IADR Abstract Archives
Polymorphisms and Serum Ltα and TNFR2 at Periodontitis and Diabetes
Objectives: The aims of this study were to determine if single nucleotide polymorphisms (SNPs) +252 A/G LT and +676T/G TNFR2 are associated with chronic periodontitis (CP) and Type 2 Diabetes (T2D) and if serum levels of LTα and TNFR2 are influenced by genetic variations or inflammation from periodontium.
Methods: Subjects (n=180) were divided into three groups: T2D+CP (group T2D), nondiabetics+CP (group PD) and healthy controls (group HC). SNPs were assessed using PCR-RFLP methods and serum levels of cytokines/receptors were measured using ELISA. Impact of periodontal inflammation on systematic inflammation was measured using Periodontal Epithelial Surface Area (PESA) and Periodontal Inflamed Surface Areas (PISA).
Results: Both +252 A/G LTα AG genotype and G allele, as the carriers of TT genotype and allele T of +676T/G SNP showed higher risk for periodontitis. There was neither difference in sLTα nor sTNFR2 level between the groups. Serum levels of studied cytokines were not influenced by SNPs. sTNFR2 were predicted by PESA and PISA parameters using regression models. TNFR2 negatively correlated with PESA and PISA at PD group. These correlations were positive at diabetics. LTα correlated positively with these parameters at diabetics. Correlation between LTα and TNFR2 were strong and significant.
Conclusions: At our sample, +252 A/G LT and +676T/G TNFR2 are risk factors for having periodontitis, but not for having both CP and T2D. Parameters that quantify burden of inflammation from periodontium on systematic level influenced the sTNFR2. Negative correlation of PESA, PISA and TNFR2 are in accordance with protective role of TNFR2 in periodontitis. Correlations of these parameters and TNFR2 are changed at diabetics compared to healthy subjects, which could lead to assumption that disturbed secretion of cytokines at diabetics diminished the influence of periodontal inflammation on general health presented at healthy subjects. At our sample, sTNFR2 could reflect action of sLTα.
Methods: Subjects (n=180) were divided into three groups: T2D+CP (group T2D), nondiabetics+CP (group PD) and healthy controls (group HC). SNPs were assessed using PCR-RFLP methods and serum levels of cytokines/receptors were measured using ELISA. Impact of periodontal inflammation on systematic inflammation was measured using Periodontal Epithelial Surface Area (PESA) and Periodontal Inflamed Surface Areas (PISA).
Results: Both +252 A/G LTα AG genotype and G allele, as the carriers of TT genotype and allele T of +676T/G SNP showed higher risk for periodontitis. There was neither difference in sLTα nor sTNFR2 level between the groups. Serum levels of studied cytokines were not influenced by SNPs. sTNFR2 were predicted by PESA and PISA parameters using regression models. TNFR2 negatively correlated with PESA and PISA at PD group. These correlations were positive at diabetics. LTα correlated positively with these parameters at diabetics. Correlation between LTα and TNFR2 were strong and significant.
Conclusions: At our sample, +252 A/G LT and +676T/G TNFR2 are risk factors for having periodontitis, but not for having both CP and T2D. Parameters that quantify burden of inflammation from periodontium on systematic level influenced the sTNFR2. Negative correlation of PESA, PISA and TNFR2 are in accordance with protective role of TNFR2 in periodontitis. Correlations of these parameters and TNFR2 are changed at diabetics compared to healthy subjects, which could lead to assumption that disturbed secretion of cytokines at diabetics diminished the influence of periodontal inflammation on general health presented at healthy subjects. At our sample, sTNFR2 could reflect action of sLTα.