Premium
The 3020insC mutation of the NOD2/CARD15 gene in patients with periodontal disease
Author(s) -
Folwaczny Matthias,
Glas Jürgen,
Török HelgaPaula,
Mauermann Daniel,
Folwaczny Christian
Publication year - 2004
Publication title -
european journal of oral sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.802
H-Index - 93
eISSN - 1600-0722
pISSN - 0909-8836
DOI - 10.1111/j.1600-0722.2004.00137.x
Subject(s) - nod2 , mutation , periodontitis , proinflammatory cytokine , medicine , gene , gene mutation , aggressive periodontitis , genetics , biology , disease , immunology , crohn's disease , inflammation
The 3020insC mutation of the NOD2/CARD15 gene leads to impaired activation of nuclear factor‐kappa B (NF‐ κ B) in vitro . As the destruction of periodontal tissue is mediated via activation of NF‐ κ B, 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.