牙周炎
结肠炎
牙槽
医学
炎症
化学
病理
内科学
牙科
作者
Guangyi Yuan,Junyu Chen,Xiaoxue Wang,Fei Hu,Xueyang Zhang,Xuanjun Chen
标识
DOI:10.1016/j.archoralbio.2022.105583
摘要
To evaluate the pathogenic role of colitis in experimental periodontitis and explore the potential serum metabolites of colitis exacerbating experimental periodontitis in mice model.C57BL/6 mice were divided into four groups (five mice in each group), including control, periodontitis, colitis and colitis+periodontitis group. Mice treated with 1.5 % dextran sulfate sodium for 14 days to induce colitis. On the seventh to fourteenth days, the experimental periodontitis model was established by installing a bacterially retentive ligature between two molars. Histological alteration of periodontium and colon was observed by hematoxylin and eosin staining. Tartrate-resistant acid phosphatase staining and micro-computed tomography was applied to evaluate alveolar bone loss. Gas chromatography-mass spectrometry was used to characterize serum metabolic profiles.Mice in colitis+periodontitis group displayed increased periodontal inflammation and alveolar bone loss when compared with the mice of periodontitis group, suggesting colitis aggravated periodontitis. Metabolomics analysis combined with enrichment analysis showed that colitis significantly (P<0.05) altered the content of compounds associated with five metabolic pathways (e.g. fatty acid biosynthesis) of periodontitis mice. Notably, colitis significantly reduced the level of serum metabolites that inhibited the formation of osteoclasts (e.g. oleic acid) or anti-inflammatory metabolites (e.g. palmitoleic acid, palmitelaidic acid and chlorogenic acid) of periodontitis mice.Our findings showed that colitis might aggravate periodontitis and this might be associated with alteration of serum metabolic profiles.
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