Collectively, these findings imply that the lack of protease 3 activation by dysfunctional cathepsin C in PLS patients leads to the deficit of antimicrobial and immunomodulatory functions of LL-37 in the gingiva, allowing for infection with A. actinomycetemcomitans and the development of severe periodontal disease.
Attention has been paid to the role of IL-1 in the pathogenesis of the disease, and to the significance of a genetic test, investigating the presence of composite two polymorphisms of IL-1 gene, as a risk factor for severe periodontitis.
Attention has been paid to the role of IL-1 in the pathogenesis of the disease, and to the significance of a genetic test, investigating the presence of composite two polymorphisms of IL-1 gene, as a risk factor for severe periodontitis.
Increased expression of hBD-2 and IL-1β was associated with slight-to-moderate periodontitis (p < 0.05), and there was a significant relationship between decreased hBD-2 and IL-1β expression and severe periodontitis (p < 0.05).
Logistic regression and other statistical analyses were used to examine the association between moderate to severe periodontitis and IL1B gene variations, including SNPs, haplotypes and composite genotypes.
A meta-analysis of the three populations supported the association between the IL-1 genotype pattern and moderate to severe periodontitis (OR 1.95; p < 0.001).
The polymorphisms observed in IL-1α(+4845) and IL-1β(+3954) single nucleotide polymorphisms (SNPs), was significantly different among the study groups (healthy controls, mild, moderate and severe periodontitis with p<0.05, d.f.=1.
The polymorphisms observed in IL-1α(+4845) and IL-1β(+3954) single nucleotide polymorphisms (SNPs), was significantly different among the study groups (healthy controls, mild, moderate and severe periodontitis with p<0.05, d.f.=1.
Study inclusion criteria focused on the analytic framework originally proposed for the IL-1 genetic effect in which overexpression of inflammatory mediators is hypothesized to result in more severe periodontitis in response to a bacterial challenge.
Study inclusion criteria focused on the analytic framework originally proposed for the IL-1 genetic effect in which overexpression of inflammatory mediators is hypothesized to result in more severe periodontitis in response to a bacterial challenge.
At T(2), a genetic test to determine the IL-1 genotype and genetic susceptibility for severe periodontal disease was performed for all 60 patients, and they were classified as IL-1 genotype positive (G+) or negative (G-) according to the test results.
At T(2), a genetic test to determine the IL-1 genotype and genetic susceptibility for severe periodontal disease was performed for all 60 patients, and they were classified as IL-1 genotype positive (G+) or negative (G-) according to the test results.
Therefore, the aim of this study is to examine the association between severe periodontitis in Japanese and the following SNPs: five in the TNF-alpha gene promoter (-1031, -863, -857, -308, -238) and three in the IL-1beta gene (-511, -31, +3953).
GCF IL-1beta was determined by ELISA at 6-8 molar sites from 29 non-smoking adults with mild, moderate, or severe periodontal disease at baseline, 2 weeks, and 24 weeks following scaling and root planing.