Rhematoid Arrhritis | Pathophysiology Mechanism

Rheumatoid arthritis (RA) is a long-term autoimmune disorder that primarily affects joints. It typically results in warm, swollen, and painful joints.[1] Pain and stiffness often worsen following rest.Most commonly, the wrist and hands are involved, with the same joints typically involved on both sides of the body.The disease may also affect other parts of the body, including skin, eyes, lungs, heart, nerves, and blood. This may result in a low red blood cell count, inflammation around the lungs, and inflammation around the heart.Fever and low energy may also be present.Often, symptoms come on gradually over weeks to months.
Arthritis of joints involves inflammation of the synovial membrane. Joints become swollen, tender and warm, and stiffness limits their movement. With time, multiple joints are affected (polyarthritis). Most commonly involved are the small joints of the hands, feet and cervical spine, but larger joints like the shoulder and knee can also be involved. Synovitis can lead to tethering of tissue with loss of movement and erosion of the joint surface causing deformity and loss of function. The fibroblast-like synoviocytes (FLS), highly specialized mesenchymal cells found in the synovial membrane, have an active and prominent role in these pathogenic processes of the rheumatic joints.
Genome-wide association studies examining single-nucleotide polymorphisms have found around one hundred alleles associated with RA risk.Risk alleles within the HLA (particularly HLA-DRB1) genes harbor more risk than other loci.The HLA encodes proteins that control recognition of self- versus non-self molecules. Other risk loci include genes affecting co-stimulatory immune pathways-for example CD28 and CD40, cytokine signaling.
RA primarily starts as a state of persistent cellular activation leading to autoimmunity and immune complexes in joints and other organs where it manifests.
The clinical manifestations of disease are primarily inflammation of the synovial membrane and joint damage, and the fibroblast-like synoviocytes play a key role in these pathogenic processes. Three phases of progression of RA are an initiation phase (due to non-specific inflammation), an amplification phase (due to T cell activation), and chronic inflammatory phase, with tissue injury resulting from the cytokines, IL-1, TNF-alpha, and IL-6.

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[@michaeleisenberg7867]

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I had to do some Google searching. This is what I came up with. Copy and paste:
Abstract
Citrullination, one of the enzymatic posttranslational modifications has become a hot topic of recent research as it is involved in various physiological and pathological processes. Antibodies against citrullinated proteins called anti-citrullinated protein antibodies, are the hallmark (diagnostic and prognostic factors) of rheumatoid arthritis, and are specific for the disease. Citrullination has an important role in the normal function of the immune system, skin keratinization, the insulation of neurons and the plasticity of the central nervous system including its essential role in gene regulation. Abnormal citrullination has been proposed to play a role in multiple sclerosis and Alzheimer's disease, and recent research has drawn attention to its implication in tumorigenesis. Still, it is unclear whether citrullination is the cause or the consequence of these pathological alterations. Here, we discuss crucial aspects of citrullination during both physiological and pathological conditions.
Copyright © 2012. Published by Elsevier SAS.

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