Association Between Interleukin‐4 Gene −590 C/T, −33 C/T,and 70‐Base‐Pair Polymorphisms and Periodontitis Susceptibility: A Meta‐Analysis

Background: Several studies have investigated the association between interleukin (IL)‐4 gene ?590 C/T, ?33 C/T, or 70–base pair (70‐bp) polymorphisms and periodontitis susceptibility but with conflicting results. Hence, a meta‐analysis was conducted to explore whether these polymorphisms are associated with periodontitis susceptibility. Methods: A comprehensive literature search was conducted of PubMed, Embase, Scopus, ScienceDirect, and Web of Science up to April 5, 2014. After the eligible studies were identified, data were extracted and quality‐assessed before performing the meta‐analysis. Results: The meta‐analysis included 23 eligible case‐control studies from 11 articles involving 12 studies of the ?590 C/T polymorphism (1,220 cases and 2,039 controls), five of the ?33 C/T polymorphism (715 cases and 967 controls), and four of the 70‐bp polymorphism (426 cases and 506 controls). The meta‐analysis showed that none of these IL‐4 gene polymorphisms were significantly associated with periodontitis susceptibility in all study participants. However, subgroup analysis showed that the IL‐4 ?590 T allele (odds ratio [OR] = 1.2, 95% confidence interval [CI] = 1.02 to 1.42, P = 0.03) and TT genotype (OR = 1.68, 95% CI = 1.05 to 2.67, P = 0.03) were associated with periodontitis in whites. Conclusions: Based on current evidence, the IL‐4 ?33 C/T and 70‐bp polymorphisms were not associated with an increased risk of periodontitis. However, the IL‐4 ?590 T allele and TT genotype were associated with increased risk of periodontitis in whites.     

Investigation of interleukin‐13 gene polymorphisms in individuals with chronic and generalized aggressive periodontitis in a Taiwanese (Chinese) population

Wu Y‐M, Chuang H‐L, Ho Y‐P, Ho K‐Y, Tsai C‐C. Investigation of interleukin‐13 gene polymorphisms in individuals with chronic and generalized aggressive periodontitis in a Taiwanese (Chinese) population. J Periodont Res 2010; 45: 695–701. © 2010 John Wiley & Sons A/S Background and Objective: The interleukin‐13 (IL‐13) ?1112 C/T polymorphisms have been analyzed previously in a North European population of patients with aggressive periodontitis. The present study was carried out to investigate the association of polymorphisms in the IL‐13 gene with susceptibility to periodontitis in a Taiwanese population. Material and Methods: The genotyping of IL‐13 ?1112 C/T polymorphisms in 60 patients with aggressive periodontitis, 204 patients with chronic periodontitis and 95 healthy controls was carried out using the polymerase chain reaction–restriction fragment length polymorphism technique. Genotypes and allele frequencies among study groups were compared using Fisher’s exact test (p < 0.05). Pearson’s chi‐square test was used for analysis of the Hardy–Weinberg equilibrium. Results: The distributions of CC genotypes and C alleles between patients with aggressive periodontitis and healthy controls were significantly different (p = 0.034 and 0.046). After adjustment for age, gender, betel nut chewing and smoking status using logistic regression analysis, the odds ratio (OR) was 6.45 [95% confidence interval (CI) = 1.99–23.72, p = 0.003] for aggressive periodontitis. However, the CC genotype was only significantly associated with the risk of aggressive periodontitis in the nonsmoking group (OR = 4.48, 95% CI = 1.31–16.93, p = 0.020). Conclusion: The CC genotype or C allele appears to increase the risk of developing aggressive periodontitis in Taiwanese subjects.     

