The effect of interleukin-20 on periodontal tissue destruction in individuals with periodontitis.

BACKGROUND AND OBJECTIVE: Periodontitis is an inflammatory disease that destroys periodontal tissues. Interleukin-20 (IL-20), on the other hand, is known as a potent angiogenic, chemotactic, and pro-inflammatory cytokine associated with various chronic inflammatory disorders. IL-20 has a significant role in the regulation of osteoclastogenesis and osteoblastogenesis. This study aimed to evaluate the effect of IL-20 on periodontal destruction. METHODS: In this study, a total of 60 participants were included, 30 of whom were systemically and periodontally healthy (control group), and 30 were systemically healthy but had periodontitis (periodontitis group). Gingival crevicular fluid (GCF) and serum samples were collected from the participants for biochemical analysis. Enzyme-linked immunosorbent assay was used to determine the levels of IL-20, tumor necrosis factor (TNF)-α, IL1ß/IL-10, RANKL/osteoprotegerin (OPG), and matrix metalloproteinase-8 (MMP8). For statistical analysis, the independent t-test, Pearson correlation coefficients, and the Chi-square test were used. RESULTS: GCF IL-20, RANKL, RANKL/OPG, serum IL-20, RANKL, RANKL/OPG, MMP-8, TNF-α, IL-1B, and IL-1ß/IL-10 values were found to be statistically significantly higher in the periodontitis group than in the control group. GCF OPG and serum IL-10 values were found to be statistically significantly higher in the control group than in the periodontitis group. No statistically significant difference was observed between the groups in serum OPG values. A statistically significantly positive correlation was observed between serum IL-20 value and serum RANKL, RANKL/OPG, MMP-8, TNF-α, IL-1ß values, and periodontal clinical parameters. The ROC curves showed: AUC = 0.788 for GCF IL-20, and AUC = 1.000 for serum IL-20. CONCLUSION: According to the results of the study, IL-20 was found to be associated with periodontitis. The role of IL-20 in periodontal pathogenesis is related to osteoclastogenesis and collagen degradation. It is conceivable that IL-20 may increase bone destruction by both affecting the RANKL/OPG ratio and proinflammatory cytokines.

Biochemical and histopathologic analysis of the effects of periodontitis on left ventricular heart tissues of rats.

BACKGROUND AND OBJECTIVE: Current epidemiological works have suggested that chronic infections, such as periodontitis, are associated with an increased risk of cardiovascular diseases, including hypertrophy and heart failure. However, mechanisms behind the association are not known. The aim of this study was to evaluate the effects of periodontitis on the serum lipid levels, inflammatory marker levels and left ventricular heart muscle tissues of rats. MATERIAL AND METHODS: Eighteen male Sprague-Dawley rats were randomly divided into two groups: control (without ligature) and experimental periodontitis (EP; ligatured). Periodontitis was induced by placing ligatures (3.0 silk) at a submarginal position of the lower first molar teeth for 5 wk. Serum samples were collected for biochemical studies (C-reactive protein, interleukin-1ß, tumor necrosis factor-α and serum lipids), after which the rats were killed and heart tissue samples were obtained for histopathological and immunological studies (nuclear factor kappa B and ß-myosin heavy chain). RESULTS: Significant increases in C-reactive protein and interleukin-1ß levels and no statistically significant increase in tumor necrosis factor-α level were observed in the EP group compared to the control group. In addition, total cholesterol, low-density lipoprotein cholesterol and triglyceride levels were significantly higher in the EP group. Stereological and immunological findings showed that the number of nuclear factor kappa B-p65- and ß-myosin heavy chain-positive cardiomyocytes increased significantly in the left ventricular tissue samples of the rats with periodontitis. CONCLUSION: Early chronic phase effects of periodontitis on heart tissue are in the form of degenerative and hypotrophic changes. Prolonging the exposure to systemic inflammatory stress may increase the risk of occurrence of hypertrophic changes.

Influence of experimental periodontitis on cardiac oxidative stress in rats: a biochemical and histomorphometric study.

BACKGROUND AND OBJECTIVE: The role of oxidative stress in the process of cardiac remodeling, hypertrophy and heart failure is a current topic. The purpose of this experimental study was to investigate the influences of periodontitis on levels of cardiac oxidative stress. MATERIAL AND METHODS: Twenty rats were separated into two groups: control and experimental periodontitis (EP). Periodontitis was induced by placing a 3.0 silk suture in the cervix of the left and right mandibular first molar teeth for 5 wk. At the end of the experiment, the animals were killed and blood samples and mandibular and ventricular cardiac tissue samples were collected. Levels of alveolar bone loss were determined using measurements performed on histological slices and radiographies. Left ventricular tissue 8-hydroxy-2'-deoxyguanosine, malonylaldehyde, glutathione peroxidase, total oxidant status, total antioxidant status (TAS) levels and serum paraoxonase-1 activity were evaluated biochemically. RESULTS: Measurements performed on the histological slices and radiographies demonstrated that applying the ligature caused obvious alveolar bone loss. Oxidative damage markers (malonylaldehyde, 8-hydroxy-2'-deoxyguanosine, oxidative stress index: total oxidant status/TAS) were significantly higher, and antioxidant markers (glutathione peroxidase, TAS) were statistically insignificantly higher, in the hearts of rats with EP when compared to the controls. In addition, reduced serum paraoxonase-1 activity was also detected in the EP group. CONCLUSION: The pronounced increase in cardiac oxidative stress caused by periodontitis was due to an excessive increase in the production of reactive oxygen species, rather than due to decreased antioxidant capacity. The results indicate that periodontitis-related cardiac oxidative stress might be one of the mechanisms that contribute to the pathological process that leads to heart failure.