Food restriction reduces hepatic alterations associated with experimental periodontitis.

BACKGROUND: Periodontitis is a chronic inflammatory and multifactorial disease that affects the periodontal structures and can cause alterations in the hepatic tissue. The aim of the present study was to evaluate whether a diet with food restriction can decrease oral and liver alterations associated with ligature-induced periodontitis. METHODS: Twenty-four female Wistar rats were used in this study, randomized into three groups (n = 8 for each group): control (regular food); periodontitis (regular food + periodontitis induced with ligatures); and food restriction (diet with food restriction and periodontitis induction). The following periodontium parameters were analyzed tooth mobility (TM), probing pocket depth (PPD), gingival bleeding index (GBI), and alveolar bone height (ABH). In the liver, the levels of oxidative stress markers-malondialdehyde (MDA), glutathione (GSH), total cholesterol, and levels of myeloperoxidase (MPO) activity were measured. Liver samples were analyzed for histopathological score. In the blood tissue, the levels of enzymes alanine aminotransferase (ALT), aspartate aminotransferase (AST), glucose, total cholesterol, and the high-density lipoprotein (HDL) were also evaluated. RESULTS: The animals that received a diet with food restriction + periodontitis showed a decrease in hepatic histopathological score (P < 0.05) when compared with the periodontitis group, the same for glucose, total cholesterol, ALT, AST, and ABH data. The group with food restriction + periodontitis showed a decrease in the histopathological liver score (P < 0.05) compared with the group with periodontitis. CONCLUSION: This study revealed that food restriction reduced oral damages, as well as hepatic, blood and alveolar bone alterations associated with ligature-induced periodontitis in rats.

Polymorphisms in the interleukin genes and chronic periodontitis: A field synopsis and revaluation by Bayesian approaches.

Periodontitis is a high prevalent disease into the clinical dentistry. Genetic variations in interleukins (IL) genes were associated with chronic periodontitis (CP) and were focus of several meta-analyses. This study aimed to assess the noteworthiness in the meta-analyses by means of a Bayesian approach to determinate possible false report associations. A systematic search was performed for meta-analyses with associations between gene polymorphisms in interleukins and CP. The calculations for the False-Positive Rate Probability (FPRP) and the Bayesian False Discovery Probability (BFDP) were performed to assess the noteworthiness with a statistical power of 1.2 and 1.5 of Odds Ratio at a prior probability of 10-3 and 10-6. As results, eight meta-analyses approaching the IL1A/rs1800587, IL1B/rs1143634, IL1RN/rs2234663, IL4/rs2243250, IL6/rs1800795/rs1800796, IL17A/rs2275913 and IL18/rs1946518/rs187238 polymorphisms have been identified. Twenty-two from 270 calculations (8.15%) were noteworthy. Herein, we have identified the IL1A and IL1B polymorphisms as noteworthy biomarkers for CP susceptibility.

Alpha-terpineol complexed with beta-cyclodextrin reduces damages caused by periodontitis in rats.

BACKGROUND AND OBJECTIVE: This study aimed to assess the effectiveness of the treatment with alpha-terpineol (αTPN) complexed with beta-cyclodextrin (ßCD) on oral, blood, and hepatic parameters in ligature-induced periodontitis. MATERIAL AND METHODS: Forty female rats were distributed among the following groups: control (vehicle solution), periodontitis (ligature + vehicle solution), 5 mg/kg of αTPN-ßCD (ligature), and 25 mg/kg of αTPN-ßCD (ligature). Compounds were administered daily via intraperitoneal injection over a 20-day period. Periodontitis was induced with the bilateral insertion of ligatures around the first lower molars of each rat. Oral parameters, as well as blood biomarkers, were measured: histopathological assessment of the hepatic tissue was carried out using light and transmission electron microscopy. RESULTS: The treatment with αTPN-ßCD significantly improved several oral parameters and blood biomarkers in comparison with rats with periodontitis. In addition, the treatment with αTPN-ßCD significantly ameliorated the steatosis score and reduced the number of lipid droplets and the amount of foamy cytoplasm in the hepatocytes of rats with periodontitis. CONCLUSION: The results obtained suggest that the treatment with αTPN-ßCD improves several oral and blood parameters in rats with experimental periodontitis. In addition, hepatic alterations caused by periodontitis were ameliorated in the rats treated with αTPN-ßCD.

High-fat diet aggravates the liver disease caused by periodontitis in rats.

BACKGROUND: Periodontitis is an inflammatory disease that causes periodontium and hepatic alterations. Liver disease is related to the intake of foods rich in fat and sugars (high-fat). The objective of this study was to evaluate whether a high-fat diet can aggravate the liver disease caused by ligature-induced periodontitis in rats. METHODS: Twenty-one female rats were divided into three groups (n = 7 in each group): control; periodontitis (periodontitis induced with ligature) and high-fat + periodontitis (received hypercaloric diet and induction of periodontitis). The rats were submitted to the analyses of the following periodontal parameters: gingival bleeding index (GBI), probing pocket depth (PPD), tooth mobility (TM), and alveolar bone height. In the hepatic tissue, the levels of malondialdehyde (MDA), glutathione (GSH), total cholesterol, and myeloperoxidase activity (MPO) were measured. Liver samples were also histopathologically evaluated. Finally, blood levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), glucose, total cholesterol, cholesterol high-density lipoprotein (HDL), and uric acid were measured. RESULTS: The high-fat + periodontitis group presented an increase in the steatosis score (P < 0.05) for the histopathologic evaluation, when compared with the periodontitis group. MDA, uric acid and ALT levels also increased, whereas GSH and HDL levels showed lower values. CONCLUSION: A high-fat diet aggravates the liver disease caused by ligature-induced periodontitis in rats.

