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Abstract Number: 2913

the Periodontal Pathogen Aggregatibacter Actinomycetemcomitans Is Associated with Subclinical Coronary Atherosclerosis in Rheumatoid Arthritis

Jon T. Giles1, Jesper Reinholdt2, Joan Bathon3, Felipe Andrade4 and Maximilian F. Konig5, 1Division of Rheumatology, Columbia University, College of Physicians and Surgeons, New York, NY, 2Department of Biomedicine, Aarhus University, Aarhus, Denmark, 3Division of Rheumatology, Columbia University, College of Physicians & Surgeons, New York, NY, 4Medicine/Rheumatology, Johns Hopkins University School of Medicine, Baltimore, MD, 5Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA

Meeting: 2017 ACR/ARHP Annual Meeting

Date of first publication: September 18, 2017

Keywords: Cardiovascular disease, pathogenesis and risk assessment, Periodontitis, rheumatoid arthritis

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Session Information

Date: Wednesday, November 8, 2017

Session Title: Rheumatoid Arthritis – Clinical Aspects VI: Comorbidities of Rheumatoid Arthritis

Session Type: ACR Concurrent Abstract Session

Session Time: 9:00AM-10:30AM

Background/Purpose: The oral pathogen Aggregatibacter actinomycetemcomitans (Aa) generates citrullinated proteins targeted by autoantibodies in RA through its pore-forming toxin leukotoxin A (LtxA).  Aa-derived LtxA is implicated in atherogenesis and atherosclerotic plaque instability, conditions over-represented in RA.  No prior studies have explored the potential link between Aa, Aa-derived LtxA, and atherosclerosis in RA.

Methods: RA patients underwent cardiac computed tomography (CT) with coronary arterial calcification (CAC), a measure of coronary atherosclerosis, assessed.  Serum levels of IgG antibodies against Aa serotype b and purified LtxA were measured by ELISA.  Healthy controls cutoffs for seropositivity were used.   Multivariable robust regression was used to model the associations of anti-Aa and anti-LtxA with CAC, adjusting for pertinent confounders.

Results: A total of 194 RA patients [mean age=59 years; 60% female: median RA duration=9 years; 79% RF or anti-CCP seropositive] were studied.  Anti-Aa was detected in n=41 (21%) and anti-LtxA in n=82 (42%).  Adjusting for relevant confounders (listed in Fig), those with anti-LtxA had a mean CAC score 65% higher than those without anti-Aa or anti-LtxA (61 vs. 37 units, respectively; p=0.005 (Fig1a)].  Those anti-Aa+/anti-LtxA– had a mean adjusted CAC score 262% higher than those with neither antibody (134 vs. 37 units, respectively; p<0.001) and 120% higher than those with anti-LtxA, with or without concomitant anti-Aa.  Among CAC-associated features, swollen joint count (SJC) was differentially associated with CAC depending on the context of anti-LtxA.   In anti-LtxA– patients, SJC was not associated with CAC (Figure 1B, open circles).  However, in anti-LtxA+ patients, each swollen joint was associated, on average, with a 6 unit higher CAC score (p<0.001).  The interaction of anti-LtxA and swollen joints was significant (p=0.002).  The association was not linear, with a marked difference noted in those with>10 swollen joints (Figure 1B, solid diamonds).  Combining the two above groups with higher CAC scores [i.e. anti-Aa+/anti-LtxA– and anti-LtxA+ and>10 swollen joints; n=32 (16% of the cohort)], the adjusted mean CAC was 171% higher vs. those without these features (114 vs. 42 units, respectively; p<0.001).

Conclusion: Infection with the periodontal pathogen Aa may contribute to atherosclerosis in RA. Anti-LtxA, a marker of exposure to leukotoxic Aa strains, was significantly associated with more CAC and identified patients in which synovitis was robustly and independently associated with the extent of CAC.  A subgroup of RA patients with isolated antibody positivity to the leukotoxic Aa serotype b showed markedly higher risk of atherosclerosis. Additional studies are warranted to elucidate the underlying mechanism, and whether Aa-specific screening and treatment may reduce CVD risk in RA patients.


Disclosure: J. T. Giles, None; J. Reinholdt, None; J. Bathon, None; F. Andrade, None; M. F. Konig, None.

To cite this abstract in AMA style:

Giles JT, Reinholdt J, Bathon J, Andrade F, Konig MF. the Periodontal Pathogen Aggregatibacter Actinomycetemcomitans Is Associated with Subclinical Coronary Atherosclerosis in Rheumatoid Arthritis [abstract]. Arthritis Rheumatol. 2017; 69 (suppl 10). https://acrabstracts.org/abstract/the-periodontal-pathogen-aggregatibacter-actinomycetemcomitans-is-associated-with-subclinical-coronary-atherosclerosis-in-rheumatoid-arthritis/. Accessed May 17, 2022.
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