Results of this study showed that there was no significant association between TNF-α (-1031 T/C promoter) gene polymorphisms and the risk of generalized aggressive periodontitis disease.
The data suggest that TNFA (-857) C/T and IL-1A (-889) C/T polymorphisms are not associated with susceptibility to GAgP in this Romanian population, potentially because of the small sample size.
We extracted genomic DNA from 45 young adults diagnosed with generalized aggressive periodontitis to study Fc receptors, formyl peptide receptor, Interleukin-6, tumor necrosis factor-alpha, and vitamin D receptor polymorphisms.
This study evaluated the frequency of the tumor necrosis factor-alpha (TNF-alpha) -308 G/A polymorphism in Brazilians with periodontal health (PH = 51), chronic periodontitis (CP = 74) and generalized aggressive periodontitis (GAgP = 38).
In GAgP group, periodontal treatment led to improvement in all examined clinical parameters and resulted in a statistically significant reduction in the total amounts of IL-1β, VEGF, and TNF-α, in comparison to baseline, already 3 months after therapy in both moderate and deep pocket sites and of PDGF-bb in deep sites (p < 0.01).
Comparing the efficiency of Er,Cr:YSGG laser and diode laser on human β-defensin-1 and IL-1β levels during the treatment of generalized aggressive periodontitis and chronic periodontitis.
In the present study, we tested polymorphisms, derived from genes of the IL-1 cluster, for association with generalized aggressive periodontitis (GAP) through both allelic association and by constructing a linkage disequilibrium (LD) map of the 2q13-14 disease candidate region.
In GAgP group, periodontal treatment led to improvement in all examined clinical parameters and resulted in a statistically significant reduction in the total amounts of IL-1β, VEGF, and TNF-α, in comparison to baseline, already 3 months after therapy in both moderate and deep pocket sites and of PDGF-bb in deep sites (p < 0.01).
Gingival samples from 18 patients with GAgP and 10 healthy subjects were collected and the level of miR-146a and its targets, including necrosis factor-alpha, interleukin-1beta, and interleukin-6, were assessed using real-time PCR.
We conclude that the polymorphic nucleotide A at position -1082 of the IL-10 gene is not associated with generalized aggressive periodontitis in the Iranian population.
The aim of this study was to investigate interleukin(IL)-6(-174) and IL-10(-597) gene polymorphisms in generalized aggressive periodontitis (GAgP) patients.
We evaluated gene polymorphisms of interleukin-10 (-592C>A, -819C>T and -1082G>A) and interleukin-12B (+16974) in patients with chronic periodontitis (n = 145) and generalized aggressive periodontitis (n = 65) in comparison with healthy controls (n = 126).
Gingival samples from 18 patients with GAgP and 10 healthy subjects were collected and the level of miR-146a and its targets, including necrosis factor-alpha, interleukin-1beta, and interleukin-6, were assessed using real-time PCR.
CP was characterized by the increased expression of genes related to responses to external stimuli and an under-expression of immune system-related genes. qRT-PCR analysis confirmed the microarray results, that KIR2DL4, IL6 and SELE were highly expressed in GAgP than CP or H patients.
CP was characterized by increased expression of genes related to responses to external stimuli and an underexpression of immune system-related genes. qRT-PCR analysis confirmed microarray results, that killer cell immunoglobulin (Ig)-like receptor, two Ig domains and long cytoplasmic tail 4; interleukin-6; and selectin E were more highly expressed in patients from the GAgP group compared with the CP and H groups.
The frequencies of the IL1RN genotype A1A2 (chi(2) test; P = 0.001) and allele A2 (chi(2) test; P = 0.006) were found to be significantly increased in patients with GAgP compared to normal subjects.
We report a novel missense mutation of CAMP gene. p.S34N mutation in CAMP gene seems to be contributing factor for generalized aggressive periodontitis, but not for chronic periodontitis.