Disease ⇒ Periodontal disease {40000225}

References Notes

Shared Reference Notes

• [1.6] 
  -Streptococcus salivarius K12 and M18 prevented immune activation induced by periodontal disease pathogens.
• [1.7] 
  - Coexisting hypertension and periodontal disease > increased Neisseria and Solobacterium genera
• [1.5] 
  - Saccharibacteria species > reduce inflammation and consequential bone loss by modulating host bacterial pathogenicity in a mouse ligature-induced periodontitis model.
• [1.8] 
  - Secretory calcium-binding phosphoprotein proline-glutamine rich 1 (SCPPPQ1), a protein normally produced by the gingival epithelium to mediate its attachment to teeth, was suggested to be bactericidal.
  - Incubation of Porphyromonas gingivalis, a major periodontopathogen, with the full-length protein resulted in decrease in bacterial number, formation of aggregates and membrane disruptions.
• [1.9] 
  - in periodontitis-diseased tissues, P. gingivalis was present, but not much LPS was evident in tissues.
  - these bacterial lipids accumulate in structures in blood vessels that can lead to thickening or blockages called atheromas.
  - in the blood of MS patients, and they found that the bacterial lipid levels were lower in MS patients, a very surprising result. They expected, if anything, that patients with the autoimmune disease would have more lipid present.
• [1.10] 
  - Transplantation of periopathogenic microbiota from the SP patients altered the caecal microbiota and induced low-grade intestinal inflammation in mice.
  - The abundance of Porphyromonadaceae and Fusobacterium, which are co-pathogens in periodontitis and intestinal inflammation was significantly enriched in the gut of the C-SP group.
  - Interestingly, Porphyromonadaceae was also enriched in the salivary samples from the humans, revealing the close relationship between the salivary and gut microbiota.