Periodontitis in Patients With Severe Obesity: From the Oral and Gut Microbiota Dysregulation to the Visceral Adipose Tissue Inflammatory and Metabolic Disorders

重度肥胖患者的牙周炎:从口腔和肠道菌群失调到内脏脂肪组织炎症和代谢紊乱

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Abstract

During periodontitis, pathogenic oral bacteria like Porphyromonas gingivalis may exert systemic effects directly by translocating into the bloodstream and indirectly by deregulating the gut microbiota, aggravating obesity-related complications. This study aimed to evaluate the links between the periodontal infection, the oral and gut microbiota composition, and the inflammatory and metabolic profile during obesity. Thirty-nine patients suffering from severe obesity, with (n = 23) or without (n = 16) periodontitis, were enrolled. We examined the subgingival microbiota composition, periodontal status and salivary inflammatory response. The fecal microbiota composition was assessed by metagenomic analysis. Inflammatory and metabolic markers were measured in the plasma and epiploon visceral adipose tissue collected during bariatric surgery. Results show that patients with periodontitis exhibited an oral microbiota dysbiosis characterized by an increased abundance of bacteria from the red and orange complexes, worsened periodontal parameters (plaque index, bleeding index, gingival recession, probing depth and clinical attachment level), and higher IL-6 salivary levels. In fecal samples of patients with periodontitis, a higher proportion of the Proteobacteria phylum and changes in functional profile of bacteria were detected. Periodontitis was also linked to higher circulating concentrations of anti-P. gingivalis IgG, total cholesterol and lipoprotein (a). Moreover, periodontitis was associated with an enhanced production of TLR2, MyD88 and TGFβ, as well as higher activities of SOD and catalase antioxidant enzymes in the adipose tissue. Overall, these findings demonstrate that during obesity, the periodontal infection correlates with deregulated oral and gut microbiota composition, higher levels of pro-inflammatory mediators, and altered markers of oxidative stress and lipid metabolism.

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