Aggregatibacter actinomycetemcomitans

It has been a long-held supposition of many doctors and researchers that dental infections and gum disease play an important role in rheumatoid arthritis (RA) and the following recent research provides additional validation.


Associations of Antibodies Targeting Periodontal Pathogens with Subclinical Coronary, Carotid, and Peripheral Arterial Atherosclerosis in Rheumatoid Arthritis. Jon T Giles et al. Arthritis Rheumatol.

In this study, multi-center researchers have identified antibodies associated with periodontal infections and atherosclerosis plaques in 197 rheumatoid arthritis (RA) patients. Of the patient sera assayed, the predominant oral pathogens identified were, Porphyromonas gingivalis (anti‐Pg), Aggregatibacter actinomycetemcomitans serotype b (anti‐Aa), and Aa leukotoxin A (anti‐LtxA). However, it was the infection Aa and/or its major virulence factor LtxA, that demonstrated immunoreactivity in the vascular atherosclerotic beds of RA patients, correlating with rheumatic disease activity. These authors conclude by suggesting that the prevention and treatment of periodontal disease may play a role in deterring coronary vascular disease in RA patients.


Aggregatibacter actinomycetemcomitans-induced hypercitrullination links periodontal infection to autoimmunity in rheumatoid arthritis. Sci Transl Med. 2016 Dec 14;8(369):369ra176.

Multi-center research conducted at numerous, prestigious medical institutions in the United States and Denmark, conclude that an oral pathogen, Aggregatibacter actinomycetemcomitans (Aa), is one of a number of organisms contributing to periodontal gum disease that can trigger the production of auto-antibody citrullinated proteins in genetically susceptible (HLA-DRB1) rheumatoid arthritis (RA) individuals. These authors state that the formation of periodontal citrullinated proteins due to Aa mirror the rheumatoid joint in which hypercitrullination occurs. Further, that Aa had the ability to cause hypercitrullination in the neutrophils of the host and led to elevation in anti-CCP and rheumatoid factor (RF). These authors conclude that Aa is a bacterial candidate for triggering RA.


 

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