Association of SOCS1 (- 820) (rs33977706) gene polymorphism with chronic periodontitis: A case-control study in Brazilians.

It is evident that the accumulation of periodontal pathogens over the teeth surface triggers periodontitis; however, its aggravation and severity depend on other elements such as environmental factors, systemic health and the host genetic and/or epigenetic background. To address this issue, we investigated the association of two genetic polymorphisms placed on promoter region of SOCS1 gene with chronic periodontal disease. SOCS1 regulates Jak/Kinase signaling pathway and changes in its mRNA expression have been related to different types of cancer and chronic inflammation, including chronic periodontitis. The frequency of alleles and genotypes of two polymorphisms in SOCS1 gene promoter (position - 820 (rs33977706) and position - 1478 (rs33989964)) were analyzed by performing RFLP and TaqMan system in a total of 257 non-smoking subjects. We found a low frequency of A allele and A/A genotype of SOCS1(- 820) polymorphism in the chronic periodontitis group, especially when severe periodontitis samples were separately analyzed (OR = 0.3933; p = 0.0084 (IC95% 0.2112 < µ < 0.7324)), suggesting that A allele plays protective effect against chronic periodontitis. We did not find association between SOCS1-1478 polymorphism and periodontitis. In addition, analysis of SOCS1 (- 820/- 1478) haplotype revealed that the frequency of A(- 820)/CA(- 1478) haplotype decreases in ChrP (p = 0.0089). In conclusion, our study found that SOCS1(- 820) polymorphism is associated with chronic periodontitis.

Interleukin-8 gene promoter polymorphism (rs4073) may contribute to chronic periodontitis.

BACKGROUND: The proinflammatory chemokine interleukin (IL)-8 is important in the regulation of the inflammatory response. Analyses of the single nucleotide polymorphism (SNP) reference sequence (rs) 4073 showed that the A allele upregulated IL-8 levels after stimulation with lipopolysaccharides. We investigated the association of the SNP rs4073 with chronic periodontitis. METHODS: Genotyping was performed by a standard polymerase chain reaction-restriction fragment length polymorphism assay in 289 genomic DNA samples of healthy control subjects and patients with chronic periodontitis; analyses were adjusted by multivariate logistic regression modeling. A real-time polymerase chain reaction performance was used to detect levels of the IL-8 mRNA. RESULTS: The analysis pointed to a statistically significant association of chronic periodontitis with the heterozygous TA genotype (P = 0.001); the results showed an increase in the frequency of the A allele in the diseased group (36% in the control group versus 48% in the periodontitis group). The higher levels of the IL-8 mRNA were found in the periodontitis group, mainly in individuals who presented the TA genotype (P = 0.03). CONCLUSION: The SNP rs4073 was associated with chronic periodontitis in non-smoker Brazilian subjects because the frequency of the A allele was higher in the disease group than in the control group, and the TA genotype was associated with increased levels of IL-8 mRNA transcripts.

DNA methylation status of the IL8 gene promoter in aggressive periodontitis.

BACKGROUND: Studies evaluating the methylation status of cytokine genes may have relevance for inflammatory diseases in which the expression of some cytokines is altered, such as periodontitis. This study observes the DNA methylation status in the interleukin-8 (IL8) gene promoter in cells of the oral epithelium of subjects affected by generalized aggressive periodontitis (AgP) and compares it to those of control subjects. METHODS: Genomic DNA from epithelial oral cells of 37 generalized AgP patients and 37 controls were purified and modified by sodium bisulphite. Modified DNA was submitted by methylation-specific polymerase chain reaction, electrophoresed on 10% polyacrylamide gels, and stained. RESULTS: Subjects who presented generalized AgP have a higher frequency of hypomethylation of the IL8 gene promoter in oral epithelium cells than that of controls (86.5% in the generalized AgP group versus 62% in the control group; P = 0.016; chi(2) test). CONCLUSIONS: A marked hypomethylated status is found in the oral epithelial cells of subjects presenting with generalized AgP, compared to controls, in the promoter region of the IL8 gene. This hypomethylated status may reflect a generalized condition of oral epithelial cells, including gingival epithelium, because gingival epithelial cells were also collected during mouthwash use.