Meta‐Analysis of Association Between Interleukin‐1β C‐511T Polymorphism and Chronic Periodontitis Susceptibility

Background: Many studies have been conducted to explore the association between interleukin (IL)‐1β C‐511T polymorphism and risk of chronic periodontitis (CP) but with different or even contradictory results. A meta‐analysis was performed to further explore their association. Methods: PubMed, Chinese National Knowledge Infrastructure, and EMBASE were searched up to September 30, 2014 for relevant case‐control studies. Two authors (D‐YL and L‐YX) independently selected studies and extracted data from included studies. The meta‐analysis was performed using comprehensive meta‐analysis software. Results: Nineteen case‐control studies involving 2,173 patients with CP and 3,900 healthy controls were included. Using a random‐effects meta‐analysis model, a non‐significant association between IL‐1β C‐511T polymorphism and CP was identified (T versus C: odds ratio [OR] = 1.03, 95% confidence interval [CI] = 0.85 to 1.25; TT versus CC: OR = 1.03, 95% CI = 0.72 to 1.46; CT versus CC: OR = 0.96, 95% CI = 0.71 to 1.30; CT + TT versus CC: OR = 1.00, 95% CI = 0.74 to 1.34; TT versus CT + CC: OR = 1.05, 95% CI = 0.81 to 1.38), and sensitivity analysis indicated that the results were robust. Subgroup analyses also revealed a non‐significant association. No publication bias was detected. Conclusions: Based on currently available evidence, IL‐1β C‐511T polymorphism is not associated with the risk of developing CP. Additional research is warranted to further explore and confirm the association of genetic polymorphism and CP.     

Impact of interleukin-8 gene polymorphisms and environmental factors on oral cancer susceptibility in Taiwan

Oral Diseases (2012) 18 , 307–314 Objectives: Interleukin‐8 (IL‐8), which is an angiogenic chemokine with a high expression level in tumor tissues, plays important roles in developing many human malignancies including oral squamous cell carcinoma (OSCC). This study was designed to examine the association of IL‐8 gene polymorphisms with the susceptibility and clinicopathological characteristics of OSCC. Methods: A total of 270 patients with OSCC and 350 healthy control subjects were recruited. Four single nucleotide polymorphisms (SNPs) of IL‐8 genes were analyzed using polymerase chain reaction–restriction fragment length polymorphism (PCR‐RFLP) genotyping analysis. Results: Results showed that four IL‐8 SNPs (?251 T/A, +781 C/T, +1633 C/T, and +2767 A/T) were not associated with oral cancer susceptibility as well as clinicopathological parameters. But among 345 smokers, IL‐8 polymorphisms carriers with betel quid chewing were found to have a 17.41‐ to 23.14‐fold risk to have oral cancer compared to IL‐8 wild‐type carriers without betel quid chewing. Among 262 betel quid chewers, IL‐8 polymorphisms carriers with smoking have a 10.54‐ to 20.44‐fold risk to have oral cancer compared to those who carried wild type without smoking. Conclusions: Our results suggest that the combination of IL‐8 gene polymorphisms and environmental carcinogens might be highly related to the risk of oral cancer.     

Association of IL1 gene polymorphisms with chronic periodontitis in Brazilians

Chronic periodontal disease (PD) is an infectious immune-inflammatory illness. Polymorphisms in IL1 genes play a role in inflammatory diseases through the modulation of cytokine levels.

Objective

This study aimed to investigate the association between polymorphisms in the IL1 gene cluster and chronic periodontitis in a Brazilian population.

Design

A sample of 113 subjects over 25 years (mean age 41.2) were grouped into: 44 healthy individuals, 31 subjects with moderate and 38 with severe periodontitis. DNA was obtained through a mouthwash and oral mucosa scraping. PCR-RFLP was used to identify the following polymorphisms: IL1A C − 889T (rs1800587), IL1B C − 511T (rs16944), IL1B C + 3954T (rs11436340), IL1RN intron 2 (rs2234663). Differences in the allele/genotype/haplotype frequencies were assessed by Chi-square test (p < 0.05). The risk associated with alleles, genotypes and haplotypes was calculated as odds ratio (OR) with 95% confidence intervals (CI).

Results

Neither IL1A (C − 889T) nor IL1B (C + 3954T) polymorphisms was associated with chronic PD. Allele T for IL1B (C − 511T) only associated with PD in the group of blacks and mulattos. Moreover, genotype 2/2 for IL1RN (intron 2) was associated with severe PD.

