雌激素受体基因多态性与慢性牙周炎相关性研究

目的探讨雌激素受体基因多态性与陕西地区慢性牙周炎易感性的关联。方法收集陕西地区109例慢性牙周炎患者和99例牙周健康对照组的颊黏膜拭子,用Chelex-100方法提取全基因组DNA, 用聚合酶链反应-限制性片段长度多态性（PCR-RFLP）技术检测雌激素α和β受体基因型分布。结果慢性牙周炎组与正常对照组在ER-α受体XbaⅠ基因型分布上有统计学差异,慢性牙周炎组XX型基因频率明显高于正常对照组,尤其在女性患者中此差异显著,男性患者中未见不同;ER-β受体RsaⅠ和AluⅠ基因型在患者组与对照组中分布未见差异。结论慢性牙周炎易感性与雌激素XbaⅠ基因型分布相关,汉族女性群体中ER-α受体XX基因型可能为慢性牙周炎的易感因子。     

Interleukin‐10 gene polymorphisms and chronic periodontitis susceptibility: Evidence based on 33 studies

The purpose of the meta‐analysis was to investigate the potential association of interleukin‐10 (IL‐10) polymorphisms with susceptibility to chronic periodontitis (CP). A total of 33 studies involving 3487 cases and 4356 controls were identified through a search of multiple electronic databases (last search was updated on 19 July 2018). Three single nucleotide polymorphisms (SNPs) were included in the meta‐analysis: ‐1082A>G(rs1800896), ‐819C>T(rs1800871), and ‐592C>A(rs1800872). Odds ratios (ORs) and their 95% confidence intervals (CIs) using allele, dominant, and recessive genetic models were computed to assess the strength of the association. The ‐1082A>G(rs1800896) polymorphism was found to be associated with decreased CP risk in both Caucasians and Latinos under the dominant model. The ‐819C>T(rs1800871) and ‐592C>A(rs1800872) polymorphisms were both associated with increased CP risk in Latinos under the allele and dominant models. In Asians, no associations were observed for any of the polymorphisms under all comparison models. The present meta‐analysis suggests that the ‐1082A>G(rs1800896) polymorphism might be a protective factor for CP in both Caucasians and Latinos, but the ‐819C>T(rs1800871) and ‐592C>A(rs1800872) polymorphisms might contribute to CP pathogenesis in Latinos.     

Association of interleukin-10 gene promoter polymorphisms with chronic and aggressive periodontitis

Oral Diseases (2012) 18 , 271–279 Objective: Interleukin‐10 gene promoter polymorphisms have been associated with interleukin‐10 decreased production, thereby playing a role in the pathogenesis of periodontitis. This study aimed to investigate whether interleukin‐10 single nucleotide polymorphisms at positions ‐1087(G/A) and ‐597(C/A) are associated with generalised chronic periodontitis and localised aggressive periodontitis. Methods: Genomic DNA samples were isolated from 276 unrelated Jordanian participants. Subjects were categorised into 86 periodontally healthy controls, 105 chronic periodontitis patients and 85 localised aggressive periodontitis patients. Genotype frequencies were calculated, and differences were determined using Pearson chi‐squared test, and odds ratio and 95 % confidence intervals were included. Results: The frequencies of the ‐1087A and ‐597A alleles were significantly more common in chronic periodontitis patients than controls. The A‐positive allele genotypes (GA, AA) at position ‐1087 and A‐positive allele genotypes (CA, AA) at position ‐597 appeared to increase the risk of having chronic periodontitis. No significant differences were observed in the genotype frequencies between localised aggressive periodontitis patients and controls. Conclusions: These findings indicate the possible use of interleukin‐10 single nucleotide polymorphisms as genetic markers in chronic periodontitis patients and further emphasise the molecular differences between chronic periodontitis and aggressive periodontitis.     

Interleukin-17 and interleukin-18 levels in saliva and plasma of patients with chronic periodontitis

Özçaka Ö, Nalbantsoy A, Buduneli N. Interleukin‐17 and interleukin‐18 levels in saliva and plasma of patients with chronic periodontitis. J Periodont Res 2011; 46: 592–598. © 2011 John Wiley & Sons A/S Background and Objective: This study was planned to investigate whether patients with chronic periodontitis exhibit different salivary and/or plasma concentrations of interleukin (IL)‐17 and IL‐18 compared with clinically healthy subjects. Material and Methods: Whole saliva and blood samples, together with full‐mouth clinical periodontal recordings, were obtained from 22 otherwise healthy untreated nonsmokers with chronic periodontitis and from 21 systemically and periodontally healthy control subjects. The concentrations of IL‐17 and IL‐18 in saliva and plasma were determined using ELISAs. Results: The healthy control group exhibited significantly lower values in all clinical periodontal measurements (p < 0.001). The salivary concentration of IL‐17 was significantly lower, and that of IL‐18 significantly higher, in patients from the chronic periodontitis group compared with healthy control subjects (p = 0.025 and p = 0.009, respectively). Plasma IL‐17 and IL‐18 concentrations were similar in the two study groups (p > 0.05). Conclusion: Within the limits of the present study, it may be suggested that an elevated salivary IL‐18 level in untreated nonsmoker chronic periodontitis patients has the potential to be a biomarker for periodontal tissue destruction.     

