Rheumatoid arthritis

RA is a chronic, systemic inflammatory disorder of autoimmune origin, which most prominently affects the lining of synovial joints.

The pathogenesis of RA involves a complex interplay between genotype and environmental triggers. Twin studies implicate genetic factors in RA, and an association with the HLA-DRB1 locus has been established. Smoking and other forms of bronchial stress increase the risk of RA among persons with certain susceptibility. Infectious agents (such as EBV, CMV, proteus species, and E. coli) have been associated with RA, possibly through a mechanism involving molecular mimicry. The onset of RA is also linked with adverse life events, an association that is postulated to occur via neuroimmunologic interactions.

The prevalence of RA in the US is estimated at 410-450 persons per 100,000 population.

Synovitis occurs when leukocytes infiltrate the synovial compartment, a process mediated by leukocyte migration and endothelial activation in synovial microvessels, which upregulates the expression of adhesion molecules and chemokines. Over time, chronic synovial inflammation leads to destruction of articular cartilage and bony erosions.

RA is associated with progressive disability, premature death, and high socioeconomic costs. Approximately 75-80% of patients achieve remission and low disease activity with modern medical therapies.