Conclusions

Genotype 2/2 of IL1RN for the whole Brazilian population and allele T of IL1B (C − 511T) in a subgroup of Afro-Americans and mulattos were suggested as putative risk indicators for chronic periodontitis.     

Single nucleotide polymorphisms of pattern recognition receptors and chronic periodontitis

Sahingur SE, Xia X‐J, Gunsolley J, Schenkein HA, Genco RJ, De Nardin E. Single nucleotide polymorphisms of pattern recognition receptors and chronic periodontitis. J Periodont Res 2011; 46: 184–192. © 2010 John Wiley & Sons A/S Background and Objective: Periodontitis is a multifactorial disease influenced partly by genetics. Activation of pattern recognition receptors (PRRs) can lead to the up‐regulation of inflammatory pathways, resulting in periodontal tissue destruction. Hence, functional polymorphisms located in PRRs can explain differences in host susceptibility to periodontitis. This study investigated single nucleotide polymorphisms of PRRs including toll‐like receptor (TLR)2 (G2408A), TLR4 (A896G), TLR9 (T1486C), TLR9 (T1237C) and CD14 (C260T) in patients with chronic periodontitis and in periodontally healthy subjects. Methods: One‐hundred and fourteen patients with chronic periodontitis and 77 periodontally healthy subjects were genotyped using TaqMan® allelic discrimination assays. Fisher’s exact test and chi‐square analyses were performed to compare genotype and allele frequencies. Results: The frequency of subjects with the CC genotype of CD14 (C260T) (24.6% in the chronic periodontitis group vs. 13% in the periodontally healthy group) and those expressing the T allele of CD14 (C260T) (CT and TT) (75.4% in the chronic periodontitis group vs. 87% in the periodontally healthy group) was statistically different among groups (p = 0.04). Homozygocity for the C allele of the CD14 (C260T) polymorphism (CC) was associated with a two‐‐fold increased susceptibility to periodontitis (p = 0.04; odds ratio, 2.49; 95% confidence interval, 1.06–6.26). Individuals with the CC genotype of TLR9 (T1486C) (14.9% in the chronic periodontitis group vs. 28.6% in the periodontally healthy group) and those expressing the T allele of TLR9 (T1486C) (CT and TT) (85.1% in the chronic periodontitis group vs. 71.4% in the periodontally healthy group) were also significantly differently distributed between groups without adjustment (p = 0.03). Further analysis of nonsmokers revealed a significant difference in the distribution of genotypes between groups for TLR9 (T1486C; p = 0.017) and CD14 (C260T; p = 0.03), polymorphisms again without adjustment. Conclusion: The CC genotype of CD14 (C260T) is related to susceptibility to chronic periodontitis in Caucasians. In addition, differences observed in the distribution of TLR9 (T1486C) genotypes between groups warrant further investigation.     

Coronary heart disease and chronic periodontitis: is polymorphism of interleukin‐6 gene the common risk factor in a Chinese population?

Oral Diseases (2011) 17 , 270–276 Objectives: Coronary heart disease (CHD) and chronic periodontitis (CP) both are multifactorial chronic diseases and related to inflammation. Interleukin‐6 (IL‐6) plays an important role in the pathogenesis of inflammatory diseases. The purpose of the study was to investigate the association among IL‐6 gene polymorphisms, CP and CHD susceptibility in a Chinese population. Material and methods: The investigation was conducted as a case‐control study involving 505 individuals: 113 patients with CHD and CP, 84 patients with CHD, 178 patients with CP and 130 control individuals. The polymorphisms of IL‐6 gene were analyzed by polymerase chain reaction‐restriction fragment length polymorphism. Relationships between the distributions of the genotypes and risk factors were also assessed. Results: Mutations at the loci ‐174 G/C, ‐597 G/A of IL‐6 were rare in a Chinese population. No significant difference for IL‐6‐572C/G polymorphism was detected among moderate CP group, severe CP group and control (P = 0.312 and 0.481), significant differences were found between CHD groups and non‐CHD groups (P ≤ 0.001). After adjustment for CHD risk factors, the G allele resulted in an increased risk (OR = 1.676‐1.856), the GG/CG genotype was nearly two times higher risk compared to CC genotype (OR = 2.010‐2.136). Conclusions: IL‐6‐572C/G polymorphism did not correlate with CP susceptibility, but might be a potential risk factor for CHD in a Chinese population.     