The Presence and involvement of interleukin‐17 in apical periodontitis

Apical periodontitis (AP) is a chronic inflammatory disease characterized by periapical tissue inflammation and destruction of the associated alveolar bone. It is caused by microbial infections within the root canal and the resultant host immune responses in the periapical tissues. The proinflammatory cytokine interleukin (IL)‐17 has been shown to play an important role in many inflammatory diseases. There is increasing evidence of the presence of IL‐17 in AP, which might be associated with disease pathogenesis. Moreover, several animal studies indicate the potential role of IL‐17 in periapical inflammation and the resultant bone resorption in AP. This article reviews recent studies regarding the collective in vitro, in vivo and clinical evidence of the presence and involvement of IL‐17 in AP. A search related to IL‐17 in apical periodontitis was conducted on PubMed, EMBASE and Web of Science databases using keywords and controlled vocabulary. Two independent reviewers first screened titles and abstracts and then the full texts that were included. A total of 25 papers were identified, of the 25 included articles, 7 involved laboratory studies on cell cultures, 11 involved animal experimentations, and 7 were observational studies using human clinical samples. In conclusion, evidence for the presence of IL‐17 in AP from human and animal models is clear. However, there is relatively little information currently available that would highlight the specific role of IL‐17 in AP.     

The Influences of Periodontal Status and Periodontal Pathogen Quantity on Salivary 8‐Hydroxydeoxyguanosine and Interleukin‐17 Levels

Background: Periodontitis is a biofilm‐initiated disease that is characterized by elevated inflammatory status. 8‐Hydroxydeoxyguanosine (8‐OHdG) and interleukin (IL)‐17 are highly associated with inflammation and bone resorption and therefore are regarded as potential biomarkers for periodontitis. In this study, the associations between salivary 8‐OHdG and IL‐17 levels and clinical and microbial parameters before and after non‐surgical treatment are investigated. Methods: Forty‐five patients with chronic periodontitis (CP) and 47 periodontally healthy volunteers were recruited for the study. Clinical parameters, including the probing depth (PD), clinical attachment level (CAL), sulcular bleeding index, and simplified oral hygiene index (OHI‐S), were examined for each participant. Microbial parameters including the quantities of Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola in the subgingival plaque and saliva were determined by real‐time polymerase chain reaction at baseline and 1 and 3 months after the non‐surgical treatment. Salivary 8‐OHdG and IL‐17 levels were detected by enzyme‐linked immunosorbent assays. Results: Compared with healthy volunteers, CP group patients had significantly higher salivary 8‐OHdG and IL‐17 levels at baseline. Baseline salivary 8‐OHdG and IL‐17 levels were positively correlated with all clinical parameters as well as the quantities of T. forsythia and T. denticola. After non‐surgical treatment, baseline levels of salivary 8‐OHdG and IL‐17 were reduced significantly at both the 1‐ and 3‐month follow‐ups. The hierarchical linear model revealed that variations in the PD, CAL, and OHI‐S had significant positive effects on variation in the salivary 8‐OHdG level. However, variations in the PD; quantity of T. forsythia in the subgingival plaque; and quantities of P. gingivalis, T. forsythia, and T. denticola in saliva were associated significantly with variation in the salivary IL‐17 levels. Conclusions: There was a strong association between salivary 8‐OHdG and IL‐17 levels and periodontitis. Variation in the salivary 8‐OHdG level was correlated with variations in the clinical parameters, whereas variation in the IL‐17 level was correlated with variation in the microbial parameters.     

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.     

Interleukin 10 gene promoter polymorphisms are associated with chronic periodontitis

BACKGROUND: Chronic periodontitis (CP) is characterized by an inflammation in the supporting tissues of the teeth caused primarily by bacterial infection. Interleukin 10 (IL10) is an anti-inflammatory cytokine whose genetic polymorphisms may influence the expression of the protein. Objective: In this study we investigated the hypothesis that single-nucleotide polymorphisms (SNPs) in the promoter of IL10 gene might be related to CP. MATERIALS AND METHODS: DNA was obtained from n=67 CP patients and n=43 control subjects. All studied individuals were non-smokers. The -1087 SNP was investigated by DNA sequencing, and the -819 and -592 SNPs by restriction fragment length polymorphism of PCR products. RESULTS: Frequencies of -819 and -592 SNPs showed differences between the control and CP groups. The ACC haplotype was more prevalent in the control group and the ATA haplotype more prevalent in the CP group. The ATA haplotype seemed to increase susceptibility to CP in women (odds ratio (OR)=2.57). The heterozygous haplotype GCC/ACC was predominant in the control group (OR=8.26; p=0.001). CONCLUSIONS: Specific haplotypes and SNPs in IL10 gene are associated with susceptibility to CP in Brazilian patients.     

