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
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.
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
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.
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.
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.