Effect of tumor necrosis factor alpha (TNF-α) -308 and -1031 gene polymorphisms on periodontitis among Saudi subjects

ObjectivesPeriodontitis is an infectious disorder that leads to irreversible loss of the surrounding attachment and bone destruction. Genetic polymorphism of cytokines has been suggested to play a role in periodontitis. This case-control study aimed to investigate the relationship between periodontitis and two single nucleotide polymorphisms (SNPs): rs1800629 (-308 G/A) and rs1799964 (-1031 T/C), in the TNF-α gene promoter area.Materials and methodsPeripheral blood was used to prepare genomic DNA from 60 subjects with stage II to stage III periodontitis, as along with 65 control subjects. Polymerase chain reaction and restriction endonuclease digestion were used to genotype TNF-α SNPs.ResultsThe distribution of both genotypes and alleles of TNF-α (-308 G/A) polymorphism did not vary between periodontitis subjects and the controls (P > 0.05). However, the CT genotype and C allele of the TNF-α (-1031 T/C) polymorphism were observed more frequently in the periodontitis subjects than in the controls, while the TT genotype and the T allele were more predominant in the control subjects than in the periodontitis patients (OR: 3.149; 95% CI: 1.494–6.639; P = 0.002 and OR: 2.933; 95% CI: 1.413–6.090; P = 0.003, sequentially).ConclusionThe TNF-α (-308 G/A) polymorphism potentially has no correlation with periodontitis susceptibility, whereas the TNF-α (-1031) CT genotype and C allele might be related to periodontitis among Saudi subjects.     

IL-1RN gene polymorphism is associated with peri-implantitis

Objectives: Interleukin (IL)‐1α, IL‐1β and their natural specific inhibitor IL‐1 receptor antagonist (IL‐1ra) play a key role in the regulation of the inflammatory response in periodontal tissues. Polymorphisms in the IL‐1 gene cluster have been associated with severe adult periodontitis. We aimed to investigate the IL‐1 gene cluster polymorphisms in patients with peri‐implantitis. Material and methods: The study included 120 North Caucasian individuals. A total of 71 patients (mean age 68 years, 76% smokers) demonstrating peri‐implantitis at one or more implants as evidenced by bleeding and/or pus on probing and bone loss amounting to >3 threads on Brånemark implants and 49 controls (mean age 66 years, 45% smokers) with clinical healthy mucosa and no bone loss around the implants were recruited for the study. The titanium implants, ad modum Brånemark, had been in function for at least 2 years. Mouthwash samples were collected and used for genotyping of the bi‐allelic polymorphisms IL‐1A^?889, IL‐1B⁺³⁹⁵³, IL‐1B^?511 and a variable number of tandem repeat IL‐1RN gene polymorphisms using PCR technique. Results: Significant differences were found in the carriage rate of allele 2 in the IL‐1RN gene between peri‐implantitis patients and controls (56.5% vs. 33.3%, respectively; odds ratios (OR) 2.6; 95% confidence interval (CI) 1.2–5.6; P=0.015). Logistic regression analysis taking smoking, gender and age into account confirmed the association between the IL‐1RN allele 2 carriers and peri‐implantitis (OR 3; 95% CI 1.2–7.6; P=0.02). Conclusions: Our results provide evidence that IL‐1RN gene polymorphism is associated with peri‐implantitis and may represent a risk factor for this disease.     

