Risk Of Chronic Periodontitis Research Articles

MMUNOHISTOCHEMICAL ANALYSIS OF NF-kB (P0/P) IN PATIENT WITH AGGRESSIVE AND CHRONIC PERIODONTITIS

Background: Nuclear factor-kappaB (NF-κB) is a protein complex that plays a role in transcription factors and in response to inflammation. Periodontitis is a periodontal disorder caused by various bacteria such as A. actinomycetemcomitan and P.gingivalis whose LPS is closely related to NFκB (p50/p65). Aim: This study observed whether NF-κB (p50/p65) played a role in aggressive and chronic periodontitis. Methods: Data were obtained from periodontal tissue 40 patients with aggressive periodontitis and 40 patients with chronic periodontitis. Samples were derived from periodontal tissue with abnormalities and NFκB (p50/p65) protein expression test was performed by immunohistochemistry. The statistical test used was the t-test. Results: In NF-κB (p50) the t value was -12 041 and significance 0.000, with α = 5%, showing significant difference in protein expression of NF-κB (p50) between patients with aggressive periodontitis and chronic periodontitis. OR estimation for the value of protein expression of NFκB (p50) was 0.64 (sign. = 0.000). It shows that if the protein expression of NFκB (p50) of the respondents is incremented by 1 (one) unit, the risk of chronic periodontitis increases 1.64 times. Box plot diagram shows that the distribution of the protein expression of NFκB (p50) between patients with aggressive periodontitis and chronic periodontitis patients is significantly different. In NF-κB (p65) the Z value was -7.137 and significance of 0000, with α= 5%, showed significant differences in protein expression of NF-κB (p65) between patients with aggressive periodontitis and chronic periodontitis. OR estimates for protein expression of NFκB (p65) was 0.66 (sign. = 0.000). This indicates that if the protein expression of NFκB (p65) respondents is incremented by 1 (one) unit, the risk of chronic periodontitis increases 1.5 times. Box plot diagram shows that the distribution of the protein expression of NFκB (p65) between patients with aggressive and chronic periodontitis patients is significantly different. Conclusion: The protein expression of NF-κB (p50/p65) has more influence on the incidence of chronic periodontitis patients, so it can be used as a marker for chronic periodontitis.

Interleukin-1α − 899 (+ 4845) C→T polymorphism increases the risk of chronic periodontitis: Evidence from a meta-analysis of 23 case–control studies

Many epidemiological studies have indicated that interleukin-1α (IL-1α) −899 (+4845) C→T polymorphism increases the risk of chronic periodontitis (CP), whereas some studies have reported opposite results. Accordingly, the aim of this meta-analysis is to investigate the association of the IL-1α −899 (+4845) C→T polymorphism with CP. We searched the PubMed database up to May 1, 2013 and finally obtained 23 case–control studies. After data extraction, we performed meta-analysis using Comprehensive Meta-Analysis v2.2 software. The overall result based on the fixed-effect model showed that IL-1α −899 (+4845) C→T polymorphism was significantly associated with increased risk of CP: [odds ratio (OR)=1.29, 95% confidence interval (CI)=1.15–1.44, p<0.001] for T vs. C; (OR=1.59, 95%CI=1.22–2.07, p=0.0005) for TT vs. CC; (OR=1.30, 95% CI=1.12–1.51, p=0.0004) for CT vs. CC; and (OR=1.40, 95% CI=1.21–1.61, p<0.001) for (CT+TT) vs. CC; (OR=1.47, 95% CI=1.16–1.87, p=0.002) for TT vs. (CT+CC). Stratified analyses revealed that there was a significantly increased risk for Caucasians and Asians. In conclusion, current evidence showed that IL-1α −899 (+4845) C→T polymorphism probably increased the risk of CP.

