Redox biomarkers in saliva and nuclear abnormalities in jugal epithelial cells of individuals with type 2 diabetes mellitus and periodontitis.

OBJECTIVE: To evaluate salivary redox biomarkers levels in individuals with periodontitis and type 2 diabetes mellitus (T2DM) and correlate with periodontal parameters and nuclear alterations in epithelial cells from jugal mucosa. DESIGN: Sixty individuals were categorized into three groups: T2DM with periodontitis (DM, n = 20), non-T2DM with periodontitis (PE, n = 20), and non-T2DM with periodontal health (HC, n = 20). All participants underwent fasting blood glucose and glycated hemoglobin measurements. After a periodontal examination, samples of epithelial cells from the jugal mucosa and saliva were collected. DNA damage was assessed by counting nuclear abnormalities using cytological analysis. Biomarkers of oxidative stress were determined through biochemical methods. Significant differences among groups were assessed using Kruskal-Wallis, Mann-Whitney, and Chi-square tests at a 5% significance level. Data were analyzed using Spearman's correlation coefficient, linear regression, and logistic regression. RESULTS: Frequencies of nuclear abnormalities, as well as levels of reduced glutathione and uric acid, were significantly higher in the DM group compared to the PE and HC groups (p < 0.05). Fasting glucose, glycated hemoglobin, nuclear abnormalities, reduced glutathione, and uric acid exhibited positive correlations with periodontal parameters (p < 0.05). Furthermore, reduced glutathione was associated with dental biofilm (OR = 1.027 [95% CI, 1.004-1.049]) and condensed chromatin (OR = 0.415 [95% CI, 0.196-0.878]). CONCLUSIONS: Periodontitis and T2DM are correlated with nuclear abnormalities, as well as salivary reduced glutathione and uric acid levels. Moreover, a higher prevalence of teeth with dental biofilm increases the likelihood of elevated levels of reduced glutathione in saliva, while the presence of condensed chromatin decreases that likelihood.

Coronary atherosclerosis and periodontitis have similarities in their clinical presentation.

Background: Periodontitis (PE) and coronary heart disease (CHD) possess multiple mechanisms for a putative association. This case-control study compared the periodontal status among CHD subjects to controls without CHD, while also investigating atheroma invasion by known periodontal pathogens. Methods: 161 subjects participated in this study were divided into three CHD groups: No CHD, chronic CHD, acute CHD. Additional analysis involved grouping subjects according to number of atheromas: no atheroma, 1-4 atheromas, 5-18 atheromas. Data were collected from medical records, periodontal examinations, and questionnaires that included demographic, behavioral, and oral health variables. Angiographic catheterizations were analyzed according to the number of atheroma lesions, lesion size, lesion location, and atheroma lesion stability. Lipoprotein profile, inflammatory markers and cells were analyzed. The microbiological branch added 30 individuals who had their atheroma lesion and subgingival plaque analyzed using polymerase chain reaction probes against the 16 s region, red complex and Aggregatibacter actinomycetemcomitans' DNA. Results: Subjects with CHD had high levels of systemic inflammatory markers and low levels of high-density lipoproteins compared to subjects without CHD. Subjects without CHD and clear coronaries had a prevalence of mild CAL, while individuals with more atheroma lesions had advanced CAL and more active PE. Subjects with more advanced CAL were 4 times more likely to have CHD compared to subjects with less, which is comparable to smoking. Only 4 subjects had the screened pathogens detected in atheroma, although these subjects also have the screened pathogens in subgingival plaque. However, 80% of atheromas had bacteria. Conclusions: CHD and PE showed similarities in progression while active PE led to more atheroma lesions that also tended to be larger in size.

Quantitative gingival crevicular fluid proteome in type 2 diabetes mellitus and chronic periodontitis.

OBJECTIVE: The aim of this study was to investigate the proteome of the gingival crevicular fluid comparing the relative abundance of proteins from type 2 diabetes mellitus (2DM) individuals and chronic periodontitis (CP) affected sites, subjects affected by both conditions and healthy individuals. MATERIAL AND METHODS: Twenty individuals were equally allocated in four groups, 2DM with CP, 2DM periodontally healthy, CP without 2DM, and periodontally healthy without 2DM. The relative quantification of proteins was accessed with iTRAQ labeling and mass spectrometry. RESULTS AND CONCLUSION: A total of 104 proteins showed significant differences in abundance in pairwise comparisons. Some presented different levels in all diseased groups as compared to control, either increasing (rap guanine nucleotide exchange factor, S100A8, S100A9, and immunoglobulins) or decreasing (actins, myristoylated alanine-rich C-kinase substrate, and glutathione S-transferase). Other differences were specific for a given condition: Titin, neutrophil elastase, and myeloperoxidase levels were higher in the DP group, cathelicidin antimicrobial peptide decreased in CP, and annexin decreased in DH. These differences in the proteome can provide clues for further studies that will validate the variation in their levels and their role in both diseases.

No association between periodontitis and preterm low birth weight: a case-control study.

