Rheumatoid Arthritis: Risk Factors, Causes, Treatment


Today, the primary treatment procedure for rheumatoid arthritis is based on suppressing the inflammation, which begins during the stage when patients’ have joint swelling. T-cell responses which cause the autoantibody production can be targeted by medications such as rituximab to prevent the disease from starting (McInnes & Schett, 2017).

Other types of treatment include bed rest and the use of both non-steroidal anti-inflammatory drugs and disease-modifying antirheumatic drugs, for example, methotrexate (McInnes & Schett, 2017).

Another way to induce tolerance is to reduce antigen expression and the formation of a pathogenic immune complex.
Finally, one of the most widespread approaches to address the disease is to stop smoking, which also has to be accompanied by weight control, dental care, and comorbidities management.


Aletaha, D., & Smolen, J. S. (2018). Diagnosis and management of rheumatoid arthritis: A Review. JAMA, 22, 10–18. Web.

Deane, K. D., Demoruelle, M. K., Kelmenson, L. B., Kuhn, K. A., Norris, J. M., & Holers, V. M. (2017). Genetic and environmental risk factors for rheumatoid arthritis. Best Practice & Research Clinical Rheumatology, 31(1), 3–18. Web.

Guo, Q., Wang, Y., Xu, D., Nossent, J., Pavlos, N. J., & Xu, J. (2018). Rheumatoid arthritis: pathological mechanisms and modern pharmacologic therapies. Bone Research, 6(15), 1–14. Web.

McInnes, I. B., & Schett, G. (2017). Pathogenetic insights from the treatment of rheumatoid arthritis. The Lancet, 389(10086), 2328–2337. Web.

Weyand, C. K., & Goronzy, J. J. (2020). The immunology of rheumatoid arthritis. Nature Immunology, 22(1), 10–18. Web.

Information on Rheumatoid Arthritis


Rheumatoid arthritis is an auto-immune condition during which chronic inflammation occurs in the synovial membrane, which eventually can lead to the destruction of juxta-articular bone and articular cartilage. Currently, there is no evidence of particular causes of the disease, yet it has been established that both genetic and environmental factors contribute to the development of the condition.

Studies have described more than one hundred genetic loci which are associated with rheumatoid arthritis and its progression. For example, some of the human leukocyte antigen class II antigens which contain amino acids in the area which are “responsible for antigen presentation to T lymphocytes are most associated with RA” (Aletaha & Smolen, 2018).

Anti-citrullinated protein antibodies (ACPAs) are also reliable predictors of the disease since they are found in 67% of all patients who have rheumatoid arthritis (Guo, 2018). Environmental aspects also can cause the condition to start progressing, for instance, smoking has been discovered to contribute to antibody formation.

Risk Factors

The development of rheumatoid arthritis is strongly associated with genetic factors since it is prevalent among withing families. The familial risk is estimated at 40-50%, and the first-degree relatives are most likely to have the disease (Deane, 2017).

The general predisposition to inflammation is another genetic factor which can act as a background for rheumatoid arthritis. Smoking accounts for 20-30% of all cases involving environmental risks since it causes lung disease and periodontal disease, which undermine the structure of joints which eventually leads to inflammation of rheumatoid arthritis (Deane, 2017).

Other major contributing factors are exposure to dust or silica in the workplace, air pollution, and obesity. Preventing the onset of rheumatoid arthritis can be possible with the help of a well-balanced diet which involves consumption of omega-3 fatty acid and fish. Some studies show that statin can also be used to reduce the risk of the development of rheumatoid arthritis.

Immune System Impact

Current research demonstrates that rheumatoid arthritis develops in the human body over a significant period of time, starting from the autoantibodies production. Then, over the course of several years, during which the process of remodeling of an individual’s immune system takes place while they do not notice any symptoms, joint inflammation begins (Weyand & Goronzy, 2020).

This becomes a result of the erosion of tissue tolerance and the emergence of T-cells, which invade tissue while macrophages which have to protect it fail (Weyand & Goronzy, 2020). Later, synovial stromal cells transform into autoaggressive effector cells, which makes the existing acute synovitis to convert into the chronic and destructive form.

When the immune system cannot cope with T cells, abnormal dynamics of the cell cycle ensues, and mitochondrial DNA instability. Eventually, the tissue-invasive effector T cells continue to produce in large quantities and cause glucose to stop generating energy and build cells instead.

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