Throughout this essay I shall critique the available evidence regarding rheumatoid arthritis (RA); particularly concerning the conclusions on its aetiology, diagnosis techniques, pharmacological management, physical therapeutics and surgical treatment interventions. I shall explore the expected prognosis and the key developments we can expect in the future.
Aetiology and Prevalence RA is a chronic, systemic and inflammatory disease that progressively impacts peripheral joints (Panayi 2011).The damage that occurs is predominantly symmetrical and polyarthropathic (Rindfleisch & Muller 2005). It affects the host’s joint synovial membranes, tendon sheaths and bursae and causes stiffness, pain and swelling to the joints…show more content… Genetics influence a high percentage of cases; according to de De Vries (2011), 50-60% of sero-positive and 30-50% of sero-negative cases are influenced by hereditary factors. A greater understanding of this area could bring new found appreciation of RA pathogenesis and treatment methods (Mikuls 2012).
Relationship of increase RA incidence with smoking is reported widespread in literature (Fisher 2012, Klareskog 2008, Sugiyama 2010, Mahdi 2009). Interaction occurs between two copies of HLA-DR SE specific genes and smoking; specific citrullinated protein antigens are induced by cigarette smoke which increases likelihood of RA. This causes a 21-flod increase risk of RA in comparison to non-smokers (Klareskog 2006).
Furthermore, literature dictates that peripheral vascular disease (PVD), steroid therapy and prednisone use have consistent supportive evidence that shows increased risk of RA (Firth et al.2008a, Maradit‐Kremers 2007, Wegner 2010).
There is little evidence to dictate a common infectious cause of RA, however some pathogenic organisms such as periodontitus, B19 parvovirus or Epstein-Barr virus (EBV) virus may stimulate the disease by activating the B cells to presence antibodies (Wegner 2010).
There is inconclusive evidence to suggest that the diet or breast implants play a role in the aetiology of RA (Tugwell et al 2001, Pattison 2006).
In RA, the immune system cannot differentiate Major