arthritis is a disease of unknown cause, and the current thinking is that an
interplay between genes, infectious agent contributes to initiate an
autoimmune disease mechanism that results in inflammation, dominantly
at limb joints, often with destructive features. The term rheumatoid
arthritis was first used by sir Archibald Garrod to describe a chronic nonsuppurative
inflammatory arthropathy (Rheuma – flux,
eidos – resemblance), a condition resembling rheumatism.
We are all familiar with the saying regarding rheumatic fever, “it
licks the joints but bites the heart.” Contrarily it can be said of rheumatoid
arthritis, “it bites the joints, licks all other systems of the body and barks
at the treating physician.”
Rheumatoid arthritis is a highly inflammatory polyarthritis often
leading to joint destruction, deformity and loss of function. Additive,
symmetric swelling of peripheral joints is the hallmark of the disease.
Extra-articular features and systemic symptoms can commonly occur and
may antedate the onset of joint symptoms. Chronic pain, disability and
excess mortality are unfortunate sequelae.
The world wide incidence of RA is approximately 3 cases per
10,000 population and the prevalence rate is approximately 1%. First
degree relatives of patients with RA have an increased frequency of
disease (2-3 %). Disease concordance in monozygotic twins is
approximately 15-20% suggesting that non-genetic factors play an
important role. Because world wide frequency is relatively constant, a
ubiquitous infectious agent has been postulated to play an etiologic role.
Females are 2-3 times more likely to develop RA than males.
The frequency of RA increases with age and peaks in persons aged
35-50 years. Nevertheless, the disease is observed in both elderly persons
The cause of rheumatoid arthritis is unknown. Genetic,
environment, immunologic, and infectious factors may play significant
roles. Socioeconomic, psychological and lifestyle factors may influence
Approximately 60% of patients with RA carry the so called
shared epitope of the HLA-DR4 cluster, which constitutes one of the
peptide binding sites of certain HLA-DR molecules associated with RA.
In addition, HLA-DR1 also carries this shared epitope and confers risk in
For many decades, numerous infectious agents have been
suggested to induce RA. Among these are Mycoplasma organisms,
Ebstein-Barr and Rubella viruses and others.
This supposition is further supported indirectly by the following: