Dose‐Effect Relation of Smoking and the Interleukin‐1 Gene Polymorphism in Periodontal Disease

Meisel, Peter; Schwahn, Christian; Gesch, Dietmar; Bernhardt, Olaf; John, Ulrich; Kocher, Thomas

doi:10.1902/jop.2004.75.2.236

Cited by 69 publications

(60 citation statements)

References 35 publications

(45 reference statements)

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“…It should also be considered that a gene-environmental interaction between smoking and the IL-1 genetic polymorphism has been recently reported: PAG-positive smokers had an enhanced smoking-associated periodontitis risk as compared to their IL-1 genotype-negative counterparts. 46 However, in GAP, Hodge et al 38 failed to detect an association with IL-1 genotypes and smoking status which, when included in the analysis as a covariate, did not influence the results.…”

Section: Discussionmentioning

confidence: 96%

Linkage disequilibrium analysis of case–control data: an application to generalized aggressive periodontitis

et al. 2004

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Several studies have shown a role for the involvement of interleukin (IL)-1 gene cluster polymorphisms in the risk of periodontal diseases. 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. The IL-1RN (VNTR) genotype distribution observed was significantly different in GAP and control subjects (P ¼ 0.019). We also observed some evidence for an association between GAP and the IL-1B þ 3953 polymorphism (P ¼ 0.039). The pattern of association in the region, represented as an LD map, identifies a recombination hot area between the IL-1B þ 3953 and IL-1B À511 polymorphisms. Multilocus modelling of association with disease gives a location for the peak association at the IL-1B þ 3953 marker, although support for the peak is not significant. Haplotype analysis identifies a IL-1B þ 3953 -IL-1B À511 haplotype as having the lowest P-value in the region. Recognition of the presence of a recombination hot area between the IL-1B þ 3953 and IL-1B À511 polymorphisms will have an important bearing on future efforts to develop higher resolution SNP analysis in this region for both this and other diseases for which this cluster is implicated.

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Section: Discussionmentioning

confidence: 96%

Linkage disequilibrium analysis of case–control data: an application to generalized aggressive periodontitis

et al. 2004

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“…Kornman et al (17) found a significantly higher prevalence of positive genotypes in non-smokers with severe PD, and Shirodaria et al (35) reported a significant association between the IL-1A polymorphism (+4845) and a higher risk of severe PD in non-smokers. However, findings of studies from 3 consecutive years (20,36,37) showed that only smokers with positive IL-1 genotype were at a higher risk of PD, concluding that tobacco use is a more important risk factor than genetics. Drozdzik et al (38) found no significant association between the presence of the IL-1B polymorphism (+3953) and the periodontal status of patients, consistent with the present study, describing plaque index and age as more influential risk factors.…”

Section: Discussionmentioning

confidence: 98%

“…However, other authors found no such correlation (18)(19)(20), thus the issue remains controversial. The aim of the present study was to examine the association between IL-1β in GCF and PD activity and to investigate the presence of IL-1 gene polymorphisms and their possible relationship with the disease, in a Spanish population.…”

Section: Introductionmentioning

confidence: 92%

Interleukin-1 gene polymorphisms and periodontal status in a Spanish population

et al. 2012

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Abstract. The aim of this study was to investigate the possible association between interleukin (IL)-1A (+4845) and/or IL-1B (+3954) gene polymorphisms and the onset and progression of chronic periodontal disease (PD), an issue that remains controversial. The relationship between IL-1β concentration in the gingival crevicular fluid (GCF) and disease activity was also evaluated. The study was performed on 25 individuals with no gingivitis or PD and on 25 subjects with active chronic PD. Two samples of GCF were obtained from each subject and IL-1β was determined by enzyme-linked immunoabsorbent assay. Blood samples (10 ml) were drawn from each subject to detect polymorphisms in IL-1A (+4845) and IL-1B (+3954) by polymerase chain reaction. Mean GCF IL-1β concentrations were higher in patients with active chronic PD compared to the control group. No significant association was found in either group between GCF IL-1β concentration and the presence of polymorphisms in IL-1A (+4845), IL-1B (+3954) or both genotypes. No significant difference was found in either group with regard to the presence of polymorphisms in IL-1A (+4845), IL-1B (+3954) or both genotypes (p=0.556). The concentration of IL-1β in GCF was almost 2-fold higher in patients with chronic PD than in the healthy individuals. The presence of polymorphisms in IL-1A (+4845) and/or IL-1B (+3954) genotypes is not associated with IL-1β overproduction in GCF and is not a risk factor for chronic PD. IL-1β is considered a suitable marker of the severity and progression of chronic PD. The presence of IL-1A (+4845) and/or IL-1B +3954 gene polymorphisms does not appear to be a risk factor for chronic PD. Therefore, the IL-1A (+4845) and/or IL-1B +3954 gene polymorphisms cannot be considered genetic markers of chronic PD. Moreover, these polymorphisms do not indicate an overproduction of IL-1β in GCF.

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“…Several studies reported relationships between IL-1-positive genotypes and smoking; however, other studies demonstrated that the association of IL-1-positive genotypes with the severity of periodontal disease was independent of smoking, suggesting no relationship between smoking and IL-1 genotypes. Logistic regression analysis revealed that odds ratios of periodontal disease, in comparison with IL-1 genotype-negative non-smokers as a reference group, was 0.98 for genotype-positive non-smokers, 2.37 for genotype-negative smokers, and 4.50 for genotype-positive smokers, suggesting synergism between IL-1 polymorphism and smoking (Meisel et al, 2004). An association between IL-6 and IL-10 genotype and periodontal status was more conspicuous in non-smokers.…”

Section: Gene-smoking Relationshipmentioning

confidence: 96%

Effects of Smoking and Smoking Cessation and Smoking Cessation Intervention

Hanioka¹,

Ojima²,

Nakamura³

2012

Periodontal Diseases - A Clinician's Guide

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Dose‐Effect Relation of Smoking and the Interleukin‐1 Gene Polymorphism in Periodontal Disease

Abstract: There is a gene-environmental interaction between smoking and the IL-1 genetic polymorphism. Smokers bearing the genotype-positive IL-1 allele combination have an increased risk of periodontitis. The IL-1 genotype has no influence in non-smokers.

Cited by 69 publications

References 35 publications

Linkage disequilibrium analysis of case–control data: an application to generalized aggressive periodontitis

Linkage disequilibrium analysis of case–control data: an application to generalized aggressive periodontitis

Interleukin-1 gene polymorphisms and periodontal status in a Spanish population

Effects of Smoking and Smoking Cessation and Smoking Cessation Intervention

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