Rheumatoid osteoarthritis is a long-lasting systemic inflammatory disorder that manifests as constant symmetric irritation of several peripheral joints. It’s among the most common Rheumatic diseases that are inflammatory and distinguished by the growth of the chronic inflammation of the synovial linings that line diarthrodial joints. This can lead to a rapid destruction of cartilage and progressive bone erosion.
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If left untreated, rheumatoid osteoarthritis frequently results in joint degeneration that is progressive or disability and eventually death. The incidence of rheumatoid arthritis within the United States is around 1 percent within the population of the base with comparable prevalence rates widely observed.
The disorder is seen three times more frequently in females than males, and is most prevalent in development in the fifth to six-year age range. Similar to SLE, rheumatoid arthritis is an autoimmune systemic disease through which an abnormal activation of T cells, as well as immune effectors in the innate system occur. Contrary to SLE most of the inflammatory activity in rheumatoidarthritis is triggered by the synovium of joints.
While the cause of rheumatoidarthritis is not known it is believed that a variety of environmental and genetic causes can contribute to susceptibility. Since the prevalence of rheumatoid arthritis is found to be similar across diverse cultures and geographical areas across the globe we can conclude that the environmental factors which trigger rheumatoidarthritis must be widespread.
The early stages of rheumatoid arthritis are closely resembled by transient inflammatory osteoarthritis that is caused by a range of pathogens that are microbial. So, although an infection-related role in the progression of rheumatoid osteoarthritis has long been speculated, it has not yet fully established.
Particularly class II MHCalleles (HLA-DR4) that share an unanimity QKRAA motif in the peptide binding groove, have been found to be linked to susceptibility to illness and greater degree of rheumatoid arthritis. A significant part of the pathological damage of rheumatoidarthritis, it is located close to the synovial linings that line joints.
Synovium typically consists of a thin cellular liner (one to three cell layers) and an interstitium underneath which is home to blood vessels but a few cells. The synovium typically provides nutrients and lubrication to the adjacent cartilage in the articular. The synovium in rheumatoid arthritis however, is quite unusual, and has a substantially larger liner of (8-10 tissues thick) comprised of activated tissue and an interstitium that is highly inflamed filled with B tissue T cells, macrophages, as well as vascular changes (including Neovascularization and thrombosis).
On sites in which articular and synovial cartilage are in close proximity the synovial tissue of rheumatoid arthritis (called the pannus) invades and damages adjacent bone and cartilage. Although the reasons behind osteoarthritis in rheumatoid patients aren’t known certain essential elements of the pathogenesis have been identified.
As previously mentioned it is important to differentiate the initiating and advancing phases of the disease, and to be aware of the fact that the well-established rheumatoid osteoarthritis characteristic is a self-sustaining, increased inflammatory state. In twins, the rates of agreement vary between 15 to 35% suggesting genetic factors that contribute to the pathogenesis of the rheumatoid arthritis.
The most striking genetic factors identified to date is a particular portion of MHC class II alleles, whose presence can be seen to significantly determine the severity of disease (sufferers homozygous for the disease-related alleles are the ones with the worst illness). These MHC molecules act as antigen-presenting scaffolds. They provide peptides to T cells of CD4 tissues.
Alleles that are associated with disease (belonging to the HLA-DR4/DR1 serotypes) have a common sequence in their antigen-presenting groove. It is referred to as”the “shared epitope.” It is possible that these alleles have crucial antigens to the T tissuethat play a role in triggering and contributing to the progression of this disease. But it is not clear what antigens have been identified.