Rheumatoid arthritis affects around 1% of the population. The disease is characterized by joint inflammation and damage. Therapy with disease modifying drugs (DMARDs) has been proved to be efficient in decreasing disease activity and progress, along with improvement in symptoms and prevention of structural damage. The sooner the therapy is initiated, the better the outcome, probably due to a decreased burden of inflammation. The therapeutic potential of early treatment led to an accelerating interest in the preclinical phase of the disease. Many studies demonstrated that there is a preclinical period that precedes the development of clinical arthritis, and the old assumption that the disease develops with the clinical symptoms is no longer valid. Apparently, many biological markers, including autoantibodies, appear years before the clinical synovitis develops. This period is called preclinical rheumatoid arthritis. In the preclinical phase, autoantibodies such as rheumatoid factor, antibodies to citrullinated proteins and many other antibodies and inflammatory markers are abundant. These findings and the evidence of genetic and environmental risk factors for rheumatoid arthritis support the theory which claims that multiple factors contribute to the development of an autoimmune process that progresses and expands until reaching a critical point where rheumatoid arthritis develops.