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Association of interleukin-6 (IL-6) haplotypes with plaque-induced gingivitis in children
LI Holla, K Musilova, J Vokurka, L Klapusova, P Pantuckova, M Kukletova, L Kukla, V Znojil
Language English Country Norway
Grant support
NR8394
MZ0
CEP Register
NR9129
MZ0
CEP Register
Digital library NLK
Full text - Article
Full text - Article
Source
Source
- MeSH
- Alleles MeSH
- Amplified Fragment Length Polymorphism Analysis MeSH
- White People MeSH
- Child MeSH
- Financing, Organized MeSH
- Gene Frequency MeSH
- Genotype MeSH
- Gingivitis etiology genetics immunology MeSH
- Haplotypes MeSH
- Interleukin-6 genetics MeSH
- Polymorphism, Single Nucleotide MeSH
- Humans MeSH
- Logistic Models MeSH
- Adolescent MeSH
- Disease Susceptibility MeSH
- Periodontal Index MeSH
- Promoter Regions, Genetic MeSH
- Case-Control Studies MeSH
- Dental Plaque complications MeSH
- Check Tag
- Child MeSH
- Humans MeSH
- Adolescent MeSH
- Male MeSH
- Female MeSH
- Geographicals
- Czech Republic MeSH
OBJECTIVES: The proinflammatory cytokine interleukin-6 (IL-6) is a key regulator of the host response to microbial infection and major modulator of extracellular matrix catabolism and bone resorption. The aim of this case-control study was to test differences between children with and without gingivitis in the distribution of IL-6 alleles at positions -174, -572, and -597 and their haplotypes. MATERIAL AND METHODS: A total of 455 Caucasian children, aged 11 to 13 years, were enrolled in this study. According to gingival bleeding on probing indices, 183 were classified as healthy subjects and 272 as children with plaque-induced gingivitis. DNA for genetic analysis was obtained from buccal epithelial cells and PCR-RFLP methods were used for genotyping three selected IL-6 promoter polymorphisms. RESULTS: Complex analysis revealed significant differences in haplotype frequencies between patients and healthy subjects (p<0.01). The CGA haplotype was significantly more frequent in children with gingivitis than in healthy subjects (41.5% versus 34.1%). In subanalyses, we found that IL-6 -174C allele was more frequent in patients (44.3%) than in healthy children (36.1%, p=0.016, P(corr)<0.05). Multivariate logistic regression analysis showed that allele C remained a risk factor for gingivitis in children (p=0.03) regardless of plaque or gender. However, the proportions of the IL-6 -597 and -572 genotypes were comparable between the two groups. CONCLUSIONS. Our results indicate that the three promoter polymorphisms in the IL-6 gene act in a cooperative fashion and suggest that IL-6 haplotypes could play a role in the pathogenesis of gingivitis in Caucasian children.
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- $a ABA008 $b cze $c ABA008 $d ABA008 $e AACR2
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- 314 __
- $a Clinics of Stomatology, St. Anne's University Hospital and Faculty of Medicine, Masaryk University Brno, Czech Republic. holla@med.muni.cz
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- $a OBJECTIVES: The proinflammatory cytokine interleukin-6 (IL-6) is a key regulator of the host response to microbial infection and major modulator of extracellular matrix catabolism and bone resorption. The aim of this case-control study was to test differences between children with and without gingivitis in the distribution of IL-6 alleles at positions -174, -572, and -597 and their haplotypes. MATERIAL AND METHODS: A total of 455 Caucasian children, aged 11 to 13 years, were enrolled in this study. According to gingival bleeding on probing indices, 183 were classified as healthy subjects and 272 as children with plaque-induced gingivitis. DNA for genetic analysis was obtained from buccal epithelial cells and PCR-RFLP methods were used for genotyping three selected IL-6 promoter polymorphisms. RESULTS: Complex analysis revealed significant differences in haplotype frequencies between patients and healthy subjects (p<0.01). The CGA haplotype was significantly more frequent in children with gingivitis than in healthy subjects (41.5% versus 34.1%). In subanalyses, we found that IL-6 -174C allele was more frequent in patients (44.3%) than in healthy children (36.1%, p=0.016, P(corr)<0.05). Multivariate logistic regression analysis showed that allele C remained a risk factor for gingivitis in children (p=0.03) regardless of plaque or gender. However, the proportions of the IL-6 -597 and -572 genotypes were comparable between the two groups. CONCLUSIONS. Our results indicate that the three promoter polymorphisms in the IL-6 gene act in a cooperative fashion and suggest that IL-6 haplotypes could play a role in the pathogenesis of gingivitis in Caucasian children.
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