白细胞介素8基因-251位点多态性与侵袭性牙周炎的相关性研究

目的研究白细胞介素8（interleukin-8,IL-8）-251位点基因多态性与侵袭性牙周炎易感性的相关性。方法采用病例对照试验设计,从广东汉族人群中选择77例侵袭性牙周炎（aggressive periodontitis,AgP）患者（AgP组）及50例牙周健康者（健康对照组）,采用聚合酶链反应—限制性内切酶片段长度多态性方法对IL-8-251位点基因进行检测,分析组间等位基因和基因型频率的分布差异。结果 IL-8-251A/T位点的基因型和A、T等位基因频率在AgP组和健康对照组的分布差异无统计学意义（P〉0.05）。结论未发现IL-8-251A/T位点基因多态性与中国广东汉族人群侵袭性牙周炎的患病易感性之间存在相关性。     

Common single nucleotide polymorphisms in cyclooxygenase‐2 and risk of severe chronic periodontitis in a Chinese population

Aim: Several common single nucleotide polymorphisms (SNPs) of the cyclooxygenase‐2 (COX‐2) gene have been reported to be functional. The association between ?1195GA, ?765GC and 8473TC of COX‐2, and severe chronic periodontitis (CP) in a Chinese population was investigated. Material and Methods: 148 cases of healthy controls (control group) and 146 cases of severe CP were recruited in this study. Genotypes of ?1195GA, ?765GC and 8473TC were determined by polymerase chain reaction restriction fragment length polymorphism (PCR‐RFLP). The distributions of genotypes and haplotypes were compared by χ² test and the odds ratios (ORs) were calculated by logistic regression analysis. Results: The prevalence of the ?1195A was more prevalent in CP group (60.62%) than control group (51.35%), and the distributions of the ?765C and 8473C were higher in control group (6.76% and 21.96%) compared with CP group (3.08% and 15.07%). Only genotype distribution of ?1195GA was significant when p‐value was corrected for multiple testing (p_c=0.033). The adjusted ORs for the ?1195AA/GA, ?765GC and 8473CC/TC were 2.49 (95% CI=1.33–4.69, p=0.005), 0.45 (95% CI=0.20–1.04, p=0.061) and 0.67 (95% CI=0.41–1.11, p=0.118). Subjects with the haplotype AGT had a significantly higher risk of periodontitis than those with the most common haplotype GGT (OR=1.91, 95% CI=1.32–2.76, p_c<0.001). Conclusions: It suggests the ?1195A variant is associated with an increased risk for severe CP.     

The association between periodontitis and interleukin-6 genetic polymorphism -174 G/C: A meta-analysis

BackgroundTo evaluate the association between periodontitis and interleukin-6 (IL6) -174 G/C polymorphism by data synthesis and subgroup analysis.MethodsEighteen case-control studies from 16 articles with 1616 cases and 1511 controls were included in this meta-analysis by searching the public databases including PubMed, Embase and Web of Science databases by Jun 2018. Data syntheses were performed using Stata 9.0.ResultsThere were inverse associations of IL6 -174 G/C polymorphism with both general periodontitis and overall periodontitis. In CC vs. GG inheritance model, whose effect was the most profound, the genetic polymorphism reduced the risks of general and overall periodontitis by 60% (95% CI = 0.25-0.65, P < 0.01) and 31% (95% CI = 0.38-0.97, P = 0.04) respectively. In addition, the G/C variation was likely to be protective against moderate (allele C vs. allele G: OR = 0.61, 95% CI = 0.43-0.87, P = 0.01; CC + GC vs. GG: OR = 0.57, 95% CI = 0.37-0.89, P = 0.01) and severe periodontitis (allele C vs. allele G: OR = 0.58, 95% CI = 0.41-0.84, P < 0.01; CC vs. GG: OR = 0.33, 95% CI = 0.13-0.82, P = 0.02) exclusively in Brazilian people. No reliable evidence was found regarding chronic periodontitis.ConclusionThis meta-analysis suggests that IL6 -174 G/C polymorphism may be negatively associated with risk of periodontitis.     

