Background Two main aims of this animal study were to inspect the possible effects of periodontitis on the structure and functions of the kidneys and the therapeutic effectiveness of melatonin. Methods Twenty‐four male Sprague‐Dawley rats were randomly divided into three groups: control, experimental periodontitis (Ep), and Ep‐melatonin (Ep‐Mel). Periodontitis was induced by placing 3.0‐silk sutures sub‐paramarginally around the cervix of right‐left mandibular first molars and maintaining the sutures for 5 weeks. Then melatonin (10 mg/kg body weight/day, 14 days), and the vehicle was administered intraperitonally. Mandibular and kidney tissue samples were obtained following the euthanasia. Periodontal bone loss was measured via histological and microcomputed tomographic slices. On right kidney histopathological and immunohistochemical, and on the left kidney biochemical (malonyl‐aldehyde [MDA], glutathione, oxidative stress [OSI], tumor necrosis factor [TNF]‐α, interleukin [IL]‐1β, matrix metalloproteinase [MMP]‐8, MMP‐9, and cathepsin D levels) evaluations were performed. Renal functional status was analyzed by levels of serum creatinine, urea, cystatin‐C, and urea creatinine. Results Melatonin significantly restricted ligature‐induced periodontal bone loss (P <0 .01) and suppressed the levels of proinflammatory cytokines (TNF‐α and IL‐1β), oxidative stress (MDA and OSI), and proteases (MMP‐8, MMP‐9, and CtD) that was significantly higher in the kidneys of the rats with periodontitis (P <0.05). In addition, periodontitis‐related histological damages and apoptotic activity were also significantly lower in the Ep‐Mel group (P <0.05). However, the markers of renal function of the Ep group were detected slightly impaired in comparison with the control group (P >0.05); and the therapeutic activity of melatonin was limited (P >0.05). Conclusion Melatonin restricts the periodontitis‐induced inflammatory stress, apoptosis, and structural but not functional impairments.

Background: The aim of this experimental rat study was to investigate the potential inflammatory effects of periodontitis on cardiac left ventricular tissue and the therapeutic activity of melatonin on these effects. Methods: Twenty-four male Sprague-Dawley rats were randomly divided into three groups: control, experimental periodontitis (Ep), and Ep-melatonin (Ep-Mel). Experimental periodontitis was induced by placing and maintaining 3.0 silk ligatures at a peri marginal position on the left and right mandibular first molars for 5 weeks. Afterward, following the removal of ligatures, melatonin (10 mg/body weight) to Ep-Mel group, and vehicle (saline) to Ep and control groups were administered intraperitoneally for 14 days. On the first day of the eighth week, mandibular and cardiac left ventricular tissue samples were obtained following the euthanasia of the rats in all groups. Alveolar bone loss measurements were made on histological and microcomputed tomographic slices. Cardiac tissue levels of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), matrix metalloproteinase-9 (MMP-9), and cardiac Troponin-T (cTnT) were evaluated by appropriate biochemical methods. Results: Measurements made on the histological and microcomputed tomographic slices showed that melatonin significantly limits the ligature-induced periodontal tissue destruction (P <0.01). In addition, melatonin was detected to cause a significant decrease of MDA, MMP-9, and cTnT levels which were found to be significantly higher on rats with Ep (P <0.05) while having no significant effect on antioxidant levels (GSH, SOD, and CAT) (P >0.05). Conclusion: Melatonin might be regarded as an important supportive therapeutic agent to reduce the early degenerative changes and possible hypertrophic remodeling at cardiac left ventricular tissues provoked by periodontitis-related bacteria and/or periodontal inflammation.

1 Technical Efficacy: Stage 4 J. Magn. Reson. Imaging 2018;47:1367-1374.

1 Technical Efficacy: Stage 2 J. MAGN. RESON. IMAGING 2018.

Background/objectives: Obesity and periodontitis are systemic subclinical inflammatory diseases with established negative renal effects. The aim of this animal study was to thoroughly investigate the possible effects of these two diseases on renal structure and function.Methods: Thirty-two male Sprague Dawley rats were divided into four groups: control (C), obesity (Ob), experimental periodontitis (Ep), and Ob + Ep. The first 16 weeks of the experiment were aimed for the induction of obesity and the last 5 weeks for the induction of periodontitis. Throughout the experimental period, the C and Ep groups were fed standard rat chow, while the Ob groups (Ob and Ob + Ep) were fed high-fat rat chow. Right after the establishment of obesity, periodontal tissue destruction was achieved by placing 3.0 silk sutures in sub-paramarginal position around the cervices of mandibular right-left first molar teeth and preserving them for 5 weeks. On the last day of the 22 nd week, following blood collection, all rats were euthanized, and kidneys and mandibles were collected. Alveolar bone loss was measured on microcomputed tomographic slices. Histopathological evaluations (light microscopy, semi-quantitative analysis of renal corpuscle area, and immunohistochemical analysis of caspase-3 activity) were done on right kidneys and biochemical evaluations (malonyl-aldehyde [MDA], glutathione [GSH], total oxidant status [TOS], total antioxidant status [TAS], oxidative stress [OSI], tumor necrosis factorα [TNFα], interleukin-1β [IL-1β], matrix metalloproteinase [MMP]-8, MMP-9, and cathepsin D [CtD] levels) were done on left kidneys. Renal functional status was evaluated with levels of serum creatinine, urea, and cystatin C.Results: Periodontal bone loss was significantly higher in the Ep and Ob + Ep groups, compared with the C and Ob groups (p < .05). All parameters except TAS and GSH were highest in the Ob + Ep group, and the differences were statistically significant compared with the control group (p < .05). Although the mean TAS and GSH levels were lower in the Ob + Ep group than the other groups, the differences were not statistically significant (p > .05). While the atypical glomeruli score was significantly higher in the Ob + Ep group than in all other groups (p < .05), the acute tubular