Periodontitis and Diabetes Complications: A Danish Population-Based Study.

Conflicting evidence suggests a link between diabetes-related microvascular complications and periodontitis. Reliable estimates have been hindered by small sample sizes and residual confounding. Moreover, the combined effects of microvascular complications and dyslipidemia on periodontitis have not been explored. Therefore, this study aimed to investigate the association between individual and combined diabetic microvascular complications (i.e., neuropathy and retinopathy) and moderate/severe periodontitis in a Danish population-based study. In addition, we assessed whether dyslipidemia modified these associations. This study comprised 15,922 participants with type 2 diabetes from the Health in Central Denmark study. Multinomial logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for individual and joint microvascular diabetes complications. The models adjusted for potential confounders, including sociodemographic factors, lifestyle behaviors, and health conditions. Inverse probability of treatment weighting (IPTW) balanced measured confounders between periodontitis and nonperiodontitis participants. Sensitivity analyses tested the findings' robustness by estimating E-values for unmeasured confounding and varying microvascular complication definitions. After IPTW, adjusted models revealed that diabetic neuropathy (OR 1.36, 95% CI 1.14 to 1.63) and retinopathy (OR 1.21, 95% CI 1.03 to 1.43) were significantly associated with moderate/severe periodontitis. Moreover, the coexistence of microvascular complications increased the odds 1.5-fold for moderate/severe periodontitis (OR 1.51, 95% CI 1.23 to 1.85). An effect modification of dyslipidemia on an additive scale was found, indicated by a positive relative excess risk due to interaction of 0.24 for neuropathy, 0.11 for retinopathy, and 0.44 for both complications. Sensitivity analysis ruled out unmeasured confounders and microvascular complication definitions as explanatory factors. Diabetic neuropathy and retinopathy, individually and combined, were associated with moderate/severe periodontitis. In addition, dyslipidemia had an additive positive effect modification on diabetic microvascular complications, elevating the odds of moderate/severe periodontitis. These findings may aid in identifying at-risk subgroups for diabetes-related microvascular complications and periodontitis, optimizing efforts to mitigate disease burden.

Co-occurrence of Periodontitis and Diabetes-Related Complications.

Periodontitis is a common finding among people with diabetes mellitus (DM) and has been cited as a DM complication. Whether and how periodontitis relates to other diabetes-related complications has yet to be explored. This study aims to examine the clustering of periodontitis with other diabetes-related complications and explore pathways linking diabetes-related complications with common risk factors. Using data from participants with DM across 3 cycles of the National Health and Nutrition Examination Survey (NHANES) (n = 2,429), we modeled direct and indirect pathways from risk factors to diabetes-related complications, a latent construct comprising periodontitis, cardiovascular diseases, proteinuria, and hypertension. Covariates included age, sex, socioeconomic status (SES), smoking, physical activity, healthy diet, alcohol consumption, hemoglobin A1c (HbA1c), dyslipidemia, and body mass index (BMI). Sensitivity analyses were performed considering participants with overweight/obesity and restricting the sample to individuals without DM. Periodontitis clustered with other diabetes complications, forming a latent construct dubbed diabetes-related complications. In NHANES III, higher HbA1c levels and BMI, older age, healthy diet, and regular physical activity were directly associated with the latent variable diabetes-related complications. In addition, a healthy diet and BMI had a total effect on diabetes-related complications. Although sex, smoking, dyslipidemia, and SES demonstrated no direct effect on diabetes-related complications in NHANES III, a direct effect was observed using NHANES 2011-2014 cycles. Sensitivity analysis considering participants with overweight/obesity and without DM showed consistent results. Periodontal tissue breakdown seems to co-occur with multiple diabetes-related complications and may therefore serve as a valuable screening tool for other well-known diabetes-related complications.

Effect of Smoking Exposure on Nonsurgical Periodontal Therapy: 1-Year Follow-up.

