Abstract
Rheumatoid arthritis (RA) and adult periodontitis share common pathogenetic mechanisms and immunologic and pathological findings. One oral pathogen strongly implicated in the pathogenesis of periodontal disease, Porphyromonas gingivalis, possesses a unique microbial enzyme, peptidylarginine deiminase (PAD), the human equivalent of which has been identified as a susceptibility factor for RA. We suggest that individuals predisposed to periodontal infection are exposed to antigens generated by PAD, with de-iminated fibrin as a likely candidate, which become systemic immunogens and lead to intraarticular inflammation. PAD engendered antigens lead to production of rheumatoid factor-containing immune complexes and provoke local inflammation, both in gingiva and synovium via Fc and C5a receptors.
MeSH terms
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Adult
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Antibody Formation / genetics
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Antibody Formation / immunology*
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Arthritis, Rheumatoid / etiology*
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Arthritis, Rheumatoid / immunology
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Arthritis, Rheumatoid / microbiology
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Arthritis, Rheumatoid / pathology
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Disease Susceptibility / etiology
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Disease Susceptibility / immunology
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Disease Susceptibility / microbiology*
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Disease Susceptibility / pathology
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Humans
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Hydrolases / immunology
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Hydrolases / metabolism
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Models, Biological*
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Mouth Mucosa / microbiology*
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Periodontitis / etiology
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Periodontitis / microbiology
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Periodontitis / pathology
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Porphyromonas gingivalis / enzymology*
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Porphyromonas gingivalis / pathogenicity
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Protein-Arginine Deiminases
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Rheumatoid Factor / biosynthesis
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Rheumatoid Factor / immunology
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Synovial Membrane / immunology
Substances
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Rheumatoid Factor
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Hydrolases
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Protein-Arginine Deiminases