dinoprost and Periodontal-Diseases

It is well accepted that glycemic control in patients with diabetes mellitus (DM) is affected by systemic inflammation and oxidative stress. The effect of periodontal therapy on these systemic factors may be related to improvement on glycemic status. The aim of the present study is to assess over a period of 6 months the effect of non-surgical periodontal therapy on serum levels of high-sensitivity C-reactive protein (hsCRP), d-8-iso prostaglandin F2a (d-8-iso) as a marker of oxidative stress, and matrix metalloproteinase (MMP)-2 and MMP-9 on patients with type 2 DM.. Sixty participants with type 2 DM and moderate to severe periodontal disease were randomized into intervention (IG) and control (CG) groups. IG received scaling and root planing, whereas CG received supragingival cleaning at baseline and scaling and root planing at 6 months. Participants of both groups were evaluated at baseline and 1, 3, and 6 months. Periodontal data recorded at each visit included probing depth, clinical attachment loss, bleeding on probing, and gingival index. Blood was collected at each visit for the assay of serum glycated hemoglobin A1c (A1c), hsCRP, d-8-iso, MMP-2, and MMP-9.. Although there was a trend to a reduction in hsCRP, d-8-iso and MMP-9 it did not reach statistical significance. MMP-2 levels remained unchanged after periodontal treatment.. Effective non-surgical periodontal treatment of participants with type 2 DM and moderate to severe periodontal disease improved significantly A1c levels but did not result in a statistically significant improvement in hsCRP, d-8-iso, MMP-2, and MMP-9 levels.

Topics: Adult; Aged; C-Reactive Protein; Chi-Square Distribution; Dental Scaling; Diabetes Mellitus, Type 2; Dinoprost; Female; Glycated Hemoglobin; Humans; Male; Matrix Metalloproteinase 2; Matrix Metalloproteinase 9; Middle Aged; Oxidative Stress; Periodontal Diseases; Periodontal Index; Prospective Studies; Statistics, Nonparametric

We sought to determine if maternal periodontal disease is associated with oxidative stress as measured by serum 8-isoprostane. A secondary analysis was conducted using prospective data from the Oral Conditions and Pregnancy Study. Healthy women enrolled at < 26 weeks' gestational age underwent oral examination and serum sampling. Maternal periodontal disease status was categorized as healthy, mild, or moderate to severe by clinical criteria. Maternal serum was analyzed for 8-isoprostane using ultrasensitive enzyme-linked immunosorbent assay. Elevated 8-isoprostane level was defined as ≥ 75th percentile. Maternal factors associated with elevated 8-isoprostane were determined using chi-square or T test. Multivariable logistic regression was used to assess association between elevated 8-isoprostane and maternal factors. Seven hundred ninety-one women had complete data. Median (interquartile) 8-isoprostane serum level was 1806 (16 to 81,870) pg/dL. Using bivariate analysis, maternal age, race, marital status, utilization of public assistance, and mild or moderate to severe periodontal disease were associated with elevated serum 8-isoprostane. Using logistic regression, moderate to severe periodontal disease (adjusted odds ratio 2.9, 95% confidence interval: 1.7 to 5.0) remained significantly associated with an elevated serum 8-isoprostane level. Maternal periodontal disease is associated with oxidative stress during pregnancy. Further study is needed to determine the role of maternal oxidative stress in periodontal disease-associated adverse pregnancy outcomes.

Topics: Adult; Chi-Square Distribution; Dinoprost; Female; Humans; Logistic Models; Maternal Age; Multivariate Analysis; Oxidative Stress; Periodontal Diseases; Pregnancy; Pregnancy Complications; Socioeconomic Factors; Young Adult

