Laboratory of Histological Analysis and Preparation (LAPHIS), Federal University of Piaui, Parnaiba, PI, Brazil.
Medicine School, Education Institute of Parnaiba Valley (IESVAP), Parnaiba, PI, Brazil.
J Periodontal Res. 2017 Oct;52(5):883-892. doi: 10.1111/jre.12459. Epub 2017 May 15.
Periodontitis may promote harmful systemic effects such as changes in hepatic tissues. The purpose of this study was to investigate whether the steatosis and oxidative stress caused by experimental periodontitis are reversible in the liver.
Twenty-four rats were divided into three groups: control, periodontitis and P20-20 (20 days with experimental periodontitis and 20 days without experimental periodontitis, to verify the reversibility of hepatic injuries). The following parameters were assessed: gingival bleeding index, probing pocket depth, myeloperoxidase activity, alveolar bone loss for periodontal tissues; liver weights, histopathological scores for steatosis, inflammation and necrosis in liver; glutathione, malondialdehyde, total cholesterol and triglyceride concentrations in hepatic tissues; and blood levels of aspartate aminotransferase, alanine aminotransferase, albumin, gamma-glutaryl transferase, total cholesterol and random glucose.
Gingival bleeding index, probing pocket depth, myeloperoxidase and alveolar bone loss parameters demonstrated the development of periodontitis. There was a significant reduction in the steatosis score of animals from the P20-20 group when compared with the periodontitis group. P20-20 group presented significantly higher glutathione (11 times) and lower malondialdehyde (nearly 23%), total cholesterol (both in blood and hepatic tissue) and triglyceride concentrations compared with the periodontitis group. For levels of aspartate aminotransferase, alanine aminotransferase, albumin, gamma-glutaryl transferase and random glucose, a significant difference between the groups was not observed.
Our results demonstrate that the microvesicular steatosis caused by periodontitis in rats is reversible after removal of the ligature, which is associated with the increase in oxidative stress and lipid peroxidation in the liver.
牙周炎可能会导致有害的全身影响,如肝组织变化。本研究旨在探讨实验性牙周炎引起的肝脂肪变性和氧化应激是否可逆。
将 24 只大鼠分为三组:对照组、牙周炎组和 P20-20 组(20 天实验性牙周炎和 20 天无实验性牙周炎,以验证肝损伤的可逆性)。评估以下参数:牙龈出血指数、探诊袋深度、髓过氧化物酶活性、牙周组织牙槽骨丧失;肝脏重量、肝组织脂肪变性、炎症和坏死的组织学评分;肝组织谷胱甘肽、丙二醛、总胆固醇和甘油三酯浓度;以及血液天门冬氨酸氨基转移酶、丙氨酸氨基转移酶、白蛋白、γ-谷氨酰转移酶、总胆固醇和随机血糖水平。
牙龈出血指数、探诊袋深度、髓过氧化物酶和牙槽骨丧失参数表明牙周炎的发展。与牙周炎组相比,P20-20 组动物的脂肪变性评分显著降低。与牙周炎组相比,P20-20 组的谷胱甘肽(增加 11 倍)和丙二醛(降低近 23%)、总胆固醇(血液和肝组织)和甘油三酯浓度显著升高。天门冬氨酸氨基转移酶、丙氨酸氨基转移酶、白蛋白、γ-谷氨酰转移酶和随机血糖水平在各组之间无显著差异。
我们的结果表明,结扎去除后,大鼠牙周炎引起的微泡性脂肪变性是可逆的,这与肝脏氧化应激和脂质过氧化增加有关。