This study investigated the influence of different levels of exposure to smoking on periodontal healing for 12 mo after nonsurgical periodontal therapy and supportive periodontal care every third month. Eighty smokers willing to quit smoking and with periodontitis were included. Participants were offered an individualized voluntary smoking cessation program. Data collection included questionnaires and a full-mouth periodontal examination. Group-based trajectory modeling was used to model smoking trajectories over the follow-up. The effect of smoking trajectory on periodontal parameters over time was estimated with mixed effects modeling. Three smoking patterns were identified: light smokers/quitters (n = 46), moderate smokers (n = 17), and heavy smokers (n = 17). For the periodontal data, the first factor, moderate periodontitis, included the number of sites with clinical attachment levels (CALs) of 4, 5, 6, and 7 mm; periodontal pocket depths (PPDs) of 4, 5, and 6 mm; and bleeding on probing. The second factor, severe periodontitis, consisted of the number of sites with a CAL ≥8 mm and PPD ≥7 mm. Heavy smokers commenced with a higher average CAL of 1.1 mm and 10 more sites with severe periodontitis than light smokers/quitters. While light smokers/quitters and moderate smokers obtained an average improvement of 0.6-mm PPD and 0.7-mm CAL, respectively, heavy smokers experienced 0.5-mm attachment loss. Heavy smokers had only a 50% reduction in the number of sites with moderate periodontitis when compared with light smokers/quitters and moderate smokers. While most participants benefited from nonsurgical periodontal therapy with results affected in a dose-response manner, the therapy had no effect on severe periodontitis among heavy smokers. Smoking cessation should be part of periodontal therapy; otherwise, limited benefits would be observed among heavy smokers, hindering the effect of treatment.

Is there a relationship between obesity and tooth loss and edentulism? A systematic review and meta-analysis.

This study conducted a systematic review to assess the bi-directional association between tooth loss/edentulism and obesity. Electronic searches were performed in four different databases. Observational studies that tested associations between tooth loss/edentulism and obesity as either exposures or outcomes were included. Additionally, meta-analyses, funnel plots and sensitivity analyses were conducted to synthesize the evidence. A total of 549 articles were identified in the electronic database search. Out of which, 16 studies were included within the meta-analyses: 75% considered tooth loss/edentulism as exposure and obesity as outcome, whereas 25% alternatively considered obesity as exposure and tooth loss/edentulism as outcome. Pooled estimates showed that obese individuals had 1.49 (95%CI 1.20-1.86) and 1.25 (95%CI 1.10-1.42) times higher odds of having any tooth loss and edentulism, respectively. Alternatively, when tooth loss or edentulism were considered as exposures, individuals with any tooth loss had 1.41 (95%CI 1.11-1.79) times higher odds for obesity, while edentates had even higher odds (OR 1.60; 95%CI 1.29-2.00). The results indicate a bi-directional association between tooth loss and obesity. Considering that all selected studies were of cross-sectional study design limiting inferences on temporality, longitudinal prospective studies are required to test the causal relationship between tooth loss/edentulism and obesity or vice a versa. © 2016 World Obesity.

Polimorfismo genético da glicose-6-fosfato desidrogenase na população da região de Araraquara, Estado de São Paulo / Genetic polymorphism of glucose-6-phosphate dehydrogenase in the population of Araraquara, State of São Paulo

The most important role played by the enzyme Glucose-6-Phosphate Dehydrogenase (G6PD) in erythrocyte metabolism is in generating energy and reducing power used to protect the cell against oxidative attack. G6PD deficiency is the erythroenzymopathy that most frequently causes hemolytic anemia, and more than 130 molecular variants have already been identified. The aim of this study was to analyze the genetic mutations in the G6PD-deficient adult males in the population of the region of Araraquara, São Paulo State. Out of 5087 male blood donors, 89 were deficient for G6PD, as confirmed by assaying the enzyme activity and electrophoresis on cellulose acetate. Thus, a frequency of 1.75% of G6PD-deficient patients was found, this value being similar to other investigations in São Paulo state. Molecular analysis was performed by amplification of genomic DNA with specific primers and digestion with restriction enzymes. In 96.6% of the patients, the G6PD A¯ variant was observed, with mutations at residues 376(A-G) and 202(G-A). Mean G6PD specific activity among the patients was 1.31 IU.g Hb-1.min-1 at 37ºC, that is 10.8% of the normal activity of the G6PD B enzyme. The variant forms G6PD A¯680(G-T) and 968(T-C) were not found. In 3.4% of the deficient individuals, the G6PD Mediterranean variant was found, with a mutation at 563(C-T). In these cases,mean enzymatic activity was 0.25 IU.g Hb-1.min-1 at 37ºC, or 2.1% of the enzymatic activity of G6PD B. Theuse of traditional techniques, allied to the identification of the different molecular variants, is important for the understanding of the structural and functional properties and hemolytic behavior of the red blood cells of the patient...