PURPOSE: This study aimed to investigate the association between periodontitis in pregnant women and adverse pregnancy outcomes by heeding confounding risk factors for preterm low birth weight infants. METHODS: This study was reported according to The Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) Statement. A case-control study was conducted. Medical records of all pregnant women attending a prenatal care clinic were screened. Those between 21 and 34 years and gestational age of 28-32 weeks were initially enrolled in the study. The exclusion criteria were then applied: diabetes mellitus, genitourinary tract infections, or HIV infection; previous multiple gestations; previous preterm birth/low birth weight infants; in vitro fertilization procedures; placental, cervical/uterine abnormalities; history of infertility; history of drug abuse; and any medical conditions that required antibiotics prophylaxis. Patients' anthropometric, demographic, and behavioral characteristics were collected. The periodontal clinical parameters were obtained from six sites per tooth: clinical attachment level, probing pocket depth, dental plaque index, and gingival bleeding index. Women were then allocated into two groups: mothers of preterm and/or low birth weight newborns (cases) and mothers of full-term and normal birth weight newborns (controls). RESULTS: Periodontal clinical parameters were analyzed and reported separately for each group, and no significant differences were observed (p > 0.05). Logistic regression analysis revealed that periodontal clinical parameters were not associated with the adverse pregnancy outcomes. CONCLUSION(S): After controlling for confounding factors, our results suggest that maternal periodontal disease is not a risk factor associated with preterm low birth weight infants.

Levels of HIV-1 in subgingival biofilm of HIV-infected patients.

AIM: The aims of the current study were to compare the levels of HIV-1 in the subgingival biofilm (SHVL) between detectable and undetectable plasmatic HIV-1 viral load (PHVL) in HIV-infected patients as well as to determine the association of SHVL with PHVL and clinical periodontal parameters. MATERIAL AND METHODS: Forty-one HIV-infected individuals were divided into two groups: detectable (21) and undetectable (20) PHVL. Subgingival biofilm samples were obtained for detection and quantification of HIV-1 by real-time RT-PCR. To estimate the effect of co-variables on the outcome undetectable SHVL, the Generalized Estimation Equation (GEE) was employed. RESULTS: Detectable SHVL was observed only in the detectable PHVL group and the detection of the HIV-1 was observed in 40% of these individuals. In the bivariate analysis between co-variables from the individual level and the outcome SHVL, significant difference was observed only for the CD4+ T lymphocytes levels (p = 0.017). The multiple logistic model demonstrated that only CD4+ T lymphocytes levels had a significant effect on the outcome undetectable SHVL [OR 8.85 (CI 3.6-9.2), p = 0.002]. CONCLUSION: HIV-1 can be detected and quantified in the subgingival biofilm of HIV-infected individuals, but these findings are not associated with PHVL and periodontal clinical parameters.

The association between detectable plasmatic human immunodeficiency virus (HIV) viral load and different subgingival microorganisms in Brazilian adults with HIV: a multilevel analysis.

BACKGROUND: This study investigates the association between detectable plasmatic human immunodeficiency virus (HIV) viral load (HVL) and high levels of periodontal- and non-periodontal-related microorganisms in the subgingival microbiota of individuals with HIV. METHODS: Thirty-seven individuals with HIV were divided into two groups: 1) detectable HVL (n = 15); and 2) undetectable HVL (n = 22). Subgingival biofilm samples were obtained, and the levels of 35 microbial species were determined by the checkerboard DNA-DNA hybridization method. Periodontal clinical measures and laboratory and sociodemographic data were also registered. χ(2) test, Fisher exact test, and Mann-Whitney U test were used to compare groups. Multilevel ordinal regression models were used to test the association between HVL and the levels of 35 microbial species in subgingival biofilm, adjusted for confounders. RESULTS: Of the 35 species studied, 11 (31.4%) showed higher mean levels in the detectable HVL group than undetectable HVL group (P <0.001). These species included Actinomyces naeslundii II, Actinomyces israelii, Actinomyces odontolyticus, Veillonella parvula, Capnocytophaga gingivalis, Eikenella corrodens, Campylobacter concisus, Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, and Candida albicans. Significant associations between detectable HVL and high levels of microorganisms, adjusted for confounders, were observed for A. naeslundii I, Actinomyces gerencseriae, C. gingivalis, E. corrodens, C. concisus, Prevotella nigrescens, T. forsythia, and Dialister pneumosintes. CONCLUSION: Detectable plasmatic HVL in individuals with HIV was associated with elevated levels of known periodontal pathogens, such as P. nigrescens, T. forsythia, and E. corrodens, as well as C. concisus, C. gingivalis, and D. pneumosintes in the subgingival biofilm.

Effect of non-surgical periodontal treatment on chronic kidney disease patients.

