Association of NOD-like receptor (NLRP3) gene variability with chronic periodontitis and type 2 diabetes mellitus
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| Year of publication | 2018 |
| Type | Conference abstract |
| MU Faculty or unit | |
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| Description | Background and Aim: Chronic periodontitis (CP) and type 2 diabetes mellitus (T2DM) are diseases characterized by an inflammation; the relationship between them is bidirectional. The NOD like receptor (NLRP3) is a part of inflammasome which is responsible for the maturation of proinflammatory cytokines and it also regulates Th2 differentiation. The aim of our study was to investigate three NLRP3 single nucleotide polymorphisms (SNPs) in diabetic patients with CP and systematically healthy subjects with/without CP in the Czech population. Methods: In total, 486 individuals were included in this case-control study: 85 patients with T2DM+CP, 210 patients with CP and 191 non-periodontitis controls. The subjects were examined by a periodontist and several parameters such as plaque index, gingival index, clinical attachment loss and the presence of selected bacteria were recorded. NLRP3 SNPs (rs4612666, rs10754558, rs3806265) were determined by the method based on qPCR using 5 nuclease TaqMan® assays. Results: Although distribution of allele and genotype frequencies of two NLRP3 SNPs (rs10754558, rs3806265) between patients and controls were similar, carriers of TT genotype vs. carriers of CT+CC genotypes NLRP3 (rs4612666) had a higher risk for development of CP in systemically healthy patients and in T2DM patients (P<0.01 and P<0.05, respectively). This finding was confirmed by haplotype analysis, TGC haplotype NLRP3 (rs4612666/rs10754558/rs3806265) was found as a risk factor for CP (OR=2.46, 95%CI=1.17-5.16, P=0.01). Conclusions: It is possible that lower NLRP3 expression in TT rs4612666 carriers has an impact on CD4+ Th1/Th2 balance. We suggest that variability in the NLRP3 gene may play an important role in the pathogenic pathways of CP in the Czech population. Acknowledgements: The study was supported by grant GACR GB14-37368G, funds provided by the Faculty of Medicine MU to junior researcher Petra Borilova Linhartova, and project MUNI/A/0948/2016. |
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