Epidemiology and Etiology of RA

RA is a chronic, destructive, inflammatory disease that is characterized by the accumulation and persistence of an inflammatory infiltrate within the synovial fluid of a patient’s joints and the destruction of the bony architecture of the joint.1-5 This ultimately leads to irreversible joint damage, loss of function and a significant burden on patients and society related to discomfort and treatment costs. It is estimated to affect 1.3 million adults in the United States (U.S.), approximately 0.5-1% of the population over the age of 35 years.1 RA affects females more frequently than males, in a 3:1 ratio, and the onset is most commonly seen in the 4th and 5th decades of life.14,15 At least three types of RA have been described in clinical studies: 1) self-limiting, 2) easily controlled, and 3) progressive.16-18 Many patients who seek care in a rheumatology clinic have a progressive form of the disease and present with a number of markers of inflammation and autoimmune disease, including rheumatoid factor, rheumatoid nodules, high erythrocyte sedimentation rate, HLA-DR4 haplotype, autoantibodies against citrullinated peptides (ACPA), and high numbers and severity of joint involvement as measured by the disease activity (DAS) score.19-22

The exact cause of RA is unknown, with many different stimuli having demonstrated an ability to activate the immune and inflammatory response seen in RA.23-26 Current understanding suggests RA may be initiated by exogenous infective agents as well as endogenous substances, such as connective-tissue proteins or immunoglobulins, in patients with a genetic predisposition.23-26 While infectious agents have been proposed as etiologic factors for RA, a single organism has not been identified, and it may be likely numerous agents may be able to initiate an RA response in susceptible individuals. Nonetheless, several agents including Gram negative anaerobic bacteria like those found in periodontitis have been implemented in the etiology of RA.27-29