Prevalence of OPG and IL-1 gene polymorphisms in chronic periodontitis

AIM: To investigate the association of polymorphisms in the osteoprotegerin (OPG) and interleukin 1 (IL-1) genes with chronic periodontitis (CP). MATERIAL AND METHODS: One hundred and ninety-four individuals (97 CP patients, 97 controls) were genotyped for the OPG polymorphisms Lys3Asn and Met256Val and for the IL-1 polymorphisms IL-1A (-889C/T) and IL-1B (+3953C/T). RESULTS: The homozygous variants coding for Lys3 were present at a higher frequency, whereas Asn3 and Met256 were present at a lower frequency in CP patients/controls (Lys3: 31%/25%, Asn3: 23%/32% and Met256: 66%/73%). Heterozygosity for Lys3Asn was observed at a higher frequency in CP patients/controls (46%/43%). Homozygosity for the Val256 genotype was observed in two CP patients (one in controls). Met256Val heterozygosity was more prevalent in CP patients/controls (32%/20%). All differences were statistically not significant between CP patients and controls. In contrast, both IL-1 polymorphisms were statistically significant. The heterozygous variant for IL-1A was present in 32% of the CP patients and in 20% of the controls (homozygosity (patients/controls) CC: 10%/21% and TT: 55%/33%). Heterozygosity for IL-1B was observed in 37% of the CP patients versus 34% in the controls (homozygosity (patients/controls) CC: 26%/57% and TT: 37%/9%). CONCLUSION: While the association between the IL-1 polymorphisms and CP was confirmed, no association between the OPG polymorphisms and CP could be found.     

Association of vitamin D receptor gene polymorphisms with chronic and aggressive periodontitis in Jordanian patients

Vitamin D acts through binding with vitamin D receptor (VDR) and is responsible for regulating bone metabolism and mineralization; it also suppresses the immune system. The aim of this study was to investigate if VDR gene polymorphisms are associated with chronic periodontitis (CP) and aggressive periodontitis (AgP) in a Jordanian population. A total of 99 patients with CP, 63 patients with AgP, and 126 controls were genotyped using PCR‐restriction fragment length polymorphism (RFLP) for BsmI, ApaI, and TaqI single nucleotide polymorphisms (SNPs). The association was determined after correcting for confounding factors using multivariate logistic regression analysis. Estimation of haplotype frequencies was carried out using the EH program, and haplotypes were constructed using the phase 2.1 program. After correcting for confounding factors, multivariate logistic regression analysis revealed that inheritance of the BsmI bb genotype or the ApaI aa genotype was associated with increased risk of developing CP (OR = 2.4 and OR = 3.4, respectively) but with reduced risk of developing AgP (OR = 0.4 and OR = 0.3, respectively). This was further supported by association of the ba haplotype with CP but not with AgP. This study supports an association of VDR gene polymorphisms with CP and AgP in a Jordanian population; however, the pattern of association was different between the two diseases.     

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.     

内皮细胞型一氧化氮合成酶Glu298Asp基因多态性与牙周炎伴Ⅱ型糖尿病的相关性研究

目的研究内皮细胞型一氧化氮合成酶（eNOS）Glu298Asp基因多态性与牙周炎伴Ⅱ型糖尿病易感性的关系。方法收集慢性牙周炎患者、慢性牙周炎伴Ⅱ型糖尿病患者、Ⅱ型糖尿病患者和牙周健康者的颊黏膜拭子,提取DNA后应用聚合酶链反应-限制性片段长度多态性法检测eNOS Glu298Asp的基因型分布。结果慢性牙周炎组、 Ⅱ型糖尿病组、慢性牙周炎伴Ⅱ型糖尿病组、正常组eNOS Glu298Asp基因型的分布差异有统计学意义（掊2＝18.503, P＝0.005）,等位基因频率分布差异也有统计学意义（掊2＝8.243,P＝0.041）。慢性牙周炎伴Ⅱ型糖尿病组与正常组相比,T基因型的OR值为0.962,95%可信区间为0.737～1.256,说明T基因型可能为糖尿病和牙周炎的保护因素;G基因型的OR值为1.043,95%可信区间为0.781～1.391,说明G基因型可能为二者的危险因素,但差异无统计学意义。结论慢性牙周炎、慢性牙周炎伴Ⅱ型糖尿病、糖尿病的易感性可能与eNOS Glu298Asp多态性有关。