Rheumatoid Arthritis Research Paper

Rheumatoid arthritis is a chronic, and generally persistent autoimmune inflammatory disease that causes functional disability, swelling of the synovium (joint lining), significant pain in the body, and can lead to premature death(1). Its origin is not clear, however, suggestions have been made that it was prevalent in early Native American populations several thousand years ago and may not have appeared in Europe until the 17th century (2). It appears to be a disease with multifactorial causes, including, cultural, genetic and environment factors (3).

As an autoimmune disease, rheumatoid arthritis occurs when an individual's own immune system attacks the synovial membrane - the soft tissue between joints (1). More specifically, B-lymphocytes, CD4+ T-lymphocytes, and macrophages penetrate the synovium and organize into distinct lymphoid masses with germinal centres (2). Swelling of the lining results from a dramatic increase in the number of macrophages and fibroblasts in the synovial fluid, as well as locally expressed degradative enzymes, which digest the extracellular matrix and destroy the synovial structures (2).

In this representation, immune complex-created rheumatoid factors (proteins produced by the immune system that can attack healthy tissue in the body) and possibly other autoantibodies (an antibody produced by the immune system that is directed against an individuals own proteins) initiate the complement system to release C5a, which mediates chemotaxis in inflammatory cells (2). It is these inflammatory cells - namely neutrophils - that are recruited and contribute to local degradation of the