Chronic rhinosinusitis increased the risk of chronic periodontitis

Although chronic periodontitis (CP) and chronic rhinosinusitis (CRS) both share immunological disturbances as pathological factors, no prior study has investigated the risk for CP among patients with CRS. This study set out to provide an estimation of risk by utilizing a cohort study design to leverage the statistical power of a population-based dataset in Taiwan. A retrospective cohort study. In total, 13,782 CRS subjects were included in the study cohort and 41,346 subjects were randomly extracted for the comparison cohort. We individually tracked each subject in this study (N = 55,128) for a 5-year period following their index date to identify those subjects who received a subsequent diagnosis of CP. Cox proportional hazards regression analysis was conducted to calculate the 5-year risk of subsequent CP following a diagnosis of CRS among the sampled subjects. The incidence rate of CP during the 5-year follow-up period was 5.12 (95% confidence interval [CI], 4.95-5.30) per 100 person-years and 3.24 (95% CI, 3.17-3.30) per 100 person-years for the study and comparison cohort, respectively. Cox proportional hazards regression revealed that the hazard ratio for CP during the 5-year follow-up period for subjects with CRS was 1.59 times (95% CI, 1.52-1.67) that of comparison subjects after adjusting for monthly income, geographic region, hypertension, diabetes, coronary heart disease, and hyperlipidemia, and censoring for cases who died during the 5-year follow-up period. This study detected an increased risk for CP among patients suffering from CRS. CRS patients should be alerted to pay particular attention to their oral hygiene practices to prevent both CP and its downstream sequelae.

Association between MMP-1 g.-1607dupG Polymorphism and Periodontitis Susceptibility: A Meta-Analysis

BackgroundMatrix metalloproteinase-1 (MMP-1) plays an important role during the destruction of periodontal tissue. Although multiple studies had focused on the association between MMP-1 g.-1607dupG and periodontitis susceptibility, the results remained inconclusive. The purpose of this meta-analysis was to explore its role in the development of periodontitis.MethodsRetrieved studies from Pubmed, Web of Science, Medline and Google Scholar Search regarding MMP-1 g.-1607dupG and periodontitis susceptibility were included into the final analysis with definite selection and exclusion criteria. Overall and stratified analyses based on disease type, severity, ethnicity and smoking status were performed. Odds ratio (OR) and 95% confidence interval (CI) were used to evaluate the association between MMP-1 g.-1607dupG and periodontitis susceptibility, while Q test and Egger’s test were adopted respectively to assess heterogeneity among studies and publication bias.ResultsA total of 1580 periodontitis cases and 1386 controls in 11 case-control studies were included in the meta-analysis. The pooled results showed significant association between periodontitis susceptibility and MMP-1 g.-1607dupG polymorphism in homozygote (2G/2G versus 1G/1G, OR = 1.50, 95% CI = 1.02–2.20) and dominant model analysis (2G/2G+2G/1G versus 1G/1G, OR = 1.28, 95% CI = 1.04–1.57). For subgroups by type of periodontitis, increased risk of chronic periodontitis was observed on heterozygote (2G/1G versus 1G/1G, OR = 2.01, 95% CI = 1.58–2.56) and dominant model (OR = 1.27, 95% CI = 1.03–1.57). Furthermore, similar association was also detected in severe chronic periodontitis (2G/2G versus 1G/1G, OR = 2.15, 95% CI = 1.35–3.43; 2G/2G+2G/1G versus 1G/1G, OR = 1.64, 95% CI = 1.12–2.39; 2G/2G versus 2G/1G+1G/1G, OR = 1.86, 95% CI = 1.31–2.64).ConclusionsOur meta-analysis demonstrated that MMP-1 g.-1607dupG polymorphism was associated with chronic periodontitis, especially the severity of the disease condition.

BRAF gene polymorphism (rs10487888) assessment in chronic periodontitis and peri-implantitis in an Iranian population

