The Pathophysiology of rheumatoid arthritis is not well understood though medical experts try to their best to understand it. However, theories do circulate trying to explain this complicated disease and how it is manifested in the human body. The genetically inherited rheumatoid arthritis is believed to develop as a result of individuals being exposed to things like trauma which in return result into proliferation of the joints lining known as synovial hypertrophy. Due to this damage of the joints, they become susceptible to inflammation and pain. The more the synovial hypertrophy is increased the more the inflammation of the joint is increased. This also leads to the damage of the joint cartilage and the joint bones as well. The low immune system caused by the body fighting against itself increases the disease progression.
The CD4 T cells, mononuclear phagocytes, fibroblasts and the osteoclasts are the main cells that are involved in the Pathophysiology of rheumatoid arthritis. The B lymphocytes on the other hand will develop the rheumatoid factors known as the auto antibodies. In the presence of rheumatoid arthritis, the synovial blood cells location otherwise known as subintimal area of synovium becomes congested with the T cells and B lymphocytes that propagate the progressing of the rheumatoid arthritis. In normal cases the subintimal area of synovium is supposed to have very few cells and when the opposite is true, the result is increased joint damage and inflammation.
The Pathophysiology of rheumatoid arthritis is also boosted by the abnormalities is causes in the body cells and also by the genetic factors of the patient. Rheumatoid arthritis is very complicated and its pathogenesis mostly includes the damage of the joint bones, cartilages and the development of fibrosis pannus. When the damage of the joints increases the inflammation is also increased as well and this will in return give rise to destruction of most the patients cells including the blood vessels, tendons, cartilages and bones. The Pathophysiology of rheumatoid arthritis is further mediated by it’s inter networking cells which include the proteolytic enzymes and the prostanoids that increase the inflammation worsening the condition of the disease.
There is a very great difference between the Pathophysiology rheumatoid arthritis patients and those who are free of the disease. In the presence of rheumatoid arthritis, the plasma becomes more correlated; the synovial and the IL-1 activities are very high. These activities of the IL-1 cause the joints to be more painful and inflamed. They are also believed to be responsible of the joint bone damage and severity of the disease. These IL-1 activities are therefore responsible of causing deformities in rheumatoid arthritis patients if not well taken care of. This is because they increase the inflammation causing agents like the nitric oxide and the cyclo-oxygenase 2. The IL-1 is also responsible of causing the cartilage proliferation as it activates the T and B lymphocytes cell. It becomes a major cause of the increment of rheumatoid arthritis. Understanding the Pathophysiology of rheumatoid arthritis is very complicated as it involves various cells playing part. However doctors are in continued research to understand this complicated disease.