Association between lactoferrin gene polymorphisms and aggressive periodontitis among Taiwanese patients

Background and Objective: A dramatic difference in the frequencies of the Lys/Arg single nucleotide polymorphism in the lactoferrin genotype between a small population of patients with localized juvenile periodontitis and healthy subjects has been reported. As the single nucleotide polymorphism could be associated with ethnicity, the present study aimed to investigate the association between polymorphisms of the lactoferrin gene and periodontitis. Material and Methods: Sixty‐five patients with aggressive periodontitis, 278 with chronic periodontitis and 88 healthy controls were genotyped for the Lys/Arg polymorphism of the lactoferrin gene at position 29 [reference sequence (rs) 1126478] in the N‐terminal alpha‐helical region. Results: The frequencies of the GG genotype and the G allele were highest in the aggressive periodontitis group, followed by the chronic periodontitis group and then the healthy controls. The frequency of the G allele was significantly higher in aggressive periodontitis and chronic periodontitis groups than in healthy controls (p = 0.0037 and 0.0212). Although the difference of the GG genotype distribution between subjects with chronic periodontitis and healthy controls did not reach significance, the distribution of genotypes between aggressive periodontitis and healthy controls was significantly different. The association of the gene polymorphism and aggressive periodontitis still existed, even after adjusting for age, gender and smoking status by logistic regression analysis (GG/AG+AA: odds ratio = 2.16, 95% confidence interval = 1.09–4.35, p = 0.0287). After the study, subjects were further stratified by their smoking status; the GG genotype was still significantly associated with the risk of aggressive periodontitis in the nonsmoking group (odds ratio = 2.69, p = 0.018). However, there were no statistical differences between chronic periodontitis vs. healthy controls and aggressive periodontitis vs. healthy controls in the smoking group. Conclusion: The present study revealed that the A/G polymorphism in the lactoferrin gene might be associated with aggressive periodontitis. The A allele might reduce the risk of development of aggressive periodontitis in a Taiwanese population. Our results also support the hypothesis that lactoferrin genetic polymorphisms could play a role in the risk for periodontitis separate from the smoking factor. The functionality of this gene’s polymorphisms has to be further elucidated.     

Effect of tumor necrosis factor alpha (TNF-α) -308 and -1031 gene polymorphisms on periodontitis among Saudi subjects

ObjectivesPeriodontitis is an infectious disorder that leads to irreversible loss of the surrounding attachment and bone destruction. Genetic polymorphism of cytokines has been suggested to play a role in periodontitis. This case-control study aimed to investigate the relationship between periodontitis and two single nucleotide polymorphisms (SNPs): rs1800629 (-308 G/A) and rs1799964 (-1031 T/C), in the TNF-α gene promoter area.Materials and methodsPeripheral blood was used to prepare genomic DNA from 60 subjects with stage II to stage III periodontitis, as along with 65 control subjects. Polymerase chain reaction and restriction endonuclease digestion were used to genotype TNF-α SNPs.ResultsThe distribution of both genotypes and alleles of TNF-α (-308 G/A) polymorphism did not vary between periodontitis subjects and the controls (P > 0.05). However, the CT genotype and C allele of the TNF-α (-1031 T/C) polymorphism were observed more frequently in the periodontitis subjects than in the controls, while the TT genotype and the T allele were more predominant in the control subjects than in the periodontitis patients (OR: 3.149; 95% CI: 1.494–6.639; P = 0.002 and OR: 2.933; 95% CI: 1.413–6.090; P = 0.003, sequentially).ConclusionThe TNF-α (-308 G/A) polymorphism potentially has no correlation with periodontitis susceptibility, whereas the TNF-α (-1031) CT genotype and C allele might be related to periodontitis among Saudi subjects.     

