Melatonin ameliorates periodontitis-related inflammatory stress at cardiac left ventricular tissues in rats.

Abstract

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. 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 (10mg/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. 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). 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.