The “red complex” of periodontal pathogens, composed of Treponema denticola (T.d.), Tannerella forsythia (T.f.), and Porphrymonas gingivalis (P.g.), are present in the majority of progressive gingival lesions of chronic periodontitis and have been identified as likely causative agents for periodontal tissue destruction.51 These organisms have a wide variety of virulence factors. P.g. expresses lipopolysaccharide (LPS), fimbrae, and hemagglutins, which allow the bacteria to invade periodontal pocket epithelium and initiate a host inflammatory response and also has a series of cysteine proteases, or gingipains, which render P.g. resistant to complement and create a feedback cycle in which the host’s attempts to clear the bacterial infection result in continued tissue damage, including bone resorption.52-56 This activation of bone resorption through activation RANKL in osteoblasts may lead to increased bone resorption at distant sites as well.57
The majority of RA cases are triggered by an autoimmune response to citrullinated proteins, which occur when proteins are enzymatically modified to replace the amino acid arginine with citrulline. This may occur for many required cell functions, including terminal differentiation of the epidermis and regulation of gene expression via chromatin remodeling.58,59 In genetically susceptible individuals, however, the generation of autoantibodies against ACPAs in synovial fluid can lead to a subsequent development of RA.60-62
P.g. is the only bacterium identified that has the capability to develop ACPAs antibodies;5,66 it has also been linked to ACPAs and their antibody formation in patients with RA and their relatives.62-66 The presence of antibodies to P.g. is associated with the development of RA (OR=2.96; 95% CI: 2.00-4.37); the strength of this association is greater than known risk factors such as smoking (OR=1.37; 95% CI 1.07-1.74).67 Similarly, expression of ACPAs were higher in patients with subgingival P.g. and with anti-P.g. antibodies than in those without evidence of P.g. infection.68 Anti-P.g. titers have also been associated with development of RA symptoms and greater disease activity in early RA patients.69
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