Maternal periodontal infection is associated with an increased risk for preeclampsia. Periodontal infection is also associated with increased oxidative stress. Our objective was to determine the relationship among maternal periodontal disease, maternal oxidative stress, and the development of preeclampsia.. A secondary analysis of prospectively collected data from the Oral Conditions and Pregnancy Study was performed. A cohort of healthy women enrolled at <26 weeks of gestation underwent an oral examination, serum sampling, and delivery follow-up. A periodontal infection was categorized by clinical parameters as healthy or mild or moderate/severe periodontal infection. Preeclampsia was defined by the American Congress of Obstetricians and Gynecologists criteria as blood pressure >140/90 mmHg and >or=1+ proteinuria on a catheterized specimen. Maternal blood was assayed for 8-isoprostane concentrations using an enzyme-linked immunosorbent assay and stratified as elevated (>or=75th percentile) or not elevated (<75th percentile). Odds ratios (ORs) for preeclampsia were calculated and stratified by periodontal disease and the level of 8-isoprostane concentration.. A total of 34 (4.3%) of 791 women developed preeclampsia. Women with an 8-isoprostane concentration >or=75th percentile at enrollment were more likely to develop preeclampsia compared to women with an 8-isoprostane concentration <75th percentile (38.2% versus 24.4%, respectively; P = 0.07; OR: 1.91; 95% confidence interval [CI]: 0.94 to 3.90). Among women with moderate/severe periodontal disease, an elevated 8-isoprostane concentration (>or=75th percentile) did not significantly increase the likelihood for preeclampsia (adjusted OR: 2.08; 95% CI: 0.65 to 6.60).. Women with oxidative stress early in pregnancy, as measured by an 8-isoprostane concentration >or=75th percentile, were at an increased risk for developing preeclampsia. The presence of periodontal disease did not appear to modify this risk.

Topics: Adult; Biomarkers; Cohort Studies; Dinoprost; Female; Humans; Odds Ratio; Oxidative Stress; Periodontal Diseases; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Infectious; Prospective Studies; Reference Values; Risk Factors; Severity of Illness Index; Statistics, Nonparametric; Young Adult

Reactive oxygen species (ROS) are implicated in the destruction of the periodontium during periodontitis. The imbalance in oxidant activity may be a key factor. The aim of this paper is to determine whether periodontitis is associated with increased oxidative damage to DNA, lipids, and proteins and modification of total antioxidant capacity (TAC) in saliva. Saliva was collected from 58 periodontitis patients and 234 healthy controls, all nonsmokers. Periodontal disease status was characterized using the Community Periodontal Index of Treatment Needs (CPITN). Assays for 8-OHdG (ELISA), 8-epi-PGF2alpha (ELISA), and total protein carbonyls (ELISA), and oxy-blotting (Western)/mass spectrometry were performed to quantify oxidative damage to nucleic acids, lipids, total and individual proteins, respectively, in whole nonstimulated saliva. Salivary TAC was measured by inhibition of ABTS oxidation by metmyoglobin. We observed (i) significantly higher levels of 8-OHdG, 8-epi-PGF2alpha, and carbonylated proteins in saliva of periodontal patients as compared with controls (P=0.0003, <0.0001 and <0.0001); (ii) 8-OHdG, 8-epi-PGF2alpha, and carbonylated proteins were independently negatively associated with CPITN (P=0.004, 0.02, and <0.0001); (iii) a positive correlation between salivary TAC and periodontal disease status in the study group (P<0.0001); and (iv) specific oxidation of transferrin, human IgG1 heavy chain fragment, and salivary amylase in periodontitis. Periodontal disease is associated with increased oxidative modification of salivary DNA, lipids, and proteins. Augmented salivary total antioxidant capacity may represent an adaptive response to oxidative stress. Salivary amylase, transferrin, and human IgG1 heavy chain fragments are particularly prone to enhanced oxidation in periodontitis.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Adult; Aged; Cross-Sectional Studies; Deoxyguanosine; Dinoprost; DNA; Enzyme-Linked Immunosorbent Assay; Female; Humans; Lipid Metabolism; Male; Metmyoglobin; Middle Aged; Oxidation-Reduction; Oxidative Stress; Periodontal Diseases; Protein Binding; Protein Carbonylation; Saliva; Severity of Illness Index; Smoking

