Abstract
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.
Highlights
Periodontal disease is a chronic inflammation of the periodontal supporting tissues resulting from the dysbiosis of the dental biofilm that causes alveolar bone loss (Page et al, 1997)
principal coordinate analysis (PCoA) based on Unweighted Unifrac indicated that the composition of intestinal microbiome significantly altered after non-surgical periodontal treatment (5 week:R∧2 = 0.344, p = 0.001; 8 week: R∧2 = 0.336, p = 0.001, Adonis test) (Figures 4A,B)
One week after the non-surgical periodontal treatment, there was no significant difference observed in the dissimilarity of bacterial structures between the non-surgical periodontal treatment group (NL group) and the ligation group (L group) but a trend of difference was showed between this two group and the control group (Figure 4C)
Summary
Periodontal disease is a chronic inflammation of the periodontal supporting tissues resulting from the dysbiosis of the dental biofilm that causes alveolar bone loss (Page et al, 1997). The relationship between the gut Periodontal Treatment Restored Gut Microbiota microbiome and specific disease such as cancer (Scanlan et al, 2008), metabolic syndromes like obesity (Delzenne et al, 2011), diabetes (Qin et al, 2012), arteriosclerotic diseases (Koeth et al, 2013) has recently been underlined These diseases are often described in association with periodontal disease (Keller et al, 2015). Several studies in mice have shown that oral administration of periodontopathic bacteria Porphyromonas gingivalis significantly change the gut microbiota composition while induce local and systemic inflammation (Arimatsu et al, 2014; Nakajima et al, 2015; Kato et al, 2018) Another possible mechanism linking inflammatory systemic diseases and periodontitis could be a disturbance of the gut microbiome
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