What is Rheumatoid Arthritis?
Clinical presentation of rheumatoid arthritis
Cells involved in RA
The synovial
membrane is made up of
cells known as fibroblast like synovial sites and these are very important in
pathogenesis of RA where we have inflammation of the synovium. The exact
trigger of the information of the disease is really not quite unknown.
Macrophages they essentially begin secreting cytokines such as
TNF – alpha, interleukin 1 and 6 which leads to inflammation. The cytokines
also stimulate the fibroblast like synovial sites. When the fibroblast like
synovial cells is stimulated, they essentially become activated and they begin
to proliferate at the same time they also begin in that rank EL expression
which together with cytokines here will stimulate osteoclast activity which
will lead to bone erosion.
When the fibroblast like synovial sites is stimulated and proliferate, they also begin secreting proteases these proteases essentially cause the cartilages to breakdown and leads to cartilage degradation.
When the fibroblast like synovium sites is that when it’s stimulated or activated, they can migrate from joint to joints so they can migrate from the hand joint on one side to the hand joint on the other this is why we get symmetrical arthritis.
We also can find T-cells in the area in the synovium T-cells make up about 50% of the immune cells in the area they are very important in the pathogenesis. T cells promote inflammation essentially and they can secrete interleukin 17 which helps to promote macrophage activity as well as stimulate the fibroblasts like synovial sites the t cells also help in the expression of rank L which stimulate osteoclast for bone erosion.
We also find plasma cells in the area only 5% of majority of immune cells and they essentially assist in inflammation through cytokines as well as through the antibodies.
In the synovial fluids we can find neutrophils and they essentially produce proteases and reactive oxygen species which will essentially cause the bone and cartilage degradation leads to inflammation.
In the synovial fluid we also find immune complexes which is feature of RA, these immune complexes are essentially antibodies that bind to one another and promote inflammation.
Cause of rheumatoid arthritis:
The main cause of RA is unknown but few theories are out there such as genetic, smoking, a bacterium called porphyromonas gingivalis which can lead to gingivitis can cause the modification of own antigen making it seem foreign and include citrullination.
Because you have modification of your own antigens this will be recognized by antigen presenting cells, activate it leads to initiate an immune response. The APC cells will migrate to lymph nodes and activate CD4 t cells this activates the b cells. The activated b cells become plasma cells and then these plasma cells produce auto antibodies against own antigen that migrates to joints.
There are 2 main antibodies found in the RA are important for helping in diagnose RA
R factor which is an IGM antibody and its present in the 75% of RA people they target the FC portion of the IgG and form immune complex that stored in the synovial fluid and promote inflammation.
Anti-citrullinated protein antibody they target citrullinated proteins these are things like fibrin and filigree.
Medication for Rheumatoid arthritis include:
- NSAIDs – Nonsteroidal anti-inflammatory drugs. NSAIDs
relives the pain and suppress the inflammation.
- DMARDs – (Disease modifying antirheumatic drugs) such as Abatacept which
suppress the T-cells, Rituximab suppress B- cells, Anakinra blocks the
interleukin-1, Tocilizumab blocks the interleukin-6, Methotrexate, Hydroxychloroquine,
Sulfasalazine.
- Steroids.
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