Voltaren No Prescription

The pathogenesis of rheumatoid arthritis are genetically determined autoimmune processes, which contributes to the emergence of a deficit of T-suppressor lymphocytes function. Unknown etiological factor causes the development of an immune response. joint damage begins with inflammation of the synovium (synovitis), and then acquires the character of proliferative (pannus) with damage to the cartilage and bone. The intensity and type of clinical inflammatory process determined by genes of the immune response. The synovium is infiltrated by T lymphocytes CD4 + (helper cells), plasma cells, macrophages. Interaction of macrophage and T-lymphocyte CD4 + (helper) triggers an immune response. Macrophages in conjunction with Class II molecules, HLA-system-DR antigen are hypothetical T-helper lymphocytes, leading to their activation. Activated T-helper cells stimulate B-lymphocyte proliferation, their differentiation into plasma cells. Plasma cells produce synovial changed aggregated IgG. In turn, it is recognized by the immune system as a foreign antigen, the plasma and synovial cells, lymph nodes, spleen begin to produce antibodies thereto - rheumatoid factors (RF). The most important is RF Class IgM, which is found in 70-80% of patients with rheumatoid arthritis. The existence of also other types of RF - IgG and IgA. When determining in the blood of patients with rheumatoid arthritis classical IgM RF suggest embodiment seropositive rheumatoid arthritis.

Rheumatoid factor can be found in healthy persons (titre not exceeding 1:64), systemic lupus erythematosus, chronic autoimmune hepatitis, Sjogren's syndrome, hemoblastoses, tumors.

In some cases, patients with rheumatoid arthritis and other auto-antibodies are detected (DNA, nuclei of cells, blood corpuscles, etc.). In patