Rheumatoid Arthritis and Periodontal Disease: A Rheumatologist's Perspective
December 2014
Abstract
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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