Peri-implantitis (PI) and chronic periodontitis (CP) are multifactorial diseases of implant/tooth supporting tissue that are caused by bacterial infection and increased host immune response. T-cell proliferation plays a pivotal role in the orchestration of host response to bacterial infection. BRAF is a positive regulator of T-cell proliferation. The aim of this study was to evaluate for the first time the role of a functional single nucleotide polymorphism (SNP) of the BRAF gene in association to PI and CP. A total of 194 individuals referred to the Periodontology Department of Shahid Beheshti Dental School, Tehran, Iran, were divided into three groups: 74 patients in the CP group (39 men and 35 women, with mean age of 48.3 years), 38 patients in the PI group (20 men and 18 women, with mean age of 50.2 years), and 82 patients in the healthy periodontium group (39 men and 43 women, with mean age of 45.4 years). DNA was extracted from fresh blood samples collected from the arm vein of participants and was transferred to KBiosience institute (United Kingdom) for genotyping. χ2 and Kruskal-Wallis tests were conducted using SPSS software v. 19 for statistical analysis (p<0.05). The allele (C/T) and genotype (CC, CT, TT) frequencies had insignificant differences among the three groups; however, the CC genotype was more prevalent in the healthy condition than in the disease conditions. The BRAF gene polymorphism (rs10487888) may not be a genetic determinant for increasing the risk of CP and PI among the Iranian population. More studies with more sample size in different populations are necessary for determining the effect of this SNP.

Association of TGF-β1 − 509 C/T, 29 C/T and 788 C/T gene polymorphisms with chronic periodontitis: A case–control study

The aim of this study was to investigate the possible association between TGF-β1 −509 C/T (rs1800469), 29 C/T (Prol10Leu, rs1800470) and 788 C/T (Thr263Ile, rs1800472) gene polymorphisms and chronic periodontitis (CP) in a sample of Iranian population. This case–control study was conducted on 100 CP patients and 100 healthy unrelated, age-, sex-, and ethnicity-matched. Genotyping was performed by tetra amplification refractory mutation system-polymerase chain reaction (T-ARMS-PCR) technique. Our findings showed that there was a significant difference between the groups regarding TGF-β1 29 C/T (rs1800470) polymorphism (χ2=23.23, P<0.0001). The CT and TT genotypes increased the risk of CP in comparison with the CC genotype (OR=4.42, 95% CI=2.16–9.06, P<0.001 and OR=5.84, 95% CI=2.32–14.71, P<0.001, respectively). The T allele increased the risk of CP (OR=2.50, 95% CI=1.66–3.74, P<0.001) in comparison with C allele. No significant association was found among the groups regarding −509 C/T and 788 C/T variants of TGF-β1 gene. This study shows that TGF-β1 29 C/T polymorphism, but not −509 C/T and 788 C/T polymorphisms, may contribute to the development of CP in a sample of Iranian population. Further studies with larger sample sizes and different ethnicities are needed to validate our findings.

MiR146a and MiR499 Gene Polymorphisms in Iranian Periodontitis and Peri-implantitis Patients

MicroRNAs (MiRs) are small noncoding RNAs that are involved in protein translation, osteoclastogenesis, and immunoregulation. Peri-implantitis and chronic periodontitis are multifactorial diseases. They are the consequence of complex interactions among host response, genetics, and environment. In the present study, we aimed to investigate the possible association between MiR146a/MiR499 gene polymorphisms and periodontitis/peri-implantitis as a first report in oral implantology. From 197 individuals referred to Periodontology Department of Shahid Beheshti Dental School, three groups were enrolled in the assessment: 75 patients in the chronic periodontitis (CP) group, 38 patients in the peri-implantitis (PI) group, and 84 healthy subjects. DNA was extracted from fresh blood samples from the arm veins of participants and transferred to KBiosience Institute (Hoddesdon, United Kingdom) for genotyping. Chi-squared and Kruskal-Wallis tests were performed using SPSS software v.19 for statistical analyses. P-value < 0.05 was considered significant. The genotype frequencies in MiR 146a and MiR 499 were significantly different among the three groups. MiR146a (rs2910146) and MiR499 (rs3746444) gene polymorphisms may be genetic determinants for increased risk of chronic periodontitis and peri-implantitis in Iranians. More studies with larger sample sizes in different populations are necessary for determining the effect of these SNPs.

