Rheumatoid Arthritis (RA) is a chronic autoimmune disease. When the immune system is functioning normally, it recognises things like harmful bacteria and viruses, and responds by creating an “army” of antibodies that seek out and fight them off. In an autoimmune disease, the body mistakenly thinks that normal tissues or organs of the body are harmful, leading to inflammation and damage.
The Merriam-Webster dictionary definition of pathophysiology is: the physiology of abnormal states; specifically, the functional changes that accompany a particular syndrome or disease.
In RA, this effectively results in the body’s immune system attacking the tissues of the joints, causing pain and inflammation. RA can cause permanent damage to joints, especially in the early years of the disease. Let’s learn a little more of the science behind the development of RA.
The pathway to development of rheumatoid arthritis
Whilst the cause of RA is not fully understood, a number of risk factors such as smoking, obesity, and family history have been implicated in the development of RA.
Broadly speaking, the combination of these factors can send a trigger to the body to create antibodies – known as autoantibodies – that seek out joint linings. These autoantibodies include rheumatoid factor (RF) and anti-cyclic citrullinated peptide antibody (anti-CCP).
This results in the production of chemicals being released including tumour necrosis factor alpha (TNF-α), Interleukin (IL)-1, IL-6, IL-8, transforming growth factor beta (TGF-β), fibroblast growth factor (FGF) and platelet-derived growth factor (PDGF).
Joint and tissue destruction
These chemicals inflame and damage the body’s cartilage, bone, tendons, and ligaments, resulting in the symptoms seen in Rheumatoid Arthritis.
- 1. Merriam Webster Dictionary.
- 2. Medscape. Rheumatoid Arthritis. Accessed 8 October 2018