Periodontitis has been associated with a variety of systematic diseases via affecting gut microbiota. However, the influence of periodontal treatment on intestinal microbiota is not known. Hyperlipidemia can significantly alter gut microbiota structure. It is proposed that the presence of hyperlipidemia can influence the impact of periodontitis on microbiota. This study was conducted to explore the influence of periodontitis and periodontal treatment on the gut microbiota on the basis of hyperlipidemia. Apolipoprotein E^−/−(ApoE^−/−) mice were ligatured to induced periodontitis and non-surgical periodontal treatment was performed for half of them after 4 weeks of ligation. Microbiota communities in the feces collected at 4, 5, 8 weeks after ligation were investigated using next-generation sequencing of 16S rDNA. Bone loss at periodontitis sites were analyzed using micro-computed tomography (Micro-CT). Morphology and mucosal architecture injury of ileum tissue were observed with hematoxylin-eosin staining. The serum lipid levels were assayed. The results showed that β-diversity index in experimental periodontitis group was differed significantly from that of the control group. Significant differences were found in β-diversity between the non-surgical periodontal treatment group and the ligation group. The samples of the non-surgical periodontal treatment group and the control group were clustered together 4 weeks after periodontal treatment. Intestinal villus height and ratio of villus height to crypt depth was found decreased after ligation and restored after non-surgical periodontal treatment. Non-surgical periodontal treatment induced the colonization and prosper of butyrate-producing bacteria Eubacterium, which was absent/not present in the ligation group. We confirmed that periodontitis led to gut microbiota dysbiosis in mice with hyperlipidemia. Non-surgical periodontal treatment had the trend to normalize the gut microbiota and improved the intestinal mucosal barrier impaired by periodontitis in apoE^−/− mice.

牙周炎已通过影响肠道菌群而与多种系统疾病相关。但是，牙周治疗对肠道菌群的影响尚不清楚。高脂血症可显着改变肠道菌群结构。有人认为，高脂血症的存在会影响牙周炎对微生物的影响。本研究旨在探讨基于高脂血症的牙周炎和牙周治疗对肠道菌群的影响。载脂蛋白E ^-/-（ApoE ^-/-）将小鼠结扎至诱发的牙周炎，结扎4周后，对其中一半进行非手术性牙周治疗。使用下一代16S rDNA测序技术研究了结扎后4、5、8周收集的粪便中的微生物群。使用微计算机断层扫描（Micro-CT）分析牙周炎部位的骨丢失。苏木精-伊红染色观察回肠组织形态及黏膜结构损伤。测定血清脂质水平。结果表明，实验性牙周炎组的β多样性指数与对照组相比有显着差异。在非手术牙周治疗组和结扎组之间，β多样性存在显着差异。牙周治疗后4周，非手术牙周治疗组和对照组的样本聚集在一起。结扎后肠绒毛高度和绒毛高度与隐窝深度之比降低，经非手术牙周治疗后恢复。非手术性牙周治疗诱导了产生丁酸盐的细菌的定殖和繁荣真细菌，在连接组中不存在/不存在。我们证实牙周炎可导致高脂血症小鼠的肠道菌群失调。非手术牙周治疗有使肠道菌群正常化的趋势，并改善了由apoE ^-/-小鼠牙周炎损害的肠粘膜屏障。