To assess the impact of systemic oxidative stress on humoral immune responses, we examined the relation between levels of serum 8-isoprostane and serum IgG antibodies against 17 microorganisms in the commensal oral biofilm among the ARIC population of community-dwelling adults (n = 4,717). Bivariately, serum 8-isoprostane was associated with age, race/center, education, smoking, serum triglycerides, and the extent of periodontal disease severity. Total IgG antibody directed to the oral biofilm was significantly associated with race/center, hypertension, triglycerides, periodontal disease severity, plaque, and serum 8-isoprostane. In multivariate models, the highest quartile of increased 8-isoprostane displayed marked reductions (44%) in biofilm IgG antibody in contrast to small increases in total IgG antibody level for the highest quartiles of oral bacterial burden or periodontal disease severity (19 and 12%, respectively; p < 0.0001). Increased 8-isoprostane was associated with decreased total IgG antibody (p < 0.0001) in subjects with or without extensive periodontal disease and/or biofilm and with suppression of IgG responses across the entire biofilm composition. Increased systemic oxidative stress is associated with a generalized decrease of serum IgG antibody responses to the oral biofilm. Levels of oral microbial burden, periodontitis severity, and smoking are, by comparison, minor modifiers of serum IgG responses to the commensal oral biofilm.

Topics: Adult; Biofilms; Cohort Studies; Dinoprost; Humans; Immunoglobulin G; Middle Aged; Mouth; Oxidative Stress; Periodontal Diseases

Prostaglandin F2alpha (PGF2alpha) is a bioactive lipid mediator which has been suggested to be involved in the pathogenesis of periodontal disease. However, the roles of PGF2alpha in periodontal lesions are poorly understood. In the present study, we investigated the effect of PGF2alpha on interleukin (IL)-6 production in human gingival fibroblasts (HGF). PGF2alpha stimulated IL-6 production in a time- and concentration-dependent fashion. IL-1beta and tumor necrosis factor alpha (TNFalpha), proinflammatory cytokines, induced IL-6 production in a time-dependent manner, and PGF2alpha synergistically enhanced IL-6 production induced by IL-1beta and TNFalpha. IL-6 mRNA was expressed in PGF2alpha-stimulated HGF, and PGF2alpha increased IL-6 mRNA levels induced by IL-1beta and TNFalpha. Fluprostenol, a selective FP receptor agonist, could mimic PGF2alpha-induced IL-6 production. Since FP receptors are coupled to elevation of intracellular calcium and activation of protein kinase C (PKC), the mechanism of IL-6 production by PGF2alpha was investigated using TMB-8, an inhibitor of Ca2+ mobilization from intracellular stores, and calphostin C, an inhibitor of PKC. TMB-8 significantly suppressed PGF2alpha-induced IL-6 production, whereas calphostin C showed a stimulatory effect on PGF2alpha-induced IL-6 production. From these data, we suggest that PGF2alpha upregulates IL-6 production through FP receptors in HGF, that PGF2alpha synergistically enhances IL-6 production in IL-1beta- and TNFalpha-stimulated HGF, and that PGF2alpha-induced IL-6 production may be dependent on intracellular Ca2+ mobilization and be downregulated by PKC activation. PGF2alpha may be involved in the pathogenesis of periodontal disease by enhancing IL-6 levels in periodontal lesions.

Topics: Calcium; Calcium Channel Blockers; Cells, Cultured; Dinoprost; Dose-Response Relationship, Drug; Down-Regulation; Drug Synergism; Enzyme Activation; Enzyme Inhibitors; Fibroblasts; Gallic Acid; Gene Expression Regulation; Gingiva; Humans; Inflammation Mediators; Interleukin-1; Interleukin-6; Naphthalenes; Periodontal Diseases; Prostaglandins F, Synthetic; Protein Kinase C; Receptors, Prostaglandin; RNA, Messenger; Time Factors; Tumor Necrosis Factor-alpha; Up-Regulation

Topics: Adult; Aged; Chromatography, High Pressure Liquid; Dinoprost; Dinoprostone; Female; Humans; Male; Middle Aged; Periodontal Diseases; Prostaglandins; Prostaglandins E; Prostaglandins F; Saliva