Epidemiology/Pathophysiology

EPIDEMIOLOGY

• 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

REFERENCES

 

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/.