Date: Sunday, October 21, 2018
Session Title: Rheumatoid Arthritis – Etiology and Pathogenesis Poster I
Session Type: ACR Poster Session A
Session Time: 9:00AM-11:00AM
Seropositivity for anti-citrullinated protein antibodies (ACPA) and rheumatoid factor (RF) is a hallmark of RA and can be present years before clinical onset has become apparent. Environmental factors, including smoking and chronic inflamed mucosal tissues of the lungs, gastro-intestinal tract or oral cavity (i.e. the periodontium), are suggested to contribute to initiation of these autoantibodies. While it is known that the inflamed periodontium contains citrullinated proteins and peptides, only Harvey et al. (2013) showed that IgG ACPA is indeed present in the periodontal exudate (n=9). As the IgA isotype is specific for mucosal immunity, we assessed in patients with and without RA whether IgA RF and IgA ACPA are present gingivocrevicular fluid (GCF), the periodontal inflammatory exudate.
Methods: RA patients fulfilling the ACR/EULAR 2010 classification criteria were recruited at the Rheumatology department of the Dr. Sardjito General Hospital, Yogyakarta, Indonesia. Patients without RA (non-RA) were recruited from the Oral Surgery department of the same hospital. Patients with diabetes or cardiovascular disease were excluded. Periodontitis was defined as periodontal inflamed surface area (PISA)>130 mm2 (Leira et al. 2017). RF and ACPA were determined by ELISA in serum (IgM RF, IgA RF, IgG ACPA, IgA ACPA) and GCF (IgA RF, IgA ACPA). In addition, total IgA and IgG were determined in GCF. IgA ACPA seropositivity and IgA RF- and IgA ACPA positivity in GCF were defined as >mean+2SD of healthy controls (non-RA patients, never smokers, no periodontitis, n=88).
In non-RA patients (n=151), PISA was correlated with total IgG and IgA in GCF (p<0.0001). IgA RF and IgA ACPA were present in GCF and correlated with total IgA in GCF (p<0.05 and p<0.01 respectively). In contrast to RA patients (n=72), IgA RF and IgA ACPA in GCF of non-RA patients were not correlated with IgA RF en IgA ACPA in serum. In non-RA patients, IgA ACPA positivity in GCF was more frequent in ever smokers (18%) than in never smokers (9.8%), the same held for presence or absence of periodontitis (18 and 9.3% IgA ACPA positivity in GCF respectively). Moreover, in non-RA patients PISA was correlated with IgA ACPA in serum (p<0.01) and GCF (p=0.05).
Conclusion: In non-RA patients, RA-associated autoantibodies are present in GCF, and are presumably the result of local formation due to periodontitis. Local production of autoantibodies may contribute to onset of RA.
Harvey et al. J Periodontal Res 2013;48:252-61
Leira et al. Acta Odontol Scand 2017 Nov 11:1-4
To cite this abstract in AMA style:Rahajoe PS, de Smit MJ, Eelsing E, Kertia N, Vissink A, Westra J. Rheumatoid Arthritis (RA)-Associated Autoantibodies Are Present in the Periodontal Exudate of Patients with and without RA [abstract]. Arthritis Rheumatol. 2018; 70 (suppl 10). https://acrabstracts.org/abstract/rheumatoid-arthritis-ra-associated-autoantibodies-are-present-in-the-periodontal-exudate-of-patients-with-and-without-ra/. Accessed August 3, 2021.
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