Osteoarthritis: A Case Study

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Osteoarthritis (OA) is a degenerative condition of articular cartilage in joints commonly affecting the knees (Sinusas 2012) and slowly develops over many years resulting from mechanical stress (Kisner and Colby 2003). Unfortunately, the risk of developing OA increases with several factors including genetics, increasing age, obesity and female gender (Sinusas 2012). OA causes pain and stiffness in the joints however it is an incurable disease and therefore physiotherapy treatment should focus on relieving symptoms and slowing the rate of progression (Brosseau et al 2004).

Articular cartilage is a smooth material which acts as a shock absorber and allows ease of movement, without pain, for the joints (Bhatia et al. 2012). When OA occurs, the articular cartilage becomes thinner and “flakes” away into the synovial fluid which in turn results in pain and difficulty when moving
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Wenham and Conaghan (2010) state that OA cannot be classed as a typical inflammatory arthropathy as there is less inflammation than in Rheumatoid Arthritis (RA), because of the lack of white blood cells, specifically neutrophils, and pro-inflammatory cytokines compared to RA. However, Pelletier et al (2001) suggested given that the symptoms of OA are swelling, pain and stiffness there is a degree of local inflammation. Man and Mologhianu (2014) states that this is caused by the synovial membrane’s lining cell layer showing hyperplasia (thickening) and infiltration of inflammatory causing cells e.g. lymphocytes and monocytes due to the products of the proteolytic breakdown of cartilage. Wenham and Conaghan (2010) also suggest that there is increased vascularity in OA affected joints. A study by Haywood et al (2003) showed that 31% of patients with OA who were about to have total joint replacements had severe synovitis and only 7 out of the 104 participants did not show any evidence of

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