Association among stress, salivary cortisol levels, and chronic periodontitis

PurposeChronic periodontitis (CP) seems to be associated with stress and depression, but little information on this possible association is available in the literature. Thus, the objective of this study was to evaluate the association among stress, the salivary cortisol level (SCL), and CP.MethodsSeventy systemically healthy subjects were included in the study from January to September 2011. Full medical and dental histories were obtained, and the following measurements were recorded: 1) probing depth; 2) clinical attachment level; 3) bleeding on probing; and 4) tooth mobility. Saliva samples were collected for the evaluation of SCL (via a highly sensitive electrochemiluminescence immunoassay), and all subjects also answered a questionnaire (i.e., the Zung Self-rating Depression Scale). The odds ratio (OR) with a 95% confidence interval (CI) was calculated, and one way analysis of variance and the Tukey-Kramer method were performed.ResultsA total of 36 subjects with CP (51.4%) and 34 without CP were evaluated. Of them, all of the subjects with CP and one periodontally healthy subject were diagnosed with depression. Subjects with moderate CP had statistically significantly higher levels of SCL than subjects with a diagnosis of slight CP (P=0.006). Also, subjects with severe CP showed the same outcome when compared to those with slight CP (P=0.012). In addition, 46 subjects presented high SCL whereas 24 had a normal level. CP was found to be correlated with the SCL, with an OR of 4.14 (95% CI, 1.43 to 12.01).ConclusionsSubjects with a high SCL and depression may show an increased risk for CP.

MMP‐9 ‐1562C&gt;T contributes to periodontitis susceptibility

The study was conducted to explore the potential association of Matrix metalloproteinases (MMP)-9 -1562C>T with susceptibility to periodontitis. Electronic literature searches of PubMed, EMBASE and EBSCO databases were performed. Fixed-effects or random-effects models were used to calculate the pooled odds ratios (ORs) for four genetic comparisons. Seven eligible studies with a total of 628 cases and 689 controls were recruited in the pooled analysis. We found MMP-9 -1562C>T contributed to decreased risk of chronic periodontitis. Furthermore, the polymorphism was associated with modified risk of periodontitis among Caucasian populations. This study indicated that MP-9 -1562C>T might be involved in the development of periodontitis. A replication of our results in independent large analysis populations is necessary to give evidence to our observation.

Modeling Susceptibility to Periodontitis

Chronic inflammatory diseases like periodontitis have a complex pathogenesis and a multifactorial etiology, involving complex interactions between multiple genetic loci and infectious agents. We aimed to investigate the influence of genetic polymorphisms and bacteria on chronic periodontitis risk. We determined the prevalence of 12 single-nucleotide polymorphisms (SNPs) in immune response candidate genes and 7 bacterial species of potential relevance to periodontitis etiology, in chronic periodontitis patients and non-periodontitis control individuals (N = 385). Using decision tree analysis, we identified the presence of bacterial species Tannerella forsythia, Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, and SNPs TNF -857 and IL-1A -889 as discriminators between periodontitis and non-periodontitis. The model reached an accuracy of 80%, sensitivity of 85%, specificity of 73%, and AUC of 73%. This pilot study shows that, on the basis of 3 periodontal pathogens and SNPs, patterns may be recognized to identify patients at risk for periodontitis. Modern bioinformatics tools are valuable in modeling the multifactorial and complex nature of periodontitis.

Association of the IL-10 polymorphisms and periodontitis: a meta-analysis

No clear consensus has been reached regarding the association of IL-10 polymorphisms and periodontitis. Therefore, we performed a meta-analysis of case-control studies and a systemic review in an effort to systematically summarize the existing knowledge. Studies were identified by searching PubMed database until December 2011. IL-10 -1082 (-1087) A>G, -819 (-824) C>T and -592 (-597) C>A polymorphisms were included in the present meta-analysis. We calculated the specific odds ratios along with their 95 % confidence intervals to compare the distribution of alleles and genotypes between cases and controls. An additive "per-allele" model (major allele vs. minor allele) was performed, and dominant and recessive models were also considered. The random-effects model was applied for the analysis. Cumulative analysis was also performed. Heterogeneity and publication bias were assessed. Nine case-control studies involving 841 periodontitis cases (644 chronic periodontitis and 197 aggressive periodontitis cases) and 748 controls were included. We found statistically significant association of IL-10 -819 (-824) C>T and IL-10 -592 (-597) C>A polymorphisms in Caucasians. The IL-10 -819 (-824) T and -592 (-597) A alleles may confer a relative increase in the risk for chronic periodontitis in Caucasians. Future studies may be important to reinforce these findings.

