AI Article Synopsis

  • The gut microbiome plays a crucial role in human health, influencing the development of various diseases, with this study focusing on the effects of a high-fat diet (HFD) on oral health and the gut microbiome.
  • The study established a dysbiosis model using high-fat diet-fed mice and compared it to probiotic treatment with LGG over 12 weeks, assessing changes in metabolic and inflammatory markers.
  • Findings indicated that the HFD resulted in decreased short-chain fatty acids and gingival blood flow, while increasing inflammation and matrix degradation, ultimately leading to periodontal disease; however, LGG treatment showed potential to counteract these negative effects.

Article Abstract

The gut microbiome has a very important role in human health and its influence on the development of numerous diseases is well known. In this study, we investigated the effect of high fat diet (HFD) on the onset of dysbiosis, gingival blood flow decreases, and the periodontal matrix remodeling. We established a dysbiosis model (HFD group) and probiotic model by GG (LGG) treatment for 12weeks. Fecal samples were collected 24h before mice sacrificing, while short chain fatty acids (SCFA) analysis, DNA extraction, and sequencing for metagenomic analysis were performed afterwards. After sacrificing the animals, we collected periodontal tissues and conducted comprehensive morphological and genetic analyses. While HFD reduced , SCFA, and gingival blood flow, this type of diet increased , lipopolysaccharide (LPS) binding protein, TLR4, pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6), matrix metalloproteinases (MMP-2 and MMP-9) expression, and also altered markers of bone resorption (OPG and RANKL). However, LGG treatment mitigated these effects. Thus, it was observed that HFD increased molecular remodeling inflammation, matrix degradation, and functional remodeling and consequently cause reduced gingival blood flow. All of these changes may lead to the alveolar bone loss and the development of periodontal disease.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7965981PMC
http://dx.doi.org/10.3389/fphys.2021.625780DOI Listing

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