College & Hospital of Stomatology, Anhui Medical University, Key Lab. of Oral Diseases Research of Anhui Province, Hefei 230032, China.
Department of Public Health Inspection and Quarantine, Anhui Medical University School of Public Health, Hefei, Anhui 230032, China.
Life Sci. 2022 Jan 1;288:120162. doi: 10.1016/j.lfs.2021.120162. Epub 2021 Nov 20.
Previous studies have demonstrated that chronic periodontitis (CP) is closely associated with the occurrence and development of a variety of systemic diseases. In this study, we successfully constructed a rat CP model through dental silk ligation, and the corresponding inflammatory reactions and fatty lesions were observed in the liver.
Sprague-Dawley rats (n = 6) underwent tooth ligation at the bilateral first molars with silk thread to induce CP and were sacrificed 8 weeks later and compared to non-ligated rats (n = 6). RNA sequencing and 16S rRNA analysis were performed to determine the molecular mechanisms of CP involved in inducing liver disease. Alveolar bone loss, liver enzymes, mandible and liver histopathology, and inflammatory responses were compared between groups.
RNA sequencing of liver tissue showed that the expression of SCD1 increased significantly in CP rats compared to controls. KEGG enrichment analysis showed that the AMPK signalling pathway may be involved in liver steatosis. The intestinal flora of faecal samples of rats were analysed by 16S rRNA sequencing, and the results indicated that the intestinal flora of the CP group was evidently imbalanced. The expression levels of tight junction proteins (ZO-1, occludin, and claudin-1) were significantly reduced in CP rats. Meanwhile, increases in serum IL-1β and lipopolysaccharide in CP rats reflected a systemic inflammatory response.
CP may be involved in the occurrence and development of hepatic injury and liver steatosis, and its mechanism may be related to the oral-gut-liver axis and SCD1/AMPK signal activation in the liver.
先前的研究表明，慢性牙周炎（CP）与多种系统性疾病的发生和发展密切相关。在本研究中，我们通过丝线结扎成功构建了大鼠 CP 模型，并观察到肝脏相应的炎症反应和脂肪病变。
将 Sprague-Dawley 大鼠（n=6）用丝线结扎双侧第一磨牙以诱导 CP，并在 8 周后处死并与未结扎大鼠（n=6）进行比较。进行 RNA 测序和 16S rRNA 分析，以确定 CP 诱导肝病的分子机制。比较各组的牙槽骨丧失、肝酶、下颌骨和肝脏组织病理学以及炎症反应。
肝组织 RNA 测序显示 CP 大鼠 SCD1 的表达明显高于对照组。KEGG 富集分析表明，AMPK 信号通路可能参与肝脂肪变性。通过 16S rRNA 测序分析粪便样本中的肠道菌群，结果表明 CP 组的肠道菌群明显失衡。CP 大鼠的紧密连接蛋白（ZO-1、occludin 和 claudin-1）表达水平显著降低。同时，CP 大鼠血清中 IL-1β 和脂多糖的增加反映了全身性炎症反应。
CP 可能参与肝损伤和肝脂肪变性的发生和发展，其机制可能与口腔-肠道-肝脏轴和肝脏中 SCD1/AMPK 信号的激活有关。
