 4 Pg. 316-9 (Aug 2004) ISSN: 0909-8836 [Print] England
• PMID: 15279649 (Publication Type: Journal Article)

Chemical References

• Carrier Proteins
• Intracellular Signaling Peptides and Proteins
• NOD2 protein, human
• Nod2 Signaling Adaptor Protein

Topics

• Adult
• Aged
• Carrier Proteins (genetics)
• Case-Control Studies
• Chi-Square Distribution
• Gene Frequency
• Humans
• Intracellular Signaling Peptides and Proteins
• Middle Aged
• Mutagenesis, Insertional
• Nod2 Signaling Adaptor Protein
• Odds Ratio
• Periodontitis (genetics)
• Polymorphism, Restriction Fragment Length
• Regression Analysis