This research was originally published in 2014 by Elliot D. Rosenstein, Laura J. Kushner & Neil Kramer.
We have curated this article as a reference point for The Larkin Protocol.
Despite advances in our understanding of the inflammatory events that underlie rheumatoid arthritis (RA), which have led to targeted therapies that more effectively control the condition, the etiology of RA is not fully understood. With the discovery that serum antibodies to citrullinated peptides (ACPA) are highly specific for RA and that Porphyromonas gingivalis, the major pathogen responsible for periodontitis (PD), contains the enzyme responsible for the citrullination of peptides, a plausible explanation for observations of increased incidence and severity of PD in RA patients and an appreciation of pathogenic similarities between the two conditions has emerged. Studies of the effect of RA treatment on the severity of PD have been limited and conflicting, especially with respect to anti-TNF agents, but indicate the potential for IL-6 as a therapeutic target for both conditions. PD treatment appears to improve clinical and laboratory evidence of RA disease activity, and the response of RA to anti-TNF therapy is abrogated by the presence of PD. Thus, evaluation and treatment of PD can be recommended for all RA patients.
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