But in the late 1990s, studies in the periodontal literature noted the presence of an enzyme (i.e., peptidyl arginine deiminase) produced by the major organism responsible for development of periodontitis (Porphyromonas gingivalis) that could lead to the production of altered (i.e., citrullinated) proteins. Simultaneously, the development of antibodies to citrullinated proteins (ACPAs) had been noted in patients with RA and the measurement of ACPAs had become the most specific and sensitive test for diagnosing RA.
When comparing studies with a periodontist, Laura Kushner, DDS, in their respective fields, they noted the intersection of the two fields. Along with colleagues in 2004, they proposed that RA could be triggered by the immune response to this periodontal organism and lead to the antibodies that contributed to development of RA.5
“Medical and dental school faculty members, even within the same university, often have little interaction with one another,” Dr. Rosenstein says. “This research demonstrates the benefit of communication and collaboration across disciplines and how disciplines devoted to disorders with shared mechanisms and pathways can inform each other.”
In the 10 years since that hypothesis was published, scores of studies have substantiated not only a clinical connection between the two conditions, but also a direct impact of one disease on the other, Dr. Rosenstein continues.
“If the exciting results of the studies done in the past 10 years since our hypothesis was proposed are borne out by more extensive testing, we are dealing with not just the treatment of RA, but the potential prevention of the disease,” Dr. Rosenstein surmises.
Additional research should focus on longitudinal observational studies and microbiome analysis to elucidate the temporal relationship between development of gum disease and RA, Dr. Rosenstein says.
“Development of inhibitors of the enzyme responsible for the alteration of proteins that cause them to become identified by the immune system (i.e., citrullination) may offer new treatment approaches,” Dr. Rosenstein says.
“Treatments of the organism responsible for PD may prove to be effective agents to treat RA, with the possibility of developing vaccines against the organism being an additional approach.”
Karen Appold is a medical writer in Pennsylvania.
References
- Rosenstein ED, Kushner LJ, Kramer N. Rheumatoid arthritis and periodontal disease: A rheumatologist’s perspective. Curr Oral Health Rep. 2015;2:9–19.
- Mercado FB, Marshall RI, Klestov AC, Bartold PM. Relationship between rheumatoid arthritis and periodontitis. J Periodontol. 2001;72:779–787.
- Scher JU, Ubeda C, Equinda M, Khanin R, et al. Periodontal disease and the oral microbiota in new-onset rheumatoid arthritis. Arthritis Rheum. 2012;64:3083–3094.
- Rosenstein ED, Kushner LJ, Kramer N, Kazandjian G. Pilot study of dietary fatty acid supplementation in the treatment of adult periodontitis. Prostaglandins Leukot Essent Fat Acids. 2003;68:231–238.
- Rosenstein ED, Greenwald R, Kushner LJ, Weissmann G. Hypothesis: The humoral immune response to oral bacteria provides a stimulus for the development of rheumatoid arthritis. Inflammation. 2004;28:311–318.
