“Rheumatoid arthritis is a chronic disease affecting over 1.3 million Americans and as much as 1% of the worldwide population.” (www.rheumatoidarthritis.org) There is a growing body of research indicating a causal association between specific periodontal pathogens and rheumatoid arthritis (RA). In a 2009 study, in Compendium of Continuing Education in Dentistry, the authors indicate that a specific perio pathogen, Porphyromonas gingivalis (P.g.), produces an enzyme capable of modifying specific proteins. The bacterial enzymes catalyze a protein folding reaction. The body recognizes this folded protein as a foreign entity. The body mobilizes an auto-immune response to these proteins, which culminates clinically in the joint destruction typically seen in RA susceptible individuals. The authors conclude that if further research affirms the initiation of rheumatoid arthritis by P.g., periodontal disease prevention and treatment may lead to the prevention of RA in susceptible individuals. A number of studies reached the same conclusions of the Smolik, et al study.1
A 2015 study, in Best Practice & Research: Clinical Rheumatology, stated the following “Converging and reproducible evidence now makes a clear case for the role of specific periodontal infective pathogens in initiating, amplifying and perpetuating rheumatoid arthritis. The unique enzymatic properties of the periodontal pathogen Porphyromonas gingivalis and its contribution to the burden of citrullinated peptides is now well established.”2
As recent as 2016, a study published in the journal Science Translational Medicine had the following conclusion “These studies identify the periodontal pathogen A.a. as a candidate bacterial trigger of autoimmunity in RA.”3
Worthy of note is this research is not indicating a relationship between periodontal disease and RA. Rather the causal link to be considered is between P.g. & RA and A.a. & RA. Interestingly, the tissue destructive mechanisms in periodontitis and rheumatoid arthritis are remarkably similar. The immunological and pathological processes occurring in periodontitis and RA are nearly identical. Both conditions are characterized by chronic inflammation in a soft tissue site adjacent to bone.
When a patient in our dental practice indicates that they have RA are we going to practice as usual? I challenge us to take into consideration the periodontal pathogens/RA link. Test for the presence of the two periodontal pathogens that have been linked to RA (A.a &P.g.). Knock down the population of these bacterial species if testing confirms their presence. This is a great opportunity to potentially impact someone’s health and quality of life.
1. Compendium of Continuing Education in Dentistry. 2009 May;30(4):188-197
2. Best Pract Res Clin Rheumatol. 2015 Apr;29(2):189-201
3. Sci Transl Med. 2016 Dec 14;8(369):369ra176
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