• Rheumatoid arthritis (RA) is one of the most common autoimmune diseases: it affects roughly 1% of the population worldwide.1
  • The annual incidence of rheumatoid arthritis (RA) has been reported to be around 40 per 100,000.2
  • The disease pattern varies from country to country, along with prevalence rates between continents, races, ages and socioeconomic levels.1
  • Women are affected two to three times more frequently than men. 2 Women are also more likely to develop RA at a younger age than men.3
  • RA generally begins to affect people between the ages of 30 and 60; however, the average person doesn’t develop symptoms of RA until they reach their 60’s. 3
  • The specific cause of RA is not known, and there is no known cure for the disease. 3




Pathophysiology (see 3D video)


  • RA is the result of an autoimmune disorder.3
  • It is not a singular disease; instead, many pathways can lead to autoreactivity with similar clinical presentations.4
  • RA is based on immune responses in which the body’s immune system attacks its own healthy cells.5
  • Symptoms are triggered when an individual’s antibodies mistakenly attack the normal synovial joint fluid, causing chronic inflammation. 3
  • Distinct physiological mechanisms regulate inflammation and matrix destruction, including damage to bone and cartilage.4
  • RA results from a complex interaction between genes and the environment, leading to a breakdown of immune tolerance and synovial inflammation in a characteristic symmetric pattern.4
  • RA susceptibility is defined by a pattern of inherited genes, with the human leukocyte antigen (HLA) and major histocompatibility (MHC) genes as the most significant.4
  • The cytokinetic network in RA is complex, with many cytokines showing pleiotropic actions at several targets. Controlling the balance between pro-inflammatory and anti-inflammatory cytokines is an essential facet of management.6
  • Two key pro-inflammatory cytokines in RA are IL-1 and TNFα. While clinical trials have shown efficacy, blockade of these cytokines often does not fully control RA in all patients.6
  • Recent discoveries of novel cytokines such as IL-4, IL-10, IL-17, IL-18 and RANK ligand (RANKL) have expanded our knowledge of the pathogenesis of RA.6



  1. Elsaman AM, et al. AB0291 Epidemiology and comorbidity of rheumatoid arthritis in upper Egypt, a hospital based study. Ann Rheum Dis. 2017. Available at:  https://ard.bmj.com/content/76/Suppl_2/1150.1.  
  2. Pauk J, et al. Infrared Thermography Sensor for Disease Activity Detection in Rheumatoid Arthritis Patients. Sensors. 2019;19(16),3444.
  3. Freeman J. RA Facts: What are the Latest Statistics on Rheumatoid Arthritis? 2018. Available at: https://www.rheumatoidarthritis.org/ra/facts-and-statistics/.
  4. Firestein G, et al. Pathogenesis of rheumatoid arthritis. UpToDate. 2019. Available at: https://www.uptodate.com/contents/pathogenesis-of-rheumatoid-arthritis.
  5. Centers for Disease Control and Prevention. Rheumatoid Arthritis. 2019. Available at: https://www.cdc.gov/arthritis/basics/rheumatoid-arthritis.html.
  6. Lubberts E, van den Berg W. Cytokines in the Pathogenesis of Rheumatoid Arthritis and Collagen-Induced Arthritis. Madame Curie Bioscience Database. 2013. Available at: https://www.ncbi.nlm.nih.gov/books/NBK6288/.


Toolkit Intro





Additional Reading