Chronic kidney disease (CKD) is a debilitating systemic condition. Our working hypothesis is that CKD predialysis patients with periodontitis would respond poorly to periodontal treatment owing to immunologic compromise. Twenty-one predialysis patients (group 1) and 19 individuals without clinical evidence of kidney disease (group 2) with chronic periodontitis were subjected to non-surgical periodontal treatment with no antibiotics. Clinical periodontal and systemic parameters were evaluated at baseline and 3 months after treatment. Both groups showed significant and similar post-treatment improvements in all periodontal parameters examined. Most interestingly, periodontal treatment had a statistically significant positive effect on the glomerular filtration rate of each individual (group 1, p = 0.04; group 2, p = 0.002). Our results indicate that chronic periodontitis in predialysis kidney disease patients improved similarly in patients with chronic periodontitis and no history of CKD after receiving non-surgical periodontal therapy. This study demonstrates that CKD predialysis patients show a good response to non-surgical periodontal treatment.

Effect of non-surgical periodontal treatment on chronic kidney disease patients

Chronic kidney disease (CKD) is a debilitating systemic condition. Our working hypothesis is that CKD predialysis patients with periodontitis would respond poorly to periodontal treatment owing to immunologic compromise. Twenty-one predialysis patients (group 1) and 19 individuals without clinical evidence of kidney disease (group 2) with chronic periodontitis were subjected to non-surgical periodontal treatment with no antibiotics. Clinical periodontal and systemic parameters were evaluated at baseline and 3 months after treatment. Both groups showed significant and similar post-treatment improvements in all periodontal parameters examined. Most interestingly, periodontal treatment had a statistically significant positive effect on the glomerular filtration rate of each individual (group 1, p = 0.04; group 2, p = 0.002). Our results indicate that chronic periodontitis in predialysis kidney disease patients improved similarly in patients with chronic periodontitis and no history of CKD after receiving non-surgical periodontal therapy. This study demonstrates that CKD predialysis patients show a good response to non-surgical periodontal treatment.

Prevalence of potential bacterial respiratory pathogens in the oral cavity of hospitalised individuals.

OBJECTIVE: To assess the prevalence of oral colonisation by bacterial respiratory pathogens in hospitalised patients. METHODS: Thirty patients undergoing myocardium revascularisation surgery were evaluated. At baseline (pre-operative phase), full-mouth clinical periodontal assessment was performed. Saliva and biofilm samples were obtained from subjects at baseline and at the post-operative phase, after orotracheal extubation. DNA was extracted from samples and species of Acinetobacter, Pseudomonas, Staphylococcus aureus and Dialister pneumosintes were detected by PCR or culture (for staphylococci isolates). RESULTS: Most of the subjects were males, with history of hypertension and smoking. Thirteen were edentulous (ED) and 17 were dentate (DE), with moderate chronic periodontitis. The most prevalent bacteria in saliva were Staphylococcus spp. (85.7%), Pseudomonas spp. (83.8%), and Acinetobacter spp. (53.3%). There was a trend for D. pneumosintes to be more frequently detected in DE (43.7%) than ED (11.5%) patients. In plaque samples, DE with >14 teeth showed a higher prevalence of Pseudomonas spp. (100%) than individuals with < or =14 teeth (69.1%; p=0.048). Conversely, P. aeruginosa was more prevalent in subjects with fewer teeth (35.5%) than with >14 teeth (5.7%; p=0.037). All staphylococci isolates were coagulase-negative, and about 11% were positive for the mecA gene. These mecA-positive isolates showed a tendency to increase in all samples, whereas P. aeruginosa reduced after surgery. A strong correlation between the presence of Acinetobacter spp. and Pseudomonas spp. was observed (rho=0.886, p<0.05). CONCLUSIONS: The oral cavity of hospitalised patients harbours high frequencies of bacterial respiratory pathogens, supporting its potential role as a reservoir for these species.

The relationship between diabetes mellitus and destructive periodontal disease: a meta-analysis.

PURPOSE: The aim of this study was to systematically review the studies on the association between diabetes mellitus (DM) and destructive periodontal disease. METHODS: The methods applied include a literature search strategy, inclusion and exclusion criteria for selecting the studies, characteristics of the studies, quality assessment and meta-analysis. Data sources included PubMed, EMBASE, SciELO and LILACS. Selected papers were articles relating to human studies investigating whether or not diabetes is a risk factor for periodontitis and if it influences the response to periodontal therapy. Those papers that were published between January 1980 and June 2007 were retrieved. RESULTS: Of the 2440 identified studies, 49 cross-sectional and eight longitudinal studies met the inclusion criteria. Twenty-seven of the 49 cross-sectional studies that are included in this review detected more periodontal disease in diabetic subjects compared with non-diabetic subjects. The greater risk of periodontal disease progression was associated with type 2 DM, and one study associated DM with response to periodontal therapy. Methodological flaws of most of the studies included inadequate control for confounders, insufficient statistical analysis and lack of information about sampling design. Random effect model showed a significant association with clinical attachment level (mean difference = 1.00 [CI 95% = 0.15 to 1.84]) and periodontal pocket depth (mean difference = 0.46 [CI 95% = 0.01 to 0.91]) between type 2 diabetics and non-diabetics. CONCLUSIONS: Type 2 DM can be considered a risk factor for periodontitis. More studies are needed to confirm the harmful effects of type 1 DM on periodontal disease.