One or two ligatures inducing periodontitis are sufficient to cause fatty liver

BACKGROUND: Periodontitis is a chronic disease that due to an intense inflammatory response triggers systemic changes such as hepatic alterations. This study aimed to compare hepatic damage in rats that received experimental periodontitis at one or two periodontal sites with ligatures. MATERIAL AND METHODS: Eighteen rats were separated into three groups: control, without ligature; periodontitis 1, with one ligature; and periodontitis 2, with two ligatures. The following parameters were assessed: gingival bleeding index, probing pocket depth, tooth mobility, alveolar bone loss, malondialdehyde (MDA) and myeloperoxidase (MPO) activity in periodontal tissue; histopathological evaluation of hepatic tissue (steatosis score); glutathione levels (GSH), MDA, MPO, cholesterol and triglycerides in the liver; and serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). RESULTS: Periodontal evaluation data showed that the periodontitis model worked well. The groups with periodontitis did not differ significantly in relation to MPO activity and MDA levels in the gingival samples, but they were significantly different when compared with the control group. Steatosis was observed in the histological analysis of the groups with periodontitis, but between the periodontitis groups, two ligatures did not cause increase in steatosis score. The levels of GSH, MDA, total cholesterol and triglycerides in the hepatic tissue were not altered between groups with periodontitis, but they showed significant differences in comparison with the control group. The activity of MPO in hepatic tissue and serum levels of AST and ALT did not present significant difference among the three groups. CONCLUSIONS: In conclusion, our results demonstrated that one or two ligatures inducing periodontitis were both sufficient to cause fatty liver. Steatosis caused by two ligatures did not present larger extension and severity than steatosis caused by one ligature

Polymorphisms in interleukins 17A and 17F genes and periodontitis: results from a meta-analysis.

Polymorphisms in inflammatory genes such as interleukins 17A and 17F are associated with the risk of development of periodontitis, although the results remain contradictory. Hence, the aim of this study was perform a meta-analysis focusing on two polymorphisms (rs2275913 and rs763780) in interleukins 17A and 17F genes, respectively, in both chronic (CP) and aggressive periodontitis (AgP). A review in literature was performed in several databases for studies published before 25, September 2016. The meta-analysis was obtained through the review manager statistical software (version 5.2) with odds ratio (OR) calculation and funnel plot (P < 0.05) for heterogeneity, as well as the comprehensive meta-analysis software (version 3.3.070) for the assessment of publication bias. Seven articles with 1540 participants composed the results in which the mutant allele in the rs2275913 polymorphism did not present significant association with the risk of CP or AgP (OR 1.56, 95% CI 0.77, 3.15, P = 0.21; OR 1.12, 95% CI 0.05, 23.44, P = 0.94, respectively) nor was the mutant allele in rs763780 associated with the risk of CP (OR 1.19, 95% CI 0.80, 1.76, P = 0.39) or AgP (OR 1.07, 95% CI 0.63, 1.84, P = 0.79). No bias of publication was observed by Egger's and Begg's tests in any allelic evaluation. This meta-analysis showed a non-significant association between the polymorphisms rs2275913 and rs763780 in interleukins 17A and 17F genes and chronic and aggressive periodontitis in the allelic evaluation.

Genetic Factors and the Risk of Periodontitis Development: Findings from a Systematic Review Composed of 13 Studies of Meta-Analysis with 71,531 Participants.

Purpose. This work aimed to synthesize the results of recent meta-analysis focusing on polymorphism in inflammatory mediators and its relation with the risk of periodontitis development. Materials and Methods. A systematic search was conducted using databases for publications prior to October 2016. Three examiners extracted data from articles with a clear association between polymorphisms in the inflammatory mediator gene and the development of periodontitis through meta-analysis using the fixed or randomized statistical models to calculate the Odds Ratio with values of P < 0.05 considered significant. Results. A total of 13 meta-analysis articles with 25 polymorphisms in seven interleukins (IL-1A, IL-1B, IL-4, IL-6, IL-8, IL-10, and IL-18), three cellular receptors (Fcγ receptors: FCGR2A, FCGR3A, and FCGR3B), and five inflammatory mediators (COX-2, MMP-2, MMP-3, MMP-8, and MMP-9), with a total of 71,531 participants, approaching different classifications of the disease. Conclusion. The study demonstrated that polymorphisms in the IL-1A, IL-1B, IL-6, IL-10, MMP-3 (chronic form), and MMP-9 (chronic form) polymorphisms were significantly associated with the risk of developing periodontitis, whereas other polymorphisms in the IL-4, IL-8, IL-18, Fcγ, COX-2, MMP-2, MMP-3 (aggressive), MMP-8, and MMP-9 (aggressive) polymorphisms had no significant association with risk of developing periodontitis.