Arthritis is a medical term for joint inflammation. It is a derived from the Greek words, “artho” and “itis,” which means joint and inflammation, respectively. It is a disorder characterised by severe chronic inflammation in at least one joint if not more and produces both pain which can be crippling enough to be disabling (Johnson & Hunter, 2014).
There are over 100 different types of arthritis. The most common is osteoarthritis but other include rheumatoid arthritis, psoriatic arthritis, and related autoimmune diseases. Whilst the causes of each of these are different, their symptoms and treatment are similar.
Osteoarthritis is a degenerative joint disease and the number of people suffering with it is steadily rising as the population grows and ages. The worldwide prevalence of knee osteoarthritis increased 26.6% from 1990 to 2010, and it affects about 9.6% of men and 18% of women more than 60 years of age. The occurrence of Osteoarthritis increases with age due to the decreased capacity to suppress inflammation, age-related sarcopenia, and increased bone turnover. Rheumatoid arthritis is a systemic inflammatory and destructive joint disease with a prevalence of about 1–2% of the adult population worldwide.
Rheumatoid arthritis (RA) is chronic autoimmune disease which can affects nearly every joint in the body. As in most cases of arthritis, the pathogenic mechanisms that underly the disease are not properly described or even understood. Systemic inflammatory response is one of the most important characterizations
throughout the occurrence, development and progression of the disease (Shrivastava & Pandey, 2013; Smolen et al., 2016).
In biological terms, nuclear factor-kappa B (NF-κB) (Roman-Blas and Jimenez, 2016), oxidative stress (Quiñonez-Flores et al., 2016) and autophagy-repated pathways (Dai & Hu, 2016) have been recognised as the most relevant parts of the process in both the pathogenesis and pathophysiology of RA. Any changes, any modulation of the expression or functions associated with various targeting proteins involved in signaling pathways is considered ripe for potential therapeutic approaches in the clinical management of arthritis generally.
References
Dai, Y., Hu, S., 2016. Recent insights into the role of autophagy in the pathogenesis of rheumatoid arthritis. Rheumatology (Oxford) 55 (3), pp. 403–410.
Goldring, S.R. (2003) Pathogenesis of bone and cartilage destruction in rheumatoid arthritis. Rheumatology (Oxford) 42 Suppl 2: ii11–ii16 https://doi.org/10.1093/rheumatology/keg327
Johnson, V.L., Hunter, D.J. (2014) The epidemiology of osteoarthritis. Best Pract. Res. Clin. Rheumatol. 28 pp. 5–15 https://www.bprclinrheum.com/article/S1521-6942(14)00005-9/abstract
Quiñonez-Flores, C.M., González-Chávez, S.A., Del Río Nájera, D., Pacheco-Tena, C., (2016) Oxidative stress relevance in the pathogenesis of the rheumatoid arthritis: a systematic review. Biomed. Res. Int. 2016, 6097417.
Roman-Blas, J.A., Jimenez, S.A., (2006) NF-kappaB as a potential therapeutic target in osteoarthritis and rheumatoid arthritis. Osteoarthr. Cartil. 14 (9), pp. 839–848.
Shrivastava, A.K., Pandey, A., (2013) Inflammation and rheumatoid arthritis. J. Physiol.
Biochem. 69 (2), pp. 335–347 https://doi.org/10.1007/s13105-012-0216-5
Smolen, J.S., Aletaha, D., Mcinnes, I.B., (2016) Rheumatoid arthritis. Lancet 388 (10055), pp. 2023–2038
Vos, T., Flaxman, A.D., Naghavi, M., et al.: (2012) Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990–2010: A systematic analysis for the Global Burden of
Disease Study 2010. Lancet. 380 pp. 2163–2196. https://doi.org/10.1016/S0140-6736(12)61729-2
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