School of Dentistry, Department of Periodontology, Recep Tayyip Erdogan University, Rize, Turkey.
School of Dentistry, Department of Periodontology, Eskişehir Osmangazi University, Eskisehir, Turkey.
J Periodontol. 2020 Nov;91(11):1486-1494. doi: 10.1002/JPER.19-0685. Epub 2020 May 19.
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 (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.
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.
本实验性大鼠研究旨在探讨牙周炎对心脏左心室组织的潜在炎症影响，以及褪黑素对这些影响的治疗作用。
将 24 只雄性 Sprague-Dawley 大鼠随机分为三组：对照组、实验性牙周炎组（Ep）和 Ep-褪黑素组（Ep-Mel）。通过在左、右下颌第一磨牙的边缘位置放置并保持 3.0 丝结扎线 5 周来诱导实验性牙周炎。结扎线去除后，Ep-Mel 组给予褪黑素（10mg/体重），Ep 组和对照组给予载体（生理盐水），腹腔内给药 14 天。在第八周的第一天，在所有组的大鼠安乐死后，获得下颌和心脏左心室组织样本。在组织学和微计算机断层扫描切片上进行牙槽骨丧失测量。通过适当的生化方法评估心脏组织丙二醛（MDA）、谷胱甘肽（GSH）、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、基质金属蛋白酶-9（MMP-9）和心肌肌钙蛋白-T（cTnT）水平。
组织学和微计算机断层扫描切片测量结果表明，褪黑素可显著限制结扎线诱导的牙周组织破坏（P<0.01）。此外，褪黑素被发现可显著降低 Ep 大鼠 MDA、MMP-9 和 cTnT 水平（P<0.05），而对抗氧化剂水平（GSH、SOD 和 CAT）无显著影响（P>0.05）。
褪黑素可被视为一种重要的支持性治疗药物，可减少牙周炎相关细菌和/或牙周炎症引起的心脏左心室组织早期退行性变化和可能的肥厚性重塑。
