Background Anti-citrullinated protein antibodies (ACPA), rheumatoid factor (RF) and anti-carbamylated proteins (anti-CarP) can be present before clinical manifestation of rheumatoid arthritis (RA). Periodontitis is regarded as a possible risk factor for RA, partly because of presence of citrullinated proteins in inflamed periodontal tissue. Porphyromonas gingivalis (PG), a periodontal pathogen that can citrullinate bacterial and human proteins is considered a possible contributor to disease onset of RA.
Objectives To assess the systemic presence of ACPA, RF and anti-CarP in serum of severe periodontitis patients and periodontal healthy persons. Reactivity to citrullinated peptides was assessed in a subgroup.
Methods In a group of 117 adult patients with severe periodontitis without other systemic disease (51±9.3 years, 58% female, 43% current smoker) and a group of 38 healthy controls with no signs of periodontitis (36±16 years, 53% female, 13% current smoker), the following serum autoantibodies were assessed by ELISA: IgG ACPA (anti-CCP2, Euro Diagnostica, cut off for positivity > 25U/ml), IgA, IgG and IgM RF (in-house, cut off for positivity > 25, >25 and >15 U/ml, respectively) and IgG anti-CarP (anti-carbamylated FCS and anti-carbamylated fibrinogen). IgA, IgG and IgM antibodies against periodontal pathogens PG and Prevotella intermedia (PI), which is closely related to PG, were also assessed. In a subpopulation of severe periodontitis patients (n=41) and periodontal healthy controls (n=13), IgG antibodies against citrullinated peptides were determined by ELISA. Extinctions were corrected for the native forms of the peptides and positive reactivity was defined as mean + 2 SD of the extinctions of periodontal healthy controls.
Results Positivity for RF (IgM 6.0% (n=7), IgA 5.3% (n=6), IgG 1.7% (n=2)) and ACPA (1.7% (n=2)) was found in severe periodontitis patients, but in none of the periodontal healthy controls. Reactivity against citrullinated peptides was higher in severe periodontitis patients (positive for cit-fibrinogen-1 (n=2), for cit-fibrinogen-2 (n=7), for cit-fibrinogen-3 (n=5), for cit-enolase (n=7) and for cit-vimentin (n=6)) compared to periodontal healthy controls (positive only for cit-fibrinogen-2 (n=1)). Positivity for anti-CarP did not differ between periodontitis patients and HC. IgG anti-PG and anti-PI were significantly increased in periodontitis patients compared to periodontal healthy controls, but there was no correlation with RA auto-antibodies.
Conclusions Positivity for RF, and ACPA, and reactivity against citrullinated peptides was found in patients with severe periodontitis but not in periodontal healthy persons. This observation suggests that to detect presence of ACPAs in an early stage, local ACPA production by B-cells in periodontium of periodontitis patients must be assessed.
Disclosure of Interest None Declared