Interleukin-10 gene polymorphisms and chronic/aggressive periodontitis susceptibility: A meta-analysis based on 14 case-control studies

Interleukin-10 (IL-10) has been described as an anti-inflammatory cytokine and IL-10 gene polymorphisms was associated with altered interleukin-10 levels, therefore, we aimed to conduct a meta-analysis assessing the association of IL-10 genetic polymorphisms with the risk of both chronic periodontitis (CP) and aggressive periodontitis (AgP). Electronic databases were acquired from PubMed, Embase, the Sinomed and WANFANG. Fourteen studies with 1438 patients and 1303 control subjects investigated the association of the three single-nucleotide polymorphisms (SNPs) of IL-10 (−1082A>G, −819C>T, −592C>A) and chronic/aggressive periodontitis risk were brought into this study. We found that there was no association between IL-10 −1082 gene polymorphism and periodontitis risk (either CP or AgP), even when we separately investigated sub-group analysis among Caucasians. The −819 polymorphism seemed to be a genetic risk factor to CP among Caucasians (T allele vs. C allele: OR=1.55, 95%CI=1.07–2.24; CT vs. CC: OR=1.64, 95%CI=1.00–2.67). When excluding one study deviated from HWE, the results showed that the T allele carriers had a significantly risk of CP in overall population (T allele vs. C allele: OR=1.23, 95%CI=1.03–1.48). Furthermore, the results of this meta-analysis showed that −592 polymorphism was associated with a significantly increased risk of CP (A allele vs. C allele: OR=1.38, 95%CI=1.04–1.85; AA vs. CA+CC: OR=1.39, 95%CI=1.05–1.85 for overall analysis; A allele vs. C allele: OR=1.97, 95%CI=1.36–3.86; AA vs. CC: OR=3.70, 95%CI=1.32–10.39; CA vs. CC: OR=2.22, 95%CI=1.36–3.64, AA+CA vs. CC: OR=2.35, 95%CI=1.46–3.79 for Caucasian descent analysis). This meta-analysis suggested that IL-10 −819 and −592 gene polymorphisms were associated with CP, especially among Caucasians. Further research is needed to assess possible gene–gene or gene-environment-lifestyle interactions on periodontal disease..

Influence of cytotoxic T lymphocyte antigen-4 (CTLA-4) gene polymorphisms in periodontitis

AimPersistent host inflammatory immune response against the pathogens results in the destruction of periodontal tissues. Cytotoxic T lymphocyte antigen 4 (CTLA-4) is a particularly important molecule in down-regulating T-cell expansion and cytokine production. This study aimed to assess three functional SNPs within CTLA-4 gene, −1722 T/C, −318 C/T, and +49 A/G in patients with aggressive or chronic periodontitis. Materials and methodsA total of 197 patients with periodontitis (71 aggressive and 126 chronic periodontitis) and 218 healthy controls were recruited. All samples were genotyped for CTLA-4 gene polymorphisms by polymerase chain reaction-amplification refractory mutation system (PCR-ARMS). ResultsThe allelic and genotype frequencies of only +49 A/G SNP were more prominence in patients with chronic periodontitis (CP) than that controls (0.0005 and 0.001, respectively). Multivariate logistic regression analysis was demonstrated that homozygosity in +49 G/G had profoundly increased susceptibility for CP, OR=3.7 (95% CI; 1.6–8.5, P=0.001). In addition, comparison of CTLA-4 SNPs between patients with CP and aggressive periodontitis (AgP) revealed that heterozygosity in −1722 T/C polymorphism of CTLA-4 gene had a significantly higher risk for CP compared with AgP with a calculated odds ratio of 2.18 (95% CI; 1.17–4.06, P=0.01). ConclusionThese results suggest that CTLA-4 gene variants might be associated to susceptibility to specific form of periodontitis and participate in the CP development.

Association between Polymorphisms in Interleukin-17A and -17F Genes and Chronic Periodontal Disease

Objective. Interleukin-17 (IL-17) is a cytokine that induces neutrophil recruitment and the release of inflammatory mediators in several inflammatory conditions; nevertheless, the involvement of IL-17 gene polymorphisms in chronic periodontitis (CP) has not been addressed yet. Our aim was to evaluate the association between periodontal status and the polymorphisms IL-17A G197A and IL-17F C7488T in subjects with CP along with their impact on levels of inflammatory mediators. Material and Methods. Genomic DNA was obtained from 30 CP patients and 30 healthy controls (HCs). IL-17A G197A and IL-17F C7488T polymorphisms were determined using PCR-RFLP. Serum and periodontal tissues were collected and processed for ELISA, myeloperoxidase (MPO), and/or microscopic analysis. Results. The frequencies of genotypes in the CP group were significantly different from those of HC. Odds ratio indicated that increased risks for CP were associated with the -197A allele, not with the -7488T allele. In addition, the -197A allele was correlated with worse clinical parameters, higher MPO activity, and increased expression of inflammatory mediators (IL-17A and IL-8) than the other genotypes. Conclusions. These results indicate that the IL-17A -197A allele is associated with increased risk for CP, likely because this genotype relates to the enhanced inflammation in periodontal tissues.

O10 Periodontal disease in rheumatoid arthritis and its significance in relation to anti CCP

Matrix metalloproteinases (MMPs) are involved in periodontal tissue remodeling and degradation. MMP polymorphisms could alter transcription and function of these enzymes. The aim of this study was to investigate MMP-2, MMP-9 and MMP-12 gene polymorphisms in relation to susceptibility to severe chronic periodontitis (CP).Genomic DNA was obtained from peripheral blood of 87 severe CP patients and 107 periodontally healthy subjects. MMP-2 −735C/T, MMP-9 −1562C/T and MMP −12357Asn/Ser gene polymorphisms were genotyped by polymerase chain reaction and restriction fragment length polymorphism. Probing depth, clinical attachment loss, supragingival plaque accumulation and bleeding on probing were recorded. The data were analyzed by chi-square, logistic regression and Mann–Whitney-U-tests.The genotype distributions and allele frequencies of MMP-2, MMP-9 and MMP-12 genes were similar in CP and healthy subjects (p > 0.05). Differences between rare allele carriage rates of CP and healthy groups regarding MMP-2, MMP-9 and MMP-12 gene polymorphisms were not significant (p > 0.05). However, T allele carriers of MMP-9 −1562 gene had less risk for CP (OR = 0.36; 95% CI = 0.16–0.81).These data suggest that MMP-2 −735C/T, MMP-9 −1562C/T and MMP-12 357Asn/Ser polymorphisms are not associated with susceptibility to severe CP in Turkish population. However, T allele of MMP-9 −1562 gene might be associated with decreased susceptibility to severe CP.

Validation of an Algorithm for Chronic Periodontitis Risk Assessment and Prognostication: Analysis of an Inflammatory Reactivity Test and Selected Risk Predictors

Patients with severe forms of chronic periodontitis present with varying degrees of decreased inflammatory reactivity. A previously reported algorithm for chronic periodontitis risk assessment and prognostication is based on the analysis of some 20 risk predictors. One of these predictors is a skin provocation test that assesses the individual patient's reactivity to a lipid A challenge. The aim of this report was to analyze results from validation data for the algorithm with respect to the contribution of results of the skin provocation test as a risk predictor for the progression of chronic periodontitis and to compare these results with the contribution from other predictors, namely smoking, angular bony destruction, furcation involvement, abutment teeth, and endodontic pathology. Data from a previously reported clinical validation sample were used for the analysis, including the calculation of quality measures and explanatory values using different types of regression analysis and non-parametric testing. Smoking, endodontic pathology, abutment teeth, angular bony destruction, and furcation involvement presented with individual explanatory values for periodontitis progression between 4% and 13% and highly significant parameter estimates. Explanatory values for the results of the skin provocation test ranged between 2.6% and 5.1% depending on the disease severity group, with a positive predictive value of 82% for the identification of high-risk patients. The skin provocation test provided a clinically significant contribution to the quality of analysis with the periodontitis risk and prognostication algorithm, in particular in the selection of high-risk patients for in-depth individual tooth analysis.

Validation of an Algorithm for Chronic Periodontitis Risk Assessment and Prognostication: Risk Predictors, Explanatory Values, Measures of Quality, and Clinical Use

The American Academy of Periodontology has recently stated that, "[risk assessment will become] increasingly important in periodontal treatment planning and should be part of every comprehensive dental and periodontal evaluation." (J Periodontol 2006;77:1608). Unaided risk assessment and prognostication show significant variability because chronic periodontitis is a multifactorial disease. This report summarizes the clinical validation of an algorithm for chronic periodontitis risk assessment and prognostication. The algorithm is a Web-based analytic tool that integrates some 20 risk predictors and calculates scores indicating levels of risk for chronic periodontitis for the dentition (Level I) and, if an elevated risk is found, prognosticates disease progression tooth by tooth (Level II). An independent clinical validation sample was generated in an open, prospective clinical trial and analyzed in a predetermined validation plan. The analyses identified two threshold scores above which significant progression of periodontitis was found. Based on these scores, sufficiently high explanatory values with significant and increasing parameter estimates for increasing risk were established in Level I, justifying detailed analysis tooth by tooth in Level II. Subsequent prognostication of chronic periodontitis in Level II was found to be accompanied by clinically relevant measures of quality in relation to rates of disease progression. Three score intervals representing increasing levels of periodontitis progression were identified corresponding to increasing levels of significant annual marginal bone loss. The predictors included in the algorithm reflect a relevant selection for periodontitis risk assessment. Risk assessment and prognostication with the algorithm provides the clinician with a validated, reliable, consistent, and objective tool supporting treatment planning.

Interleukin-6 polymorphisms modify the risk of periodontitis:a systematic review and meta-analysis

To clarify the association of IL-6 polymorphisms and periodontitis, a meta-analysis of case-control studies and a systemic review were conducted. We performed a literature search using PubMed and Medline database to May 2009, with no restrictions. We also reviewed references from all retrieved articles. Six case-control studies involving 1 093 periodontitis cases and 574 controls were selected for meta-analysis to assess the purported associations between IL-6 polymorphisms and the risk of periodontitis. IL-6 -174 G/C and -572 C/G polymorphisms were included in the present meta-analysis, and the association between IL-6 -6331 T/C polymorphism and the risk of periodontitis was adequately reviewed as well. The present meta-analysis indicates that the IL-6 -174 G allele could not modify the risk of chronic periodontitis, but increased the risk of aggressive periodontitis. And -572 C/G polymorphism is associated with the pathogenesis of periodontitis, including chronic periodontitis or aggressive periodontitis.

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

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. 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 chi(2) test and the odds ratios (ORs) were calculated by logistic regression analysis. 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). It suggests the -1195A variant is associated with an increased risk for severe CP.

Renin–angiotensin gene polymorphisms in relation to severe chronic periodontitis

Evidence suggests that the ultimate product of the renin-angiotensin system (RAS), angiotensin II, exerts inflammatory actions. The present study aimed to evaluate the inter-relation between gene polymorphisms of the RAS components; angiotensin converting enzyme (ACE), angiotensinogen (AGT) and angiotensin II type-I receptor (AT1R), and severe chronic periodontitis (CP). DNA was obtained from peripheral blood of 90 CP patients and 126 periodontally healthy subjects, and the clinical parameters were recorded. ACE I/D, AGT M235T and AT1R A1166C polymorphisms were genotyped by the PCR-RFLP method. Chi-square, anova and logistic regression methods were used in statistical analyses. The frequency of the ACE D allele was significantly lower in the CP group than the healthy group (p(corr)=0.015). CP subjects exhibited increased C allele carriage and C allele frequency of the AT1R gene (p(corr)=0.03 and p(corr)=0.03, respectively). All clinical parameters of CP patients were found to be similar in variant allele-carrying and non-carrying subjects (p>0.05). The present findings suggest that ACE I/D and AT1R polymorphisms might be associated with susceptibility to CP but not with disease severity. The D allele of ACE I/D might be associated with decreased, whereas the C variant of AT1R A1166C might be associated with an elevated risk for CP in Turkish population.