The disorder is seen three times more frequently in females than males
Rheumatoid osteoarthritis is a long-lasting systemic inflammation disease that is characterized by constant symmetric irritation of several peripheral joints. It’s one of the most well-known Rheumatic diseases that are inflammatory and defined by the increase in the chronic inflammatory growth of the synovial linings that line diarthrodial joints. This leads to a rapid destruction of cartilage and progressive bone erosion.
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When left untreated, rheumatoid arthritis results in joint degeneration that is progressive or disability and eventually death. The incidence of rheumatoid arthritis across the United States is around 1 percent of the general population with comparable prevalence rates widely observed.
The disorder is seen three times more frequently in females than males. Its peak beginning in the fifth or sixth decade. As with SLE, rheumatoid arthritis is a systemic autoimmune disorder 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 rheumatoid arthritis is located in the synovium of the joint.
Although 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 rheumatoidarthritis has been found to be similar across different cultures and areas across the globe we can conclude that the environmental triggers that trigger rheumatoid arthritis should be widespread.
The early stages of rheumatoid arthritis are closely mimicked by transient inflammation osteoarthritis that is caused by a range of pathogens that are microbial. Thus, even though the role of infection in the development 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 within the peptide-binding groove, are linked to susceptibility to illness and to a higher degree of rheumatoid arthritis. A significant part of the pathological damage of rheumatoidarthritis, it is located close to the synovial linings that line joints.
The typical synovium is comprised of a thin cellular liner (one to three layers) and an interstitium beneath which is home to blood vessels however, there are a few cells. Synovium is a place where nutrients are provided and lubrication for adjacent cartilage in the articular. The synovium of rheumatoid arthritis, is, however, markedly abnormal, with a dramatically larger liner of (8-10 thickness of tissue) comprised of activated tissue and an interstitium that is highly inflamed filled with B tissue T cells, macrophages as well as changes in vascular structure (including the neovascularization and thrombosis).
At sites where articular cartilage and synovium are connected 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 several of the key components of pathogenesis are well-known.
As we have discussed it is important to differentiate the initiating and spreading phases from the disease and also to understand the way in which the rheumatoid arthritis characterizes a self-sustaining and increased inflammatory state. The rates of concordance in twins vary between 15 to 35% indicating genetic factors as the cause of the rheumatoid arthritis.
The most striking genetic factors identified to date is a particular part of MHC class II alleles, whose presence is believed to primarily reveal the severity of the disease (sufferers homozygous for the disease-related alleles are the ones with the worst illness). These MHC molecules act as antigen-presenting scaffolds. They deliver peptides to the CD4 T tissues.
Alleles that are associated with disease (belonging to the HLA-DR4/DR1 serotypes) share a common sequence along their antigen-presenting groove. It is referred to as”the “shared epitope.” It is possible that these alleles possess crucial antigens to T tissues, which play a role in triggering and contributing to the progression of this disease. But it is not clear what antigens have been identified.