Matrix Metalloproteinase (MMP)‐8 and Tissue Inhibitor of MMP‐1 (TIMP‐1) Gene Polymorphisms in Generalized Aggressive Periodontitis: Gingival Crevicular Fluid MMP‐8 and TIMP‐1 Levels and Outcome of Periodontal Therapy

Background: The aim of the present study is to investigate matrix metalloproteinase (MMP)‐8 and tissue inhibitor of MMP‐1 (TIMP‐1) gene polymorphisms in generalized aggressive periodontitis (GAgP) and to assess the effects of MMP‐8 and TIMP‐1 genotypes on the outcomes of non‐surgical periodontal therapy. Methods: Genomic DNA was obtained from peripheral blood of 100 patients with GAgP and 167 periodontally healthy controls. MMP‐8 +17 C/G, ?799 C/T, ?381 A/G and TIMP‐1 372 T/C, *429 T/G polymorphisms were determined by polymerase chain reaction‐restriction fragment length polymorphism. Patients with GAgP received non‐surgical periodontal therapy and were followed for 6 months. Clinical periodontal parameters and gingival crevicular fluid (GCF) samples were collected at baseline and at follow‐up visits. GCF biomarkers were analyzed by immunofluorescence assay and enzyme‐linked immunosorbent assay. Results: Distribution of the MMP‐8 ?799 C/T genotypes was significantly different between the GAgP and control groups (P <0.005). TIMP‐1 372 T/C and *429 T/G genotypes in males were also significantly different between study groups (P <0.004). GCF MMP‐8 levels decreased until 3 months after non‐surgical therapy compared with baseline in T and G alleles, as well as G and C allele carriers (P <0.0125), whereas no significant decreased was observed in non‐carriers (P >0.0125). Conclusion: On the basis of the present findings, it can be suggested that MMP‐8 ?799 C/T and TIMP‐1 372 T/C, *429 T/G gene polymorphisms in males may be associated with the susceptibility to GAgP in the Turkish population.     

Interleukin-2 −330 and 166 gene polymorphisms in relation to aggressive or chronic periodontitis and the presence of periodontopathic bacteria

Background and Objective: As a pro‐inflammatory cytokine, interleukin‐2 mediates the activation, growth and differentiation of T and B lymphocytes and natural killer cells. Promoter polymorphisms of the interleukin‐2 gene have been associated with altered interleukin‐2 production or identified as prognostic markers for various infectious diseases. Therefore, the aim of this study was to evaluate two polymorphisms at positions ?330 T/G and 166 G/T in patients with generalized chronic periodontitis (n = 58) or generalized aggressive periodontitis (n = 73) in comparison with periodontitis‐free controls (n = 69). Material and Methods: Both interleukin‐2 polymorphisms were analyzed using the polymerase chain reaction with sequence‐specific primers. Distributions of single alleles, genotypes and haplotypes were calculated using the chi‐square test. Risk factor analyses were carried out by logistic regression with respect to established cofactors for periodontitis. The presence of subgingival bacteria in an individual were analyzed using a molecular biological method (the micro‐Ident^® test). Results: The interleukin‐2 genotype ?330 TG occurred less frequently in patients with chronic periodontitis (25.9% vs. 49.3%). Moreover, this genotype decreased the adjusted odds ratio for chronic periodontitis (odds ratio = 0.394), whereas the interleukin‐2 genotype 166 TT and the haplotype combination interleukin‐2 ?330,166 TT : TT were associated with an increased adjusted odds ratio (odds ratio = 2.82 or 2.97). For the latter interleukin‐2 combination, a positive association for the subgingival presence of Porphyromonas gingivalis (81.3% vs. 59.5%) and bacteria of the ‘red complex’ (78.1% vs. 56.0%) was shown. Conclusion: The interleukin‐2 genotypes ?330 TG and 166 TT, as well as the combination genotype interleukin‐2 TT : TT, could be putative prognostic factors for chronic periodontitis.     

Cyclooxygenase-2 Gene-765 single nucleotide polymorphism as a protective factor against periodontitis in Taiwanese

