This overview of the pathophysiology of rheumatoid
arthritis is provided to help facilitate the understanding of the study
outcomes, as well as the proposed mechanisms of actions suggested later in the
website.
Rheumatoid arthritis (RA) is a chronic multisystemic
disease of unknown etiology. The characteristic feature of RA is a
persistent inflammatory synovitis, involving the peripheral joints in a
symmetric fashion. The hallmark of the disease is the synovial
inflammation that causes cartilage damage and bony erosions, resulting in
changes in joint integrity. Despite this destructive potential, the course
of RA can be variable.
RA is one of the most common autoimmune diseases, with a
prevalence of approximately 1%. It has a female-to-male ratio of about
3:1, with onset most common in the 30's through 50's.
The inflammatory process in the synovial space and joint
fluid causes symptoms of joint pain and swelling. This is the result of
polymorphonuclear cells activating the release of prostaglandins and
leukotrienes, with the generation of reactive oxygen species. The destruction of
cartilage and bone is caused by activated lymphocytes and monocytes that release
inflammatory proteinases and prostanoids.
Adapted from-
Treatment of
Rheumatoid Arthritis: New Therapeutic Approaches with Biological Agents
The production of interleukin-1 (IL-1) and
tumor necrosis factor-α (TNF-α) by monocytes is central to the inflammatory process. In
particular, IL-1 is responsible for for stimulating prostaglandin E2
(PGE2), while TNF-α
is key in activating matrix proteinases. The activated proliferating
synovial tissue invades the cartilage and bone and functions like a locally
invasive tumor. Cytokines such as IL-6, induced by IL-1 and TNF-α,
as well as IL-1 itself, contribute to the systemic
features of the disease such as fever, myalgia, and weight loss.
Adapted from-
Hypersensitivity and Chronic Inflammation
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