RA is serious arthritis of inflammatory nature of unknown cause. In most patients this disease involves bilaterally symmetric chronic low-grade inflammation eventually progressing to involve multiple joints with periodic inflammatory flares (Kraus and Wiggin, 2009).
The onset of the disease is most frequent in fourth and fifth decades of life (Luqmani et al., 2006).
The aetiology of the disease is not specifically known and has been suggested to be multifactorial. The class II major histocompatibility complex allele HLA-DR4 and related alleles are known to be major genetic risk factors for RA. It has been suggested that RA might be a manifestation of the response to an infectious agent in a genetically susceptible host. Activation of autoimmune mechanisms is the key aetiologic event in sustaining the chronic inflammatory process so characteristic of RA (Scott et al., 2000).
The main event in pathophysiology is inflammatory synovitis. Subsequently through a cascade of multiple immune events through mediation of a host of immune cells, the synovial fibroblasts are activated. Added to cartilage degradation, osteoclasts are activated that leads to erosion of bone. The chemokines and cytokines lead to synovitis, cartilage and bone damage, and systemic manifestations of RA (Luqmani et al., 2009). Altman (2008) notes that these immunologic abnormalities arise from various immune complexes, which originate from the inflamed synovial cells that serve as a target for such immune injuries. The plasma cells that are recruited produce antibodies known as rheumatoid factors. These actively contribute to these complexes which ultimately lead to joint destruction. ...