Aim: Prostaglandin E₂ (PGE₂) is considered to be an important mediator of tissue destruction in periodontitis. The cyclooxygenase (COX) catalyses the production of PGs. COX‐2, which is induced in an inflammatory response, is responsible for PGs synthesis at sites of inflammation. A single nucleotide polymorphism of COX‐2^?765 has been shown to alter the expression of the COX‐2 gene. The purpose of the present study was to evaluate the association of the COX‐2^?765 polymorphism and susceptibility to periodontitis in Taiwanese. Material and Methods: Eighty‐five cases of aggressive periodontitis (AgP), 343 cases of chronic periodontitis (CP) and 153 cases of healthy controls (HC) were recruited for the study. Genotypes of COX‐2^?765 were determined by polymerase chain reaction‐restriction fragment length polymorphism (PCR‐RFLP). The distribution of genotypes among groups was compared by logistic regression analyses. The risk for periodontitis associated with genotypes was calculated as the odds ratio (OR). Results: The prevalence of the GC and CC genotypes was significantly lower in AgP (5%) and in CP (29%) compared with the HC (42%). The ORs for carriage of the ?765C allele (GC+CC versus GG) in AgP and CP were 0.068 (95% CI=0.020–0.173, p<0.0001) and 0.571 (95% CI=0.385–0.849, p=0.006), respectively. After adjustment for age, gender and smoking status, the OR was 0.071 (95% CI=0.017–0.219) and 0.552 (95% CI=0.367–0.829) for AgP and CP, respectively. Conclusions: The results of the study suggest that the ?765G to C polymorphism of the COX‐2 gene is associated with a decreased risk for periodontitis in Taiwanese, especially in AgP. However, the biological meaning needs further investigation.     

TLR4 and IL-18 gene variants in aggressive periodontitis

Aim: We aimed to assess the association of different genotypes with increased aggressive periodontitis susceptibility by studying functional relevant variants in the pathogen‐recognition receptor Toll‐like receptor 4 (TLR4) and variants in the promoter region of the pro‐inflammatory cytokine interleukin‐18 (IL‐18). Material and Methods: One hundred and eleven patients with aggressive periodontitis and 80 periodontally healthy controls were genotyped for four functional variants in the TLR4 gene (c.896A>G and c.1196C>T) and in the IL‐18 promoter (c.?368G>C and c.?838C>A). The genotype and allele frequencies, as well as the frequency of combined genotypes were compared between study groups. Results: There were no statistical differences in genotype and allele frequencies within the four variants between the groups. All study subjects were further classified into carriers and non‐carriers of at least one variant of both genes. The logistic regression analysis adjusted for gender and smoking showed no association between carrier status of at least one variant of both genes and periodontal status (OR=1.41, 95% CI: 0.43–4.70). Conclusions: Our results reject the hypothesis that functionally relevant IL‐18 and TLR4 gene mutations have a major effect on aggressive periodontitis susceptibility alone or in combination.     

The IL1A (-889) gene polymorphism is associated with chronic periodontal disease in a sample of Brazilian individuals

BACKGROUND AND OBJECTIVE: It has been proposed that genotypes reflective of polymorphisms in cytokine genes can predispose individuals to disease by enhancing inflammatory processes. The C/T polymorphism at position -889 of the IL1A gene influences interleukin-1alpha expression, with the T allele inducing higher expression. The aim of this study was to evaluate the association of the IL1A (-889) gene polymorphism in Brazilian individuals with different clinical forms of periodontitis and severity of disease. MATERIAL AND METHODS: DNA was obtained from oral swabs of 163 Brazilian individuals and was amplified using the polymerase chain reaction (PCR). Products were submitted to digestion and were analyzed by electrophoresis to distinguish the C and T alleles. RESULTS: A significant difference in the genotype distribution was observed when comparing the chronic periodontitis group with the control group, evaluating only nonsmokers (chi-squared analysis = 9.91; p = 0.007), as well as when smokers were included (chi-squared analysis = 6.36; p = 0.04). Moreover, we observed a higher incidence of the T allele in the chronic periodontitis group (37.8%) when compared with the control group (18.4%) in nonsmokers (p = 0.006, odds ratio = 2.69, confidence interval = 1.27-5.68) and also when smokers were included (p = 0.03, odds ratio = 1.87, confidence interval = 0.98-3.56). No statistical difference was observed when the aggressive periodontitis group was compared with the control group. With regard to severity of disease, no statistical difference was observed. CONCLUSION: These data show an association of the IL1A (-889) polymorphism with chronic periodontitis in Brazilian individuals.