Newswise — Moderate to severe perodontitis has been linked to the development of rheumatoid arthritis among non-smokers, according to research presented this week at the American College of Rheumatology Annual Scientific Meeting in Philadelphia, Pa.
Rheumatoid arthritis is a chronic disease that causes pain, stiffness, swelling, and limitation in the motion and function of multiple joints. Though joints are the principal body parts affected by RA, inflammation can develop in other organs as well. An estimated 1.3 million Americans have RA, and the disease typically affects women twice as often as men.
Periodontal disease is a gum disease characterized by inflammation that leads to separation of the teeth from the gums, loss of bony support, and possible tooth loss.
Researchers recently set out to determine the risk for developing RA based on periodontitis as well as asses the levels of protein-attacking antibodies and rheumatoid factor in these patients.
The researchers studied 6,616 people who were a part of a separate epidemiological study who had been examined four times between 1987 and 1998. Each individual was assessed for periodontal disease between 1996 and 1998.
Each participant was characterized as having no, mild, moderate or severe periodontitis and either prevalent RA (having been hospitalized with a diagnosis of RA within the nine years before their periodontal exam) or new RA (having been hospitalized with a diagnosis of RA within eight years after their periodontal exam). In addition, researchers performed anti-cyclic citrullinated peptide antibody tests on blood samples collected during their study visits.
The risk of developing RA was over twice as high in persons with moderate to severe periodontitis, compared to those with no-mild periodontitis. The risk of developing RA was even higher among non-smokers with moderate to severe periodontitis compared to non-smokers with no to mild periodontitis.
People with peridontitis were also more likely to develop higher levels of the anti cyclic citrullated antibody, which has been associated with more severe, damaging RA. Those individuals with positive anti-cyclic citrullinated antibodies were more likely to have moderate to severe periodontitis and to be smokers than those who did not have both of those putative RA risks.
The researchers conclude that moderate to severe periodontitis may be a risk for developing RA, in non-smokers, and that it may increase the risk of anti-CCP antibody positivity in smokers.
“Moderate to severe periodontitis, a chronic infectious disease of the gums leading to loosening of the teeth, may also increase the risk of developing rheumatoid arthritis,” explains Jerry A. Molitor, MD, PhD; associate professor, department of medicine, division of rheumatology and autoimmune disease, University of Minnesota Minneapolis, Minn., and lead investigator in the study.
“Furthermore, among those who smoke, moderate to severe periodontitis may increase the risk of developing a specific type of antibodies associated with more severe, damaging rheumatoid arthritis. These studies point out the importance of further studies into how periodontitis may predispose to RA, and the possible value of dental care in prevention of RA."
The ACR is an organization of and for physicians, health professionals, and scientists that advances rheumatology through programs of education, research, advocacy and practice support that foster excellence in the care of people with or at risk for arthritis and rheumatic and musculoskeletal diseases. For more information on the ACR’s annual meeting, see www.rheumatology.org/annual.
Editor’s Notes: Dr. Molitor will present this research during the ACR Annual Scientific Meeting at the Pennsylvania Convention Center at 2:30 PM on Monday, October 19 in Room 103 A. Dr. Molitor will be available for media questions and briefing at 8:30 AM on Monday, October 19 in the on-site press conference room, 109 A.
Presentation Number: 1160
Moderate to Severe Adult Periodontitis Increases Risk of Rheumatoid Arthritis in Non-Smokers and Is Associated with Elevated ACPA Titers: The ARIC Study
J. A. Molitor, MD, PhD, Rheumatic/Autoimmunie Diseas, Univ of MN, Minneapolis, MN A. Alonso, PhD, School of Public Health, Univ of MN, Minneapolis, MN M.H. Wener, M.D., Univ of WA, Seattle, WA B.S. Michalowicz, MS, Department of Developmental and Surgical Sciences, Univ of MN, Minneapolis, MN J. Beck, PhD, Dental Ecology, Univ of NC, Chapel Hill, NC V. H. Gersuk, PhD, Benaroya Rsch Ini., Seattle, WA J.H. Buckner, M, M.D., Benaroya Rsch Ini., Seattle, WA A.R. Folsom, MPH, School of Public Health, Univ of MN, Minneapolis, MN
Purpose: Genetic risks for the development of anti-citrullinated peptide antibodies (ACPA) have been established, but the only environmental exposure consistently associated with ACPA+ Rheumatoid Arthritis (RA) risk is tobacco exposure (TE).
Objectives: 1. Establish the risk for development of incident (new) RA cases in a large cohort characterized for periodontitis severity and smoking status. 2. Assess ACPA and RF seropositivity of RA cases.
Method: We studied 6616 participants in the Atherosclerosis Risk in Communities (ARIC) study who were examined 4 times during the period 1987-1998 and for whom a detailed periodontal assessment was made in 1996-1998. Periodontitis status (no, mild, moderate or severe disease) was determined using published criteria. Subjects hospitalized with a discharge code of RA in the 9 years before their periodontal exam were designated as having “prevalent” RA; those with a first-time RA discharge code up to 8 years following their periodontal assessment were designated as having “incident” RA. Hazard ratios (HR) were determined using the Cox proportional hazards model adjusting for age, sex, and race. Available sera from 1990-92 and 1996-98 from both the incident and prevalent RA cases were examined with a second-generation ACPA ELISA and ELISA for IgG-RF, IgA-RF, and IgM-RF. HLA- DR4 alleles were determined by quantitative real-time PCR.
Results: Incidence rates of RA in the ARIC cohort were comparable to those in Olmsted County, MN. The HR of developing RA in subjects with moderate to severe periodontitis (n= 27) was 2.6 (95% CI=1.0-6.4, p=0.04), compared to those with no to mild periodontitis (n= 6). Among lifetime non-smokers, the HR was 8.8 (95% CI=1.1-68.9, p=0.04). In adjusted analyses, periodontitis severity was not associated with RA incidence among current and former smokers. ACPA levels were significantly higher in participants with moderate-severe periodontitis than in those with no-mild periodontitis (222.5 U vs. 8.4 U, p=0.04). Of 13 cases with ACPA+ at either sampled visit, 11 were both smokers and had moderate-severe periodontitis (85%, vs 47% predicted, chi-square, P=0.007), indicating a possible interaction between smoking and periodontitis in the production of ACPA. Of 12 DR4+ participants, 6/7 ACPA+ were both smokers and had moderate-severe periodontitis, whereas only 1/5 ACPA-/DR4+ individuals was both a smoker and had moderate-severe periodontitis (p=0.07, Fisher’s exact test). Conclusion: Moderate to severe periodontitis may be a risk factor for the development of RA in non-smokers. Individuals with moderate to severe periodontitis have higher ACPA titers than those with no or mild periodontitis. There is evidence of an interaction between smoking and periodontitis increasing the likelihood of high-titer ACPA.
Supported by the Minnesota Medical Foundation and RO1DE11551.
Disclosure: J. A. Molitor, None; A. Alonso, None; M. H. Wener, None; B. S. Michalowicz, None; J. Beck, None; V. H. Gersuk, None; J. H. Buckner, None; A. R. Folsom, None.
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