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Rheumatoid Arthritis (RA) is a systemic inflammatory disease that predominantly manifests in the synovial membrane of diarthrodial joints. The inflammation develops in a genetically predispose host.

Exogenous events that precipitate the development of the disease have not been identified.

The chronic inflammatory process induces changes in the cellular composition and the gene expression profile of the synovial position and the gene expression profile of the synovial membrane, resulting in hyperplasia of synovial fibroblasts and structural damage of cartilage, bone, and ligaments.

Extra-articular disease affecting a variety of organs occurs in the majority of the patients. It’s a significant factor in morbidity and mortality of people with RA. The severity of RA encompasses a wide spectrum, ranging from self-limiting disease to chronic progressive disease, causing varying degrees of joint destruction and clinically evident extra-articular organ involvement. This clinical heterogeneity is determined by genetic and environmental factors that control the progression, degree, and pattern of the inflammation.

Epidemiology

Rheumatoid Arthritis has a worldwide distribution and affects all ethnic groups. The disease can occur at any age, but its prevalence increases with age, the peak incidence is between the fourth and sixth decades RA is a disease of an aberrant immune response in a genetically predisposed host that leads to chronic progressive synovial inflammation and destruction of the joint architecture.
 

Research efforts have shed light on the genetic factors, the immunoregulatory defects, and the effector mechanisms leading to tissue injury.

Although the impact of genetic factors is obvious, the genetic basis is complex and not sufficient to explain the triggering of the immune insult. Precipitating factors have not been identified, and it remains a matter of debate whether the disease is triggered by an exogenous infectious agent, a breach in tolerance leading to classical autoimmunity, or merely stochastic events that have accumulated with age.

Rheumatoid arthritis treatment

Rheumatoid Arthritis is a Chronic Disorder for which there is no known cure. Fortunately, in the last few years, a shift in strategy toward the earlier institution of disease modifying drugs and the availability of new classes of medication have greatly improved the outcomes that can be expected by most patients.

The optimal treatment of RA requires a comprehensive program that combines medical, social and emotional support for the patient. Treatment options include medications, reduction of joint stress, physical and occupational therapy, en surgical intervention.

Pharmacological strategies

There are three general classes of drugs commonly used in the treatment of rheumatoid arthritis: nonsteroidal anti-inflammatory agents (NSAIDS), CORTICOSTEROIDS, AND DISEASE MODIFYING ANTI-RHEUMATIC DRUGS (DMARDs). NSAIDs and corticosteroids have a short onset of action while DMARDs can take several weeks or months to demonstrate a clinical effect.

DMARDs include methotrexate, sulfasalazine, leflunomide (arava) etanercept (Enbrel) infliximab (Remicade) adalimumab (Humira), certolizumab pegol (Cimzia), rituximab (rituxan) antimalarials (plaquenil) and others. Also, immunomodulators are occasionally used including azathioprina (Imuran) and cyclosporine. Analgesics are also sometimes helpful in decreasing pain until DMARDs take effect.