High-fat diet exacerbates periodontitis: is it because of dysbacteriosis or stem cell dysfunction?

Abstract

Previous studies have shown that high-fat diet (HFD) may aggravate periodontitis, however the underlining mechanism remains to be further clarified. This study aims to explore whether HFD promotes periodontitis by inducing periodontal microbiota dysbiosis or stem cell dysfunction. A high-fat diet was given to four-week-old male Sprague-Dawley rats for 12 weeks. Periodontitis was induced during the latter 4 weeks. At the end of the 12th week, samples were collected after euthanasia. Maxillae were harvested for histological or microbial analysis. The microbial 16S rRNA gene sequencing was performed with the Illumina MiSeq platform. The data was analyzed through RDP Classifier against the SILVA database. The mandible molars were harvested for isolating periodontal ligament stem cells (PDLSCs). The protein level of p27, p21, and p16, which are negative regulators of the cell cycle, in PDLSCs were detected. Markers of osteogenic differentiation and pro-inflammatory mediators were detected by real-time polymerase chain reaction. Activation of pro-inflammatory signaling pathways was detected by Western blotting. We found that HFD significantly increased ligature-induced alveolar bone loss. HFD resulted in a less diverse periodontal microbiota, with increased proportions of Lactococcus, Bacillus, Alloprevotella, Carnobacterium, and Exiguobacterium and decreased proportion of Nitrospira. HFD increased the protein levels of p27, p16, and p21, and upregulated the expression of osteogenic biomarkers, IL-1β and IL-10 with the ERK1/2 signaling pathway activated in PDLSCs.