A importância da enzima Glicose-6-fosfato desidrogenase (G6PD) no metabolismo eritrocitário está na obtenção de energia calórica e redutora para a proteção celular contra agressões oxidativas. A deficiência de G6PD é a eritroenzimopatia que causa mais frequentemente anemia hemolítica, com mais de 130 variantes moleculares identificadas. O objetivo deste estudo foi realizar a análise molecular da deficiência de G6PD em uma população masculina adulta da região de Araraquara, SP, para a identificação das mutações genéticas. Nos 5087 doadores de sangue do sexo masculino pesquisados, foram encontrados 89 deficientes de G6PD, confirmados pela determinação da atividade enzimática e eletroforese em acetato de celulose, com frequência de 1,75%, valores semelhantes aos encontrados por outros pesquisadores no Estado de São Paulo. A análise molecular realizada pela amplificação do DNA genômico com iniciadores específicos e digestão com enzimas de restrição, demonstrou que 96,6% dos deficientes apresentaram a variante G6PD A¯, com as mutações 376(A-G) e 202(G-A) e atividade enzimática média de 1,31 UI.g de Hb-1.min-1 a 37ºC, correspondendo a 10,8% da atividade enzimática da enzima normal G6PD B. Não foram encontradas as formas variantes G6PD A¯ 680(G-T) e 968(T-C). Em 3,4% dos indivíduos deficientes, foi encontrada a variante G6PD Mediterrânea, mutação 563(C-T) e atividade enzimática média de 0,25 UI.g de Hb-1.min-1 a 37ºC, correspondendo a 2,1% da atividade enzimática da G6PD B. A utilização das técnicas tradicionais, aliadas à identificação da variante molecular, são importantes na compreensão das propriedades estruturais, funcionais e comportamento hemolítico dos glóbulos vermelhos do paciente...

A double-blind randomised clinical trial of two techniques for gingival displacement.

Knowledge about security and the potential damage originated by the gingival displacement techniques has not been described through randomised clinical studies. This crossover, double-blind, randomised clinical trial evaluated clinical and immunological factors related to conventional and cordless gingival displacement (GD) techniques, and patients' perceptions in 12 subjects with the employment of 2 GD techniques: conventional (gingival cord + 25% AlCl3 astringent gel) and cordless (15% AlCl3 astringent-based paste). In each subject, two anterior teeth were treated and a 10-day wash-out period separated the two treatments. Periodontal indices were evaluated before (baseline) and 1 and 10 days after GD. Interleukin 1ß, interleukin 6 and tumour necrosis factor α concentrations in gingival crevicular fluid were measured before and 1 day after GD. Subjective parameters (pain, unpleasant taste and stress) were also evaluated. Data were analysed by one-way repeated-measures analysis of variance and Tukey's test (immunological factors), the Friedman test (periodontal parameters) and Fisher's exact or chi-squared test (subjective parameters), with a significance level of 95%. Gingival bleeding index, probing depth and plaque index values did not differ significantly between groups at any timepoint. Neither technique resulted in worse periodontal indices. Both techniques yielded similar results for pain and unpleasant taste, but conventional GD was significantly more stressful than cordless GD for volunteers. Both treatments significantly increased mean concentrations of the three cytokines, with the conventional technique producing the highest cytokine levels. Cordless GD is less stressful for patients and results in lower post-treatment levels of inflammatory cytokines compared with conventional GD.