Background Chronic Porphyromonas Gingivalis (PG) infection is associated with parodonditis and the later is associated with rheumatism arthritis (RA). PG contains a bacterial deiminase able to citrullinate bacterial and human antigens. Thus it is logical to suspect an association with chronic PG infection and anti-CCP + RA.
Objectives To investigate a possible link between PG infection and RA antibody profile and structural damage.
Methods For assessing chronic PG infection we look at serum anti PG antibodies (titers were log-transformed) at baseline in the ESPOIR cohort consisting of 813 patients with early arthritis (more than 6 weeks and less than 6 months) not treated with steroid or DMARD. RA was defined according to ACR/EULAR 2010 criteria or ACR 1987 criteria. RA patients were divided between anti-CCP+ and -. Sex and age-matched control were also studied.
Results Among the 812 patients included in the ESPOIR cohort, 694 (78% female, mean age 48.5±12.3, mean DAS28 5.3±1.2) had RA according to ACR/EULAR 2010 criteria and 641 according to ACR 1987 criteria. Whatever the used criteria set, the level of anti-PG antibodies did not significantly differ between RA and non-RA patients. Likewise, the mean level of anti-PG antibodies in the 694 RA patients did not differ from that of 70 healthy controls (1.53±0.50 vs 1.47±0.43; p=0.20). The mean level of anti-PG antibody did not differ between anti-CCP positive and negative RA patients (1.48±0.43 vs 1.46±0.43; p=0.63), and did not correlate with anti-CCP levels.
Anti-PG antibody level did not correlate with DAS28 (rho=-0.01; p=0.76) or other parameters of disease activity or serum level of inflammatory cytokines (IL.6, IL1b, INFg or TNFa). Anti-PG antibody levels were higher in the 361 never smoker patients compared to the 333 ever smokers (1.51±0.42 vs 1.43±0.43; p=0.01). In sensitivity analyses, significantly more never smoker had high anti-PG level (>mean+2SD of healthy controls) than ever smoker (35.7% vs 27.6%; p=0.02). There was a trend for a higher frequency of baseline erosive change (mSharp score ≥1) in patients with high anti-PG levels compared to those with low levels (46.7% vs 32.4%; p=0.008). But the level of anti- PG antibodies was neither associated with baseline modified Sharp score (mSharp) nor with structural progression (defined by a >1 point increase of mSharp).
Conclusions Like in a much smaller study recently published, we could not detect in this large cohort of patients with early arthritis any association between anti PG antibodies with RA or anti CCP+ RA. However, we found an association between anti-PG levels and baseline erosive change in never smokers patients, suggesting a possible association in this population not exposed to this major pathogen.
Disclosure of Interest None Declared