Arthritis is a general term for the inflammation of joints. Arthritis can affect one or multiple joints, hence the different types of arthritis. The two common types are rheumatoid arthritis (RA) and osteoarthritis (OA). RA and OA are two different types of diseases with RA as an autoimmune disorder while OA is a degenerative disease caused by wear and tear on joints (Woetzel et al., 2014). OA is the most popular form of arthritis affecting over 27 million Americans, while RA is less common.
OA and RA have different pathophysiology, but there are some similarities. According to Ashkawand et al. (2013), many factors lead to the initiation and progression of OA. The cause of OA is the changes in cartilage, which can be caused by mechanical, cellular and biochemical processes that lead to the abnormal reparation of cartilage and cartilage degradation. OA is characterized by progressive cartilage loss and thickness of the subchondral plate, osteophytes, and subchondral bone cysts. As OA progresses, vascular invasion and calcification of nearby articular cartilage take place causing decreased thickness of articular cartilage. Over time, OA leads to bone remodeling and further cartilage deterioration. Inflammation caused by OA involves periarticular tissues, and it is not as severe as the inflammation caused by RA.
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On the other hand, the pathophysiology of RA is different from that of OA. The initial trigger for RA is unclear, but studies suggest that hormones, genetics, and environmental factors play a role. When the immune response is triggered, the immune system produces autoantibodies and inflammatory cytokines that lead to inflammation causing the formation of pannus which destroys cartilage and bone. As RA progresses, additional joint damage and systemic complications occur in the affected joint (Woetzel et al., 2014).
OA and RA have notable similarities. Joint pain, stiffness and morning stiffness are some of the common symptoms of OA and RA which is why the diagnosis of the two conditions can be confusing. However, RA has a rapid onset, and it can worsen within weeks, unlike OA which develops slowly and worsens over time. RA symptoms affect joints all over the body, while OA tends to affect small finger joints, thumb, and knees. RA symptoms are also symmetrical because they affect both sides of the body equally unlike OA.
Patient factors such as gender, genetics, and age affect the pathophysiology of OA and RA. According to Ashkavand et al. (2013), OA is higher in women than men as revealed by studies. Ashkavand et al. (2013) refer to a study conducted in patients over the age of 65, and it concluded that OA was high as 68% in women and 58% in men. The alignment of women’s bodies put them at a higher risk for knee injuries that can lead to OA in later life. Additionally, women who play sports or engage in physically demanding activities increase their risk for OA. Alternatively, Kurko et al. (2013) state that the heritability of RA is estimated at 60% as genetic factors such as class II major histocompatibility antigens and non-HLA genes are implicated in the pathophysiology of RA.
OA and RA are diagnosed differently. The diagnosis for RA involves a physical examination for symptoms, family, and medical history (Li et al., 2014). A blood test is conducted to determine the antibodies that trigger RA and imaging tests are done to assess joint damage and inflammation. Imaging tests, including X-rays and MRIs, are used to show the progressive damage and joint deterioration. OA cannot be diagnosed using a blood test.
Lastly, both OA and RA do not have a known cure. The goal of treatment for OA and RA is to reduce pain, manage symptoms and prevent further damage to the joints. Anti-inflammatory medications such as ibuprofen are prescribed to manage symptoms of joint pain and swelling. Since RA is an autoimmune disorder, there are medications to prevent further immune system attacks and damage. Patients with RA and OA require physical and occupational therapy as well as lifestyle changes.
References
Ashkavand, Z., Malekinejad, H., & Vishwanath, B. S. (2013). The pathophysiology of osteoarthritis. Journal of Pharmacy Research , 7 (1), 132-138.
Kurkó, J., Besenyei, T., Laki, J., Glant, T. T., Mikecz, K., & Szekanecz, Z. (2013). Genetics of rheumatoid arthritis—a comprehensive review. Clinical reviews in allergy & immunology , 45 (2), 170-179.
Li, Z. C., Xiao, J., Peng, J. L., Chen, J. W., Ma, T., Cheng, G. Q., & Liu, Z. D. (2014). Functional annotation of rheumatoid arthritis and osteoarthritis associated genes by integrative genome-wide gene expression profiling analysis. PloS one , 9 (2), e85784.
Woetzel, D., Huber, R., Kupfer, P., Pohlers, D., Pfaff, M., Driesch, D., & Kinne, R. W. (2014). Identification of rheumatoid arthritis and osteoarthritis patients by transcriptome-based rule set generation. Arthritis research & therapy , 16 (2), R84.
