Periodontitis and Seropositive RA | Arthritis Information

Share
 

FRI0129   MODERATE TO SEVERE ADULT PERIODONTITIS IS ASSOCIATED WITH INCREASED RISK OF SEROPOSITIVE RHEUMATOID ARTHRITIS IN NON-SMOKERS: THE ARIC STUDY

J. A. Molitor*1, A. Alonso2, M. H. Wener3, B. S. Michalowicz4, J. D. Beck5, A. R. Folsom2
1Medicine, 2Epidemiology, University of Minnesota, Minneapolis, 3Medicine, University of Washington, Seattle, 4Developmental and Surgical Sciences, University of Minnesota, Minneapolis, 5Dental Ecology, University of North Carolina, Chapel Hill, United States

Background: Genetic risks for the development of anti-citrullinated peptide antibodies (ACPA) have been established, but the only environmental exposure proven to contribute to ACPA+ Rheumatoid Arthritis (RA) risk has been tobacco exposure (TE). A large proportion of ACPA+ RA cases cannot be attributed to TE, however.
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 rheumatoid factor(RF) seropositivity of all RA cases in the cohort.
Methods: We examined hospitalization discharge codes of 5413 participants in the Atherosclerosis Risk in Communities (ARIC) study (1) from whom serum was obtained at the time of a detailed periodontal assessment in 1996-1998 (2). Periodontitis status (no, mild, moderate or severe disease) was determined using published criteria. Subjects who were 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) for incident RA were determined using the Cox proportional hazards model adjusting for age, sex, and race. Available sera from incident and prevalent RA cases were examined with a second-generation ACPA ELISA and ELISA for IgG-RF, IgA-RF, and IgM-RF.
Results: Incidence rates of hospitalization with a diagnosis of RA (n=33) for Caucasian ARIC participants were 1.1 per 1000 persons per year(female) and 0.8 per 1000 persons/year (male), comparable to the RA incidence previously described in Olmsted County, MN (3). 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), comparable to that seen in NHANES III (4). Among lifetime non-smokers, the HR was 8.8 (95% CI=1.1-68.9, p=0.04). Periodontitis severity was not independently 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).

Interesting. I had periodontitis a couple years  before RA diagnosis.  I'm seropositive. I know that any infection in the mouth can travel throughout your body. Hmmm.  (Don't have any problems with my mouth now, I go in three times a year for cleaning and have a sonic care toothbrush, floss alot.) 
Copyright ArthritisInsight.com