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.
Two polymorphisms located at +4845 bp in the IL-1 alpha region and at +3954 bp in the IL-1 beta region were evaluated by a polymerase chain reaction method; 35.3% of the examined subjects were positive for specific combinations of allotypes of the IL-1 gene complex previously associated with an increased risk for severe periodontitis.
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.
This study demonstrates that specific genetic markers, that have been associated with increased IL-1 production, are a strong indicator of susceptibility to severe periodontitis in adults.
Former moderate smokers (>5 pk/yr and <10 pk/yr) who were IL-1 genotype negative were at increased odds ratio of having moderate to severe periodontal disease of 7.43 (95% CI: 1.20-46.20) compared to non-smokers or former light smokers who were IL-1 genotype negative.
Two polymorphisms located at +4845 bp in the IL-1 alpha region and at +3954 bp in the IL-1 beta region were evaluated by a polymerase chain reaction method; 35.3% of the examined subjects were positive for specific combinations of allotypes of the IL-1 gene complex previously associated with an increased risk 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).
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.
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).
Former moderate smokers (>5 pk/yr and <10 pk/yr) who were IL-1 genotype negative were at increased odds ratio of having moderate to severe periodontal disease of 7.43 (95% CI: 1.20-46.20) compared to non-smokers or former light smokers who were IL-1 genotype negative.
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.
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.
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.
Cross-sectional studies have demonstrated that a specific polymorphism (allele 2 of both IL-1A +4845 and IL-1B +3954) in the IL-1 gene cluster has been associated with an increased susceptibility to severe periodontal disease and to an increased bleeding tendency during periodontal maintenance.