Oral bacterium P. gingivalis has been well-documented as a mediator of periodontal disease. Furthermore, hosts harboring this pathogen have been shown to have greater risk for rheumatoid arthritis. Researchers are elucidating the mechanisms by which P. gingivalis contributes to the pathogenesis of arthritic and their related disorders. Upregulation of intestinal lipopolysaccharides and subsequent inflammation, as well as citrullination of alpha-enolase, which shares homology with human tissue α-enolase, are described mechanisms of autoimmunity.
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Oral bacterium P. gingivalis has been well-documented as a mediator of periodontal disease. Furthermore, hosts harboring this pathogen have been shown to have greater risk for rheumatoid arthritis.
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AA/EPA, Akkermansia muciniphila, Alloprevotella, Alpha Gliadin IgG, Alpha-Beta Gliadin IgG, Amylase/Protease Inhibitors IgG, Anti-Actin IgG, Anti-LPS (IgG + IgM), Anti-LPS IgA, Anti-Zonulin IgG, Arachidonic acid (AA), Bacillus coagulans, Bacteroides, Bifidobacterium bifidum, Bifidobacterium infantis, Bifidobacterium lactis, Clostridium, Clotridiales Incertae Sedis IV, Copper to Zinc Ratio, Eggerthella lenta, Escherichia coli Nissle, Faecalibacterium, Farinins IgG, Gamma Gliadin IgG, Globulins IgG, Gluteomorphin IgG, HMW Glutenin IgG, Lactobacillus animalis, Lactobacillus paracasei, Linoleic acid (LA), LMW Glutenin IgG, Omega Gliadin IgG, Oscillospira, Porphyromonas gingivalis, Prodynorphin IgG, Pseudobutyrivibrio, Purinin IgG, Serpin IgG, Streptococcus, Total Omega-6, Tyzzerella