**1. Introduction**

Rheumatoid arthritis (RA) is a relatively common, disabling, autoimmune disease that is characterized by progressive joint disorder, significant pain and functional disability. Its prevalence is estimated at 0.5 - 1.0 percent of adults worldwide (Kvein, 2004), and the disease continues to cause significant morbidity and premature mortality.

 Symmetric highly inflammatory polyarthritis of peripheral joints is the hallmark of the disease. The condition is also systemic in that it often affects many extra-articular tissues throughout the body, including skin, blood vessels, heart, lungs, and muscles. The gradual involvement of multiple joints into pathophysiological process eventually results in articular destruction, ensuing instability, deformity and collateral pain. As the pathology progresses, chronic pain and functional disability dominates one's life and lessens everyday enjoyment and comforts.

Physical in nature, the disease also exacts an emotional toll that often leads to unfortunate psychiatric sequelae. It is not at all surprising that in addition to joint deformity, disability, dolour, and excess mortality, on average one in five patients with rheumatoid arthritis will experience depression.

Many new insights into epidemiology, pathogenesis, outcomes measurement, and pharmacologic treatment of rheumatoid arthritis have occurred in recent years. Applications of historical analyses to the development of a cogent etiologic theory of rheumatoid arthritis have been limited to date (Entezami et al, 2011). In this chapter, the author presents the major points of evidence and conclusions that have been drawn from historical, clinical and research material in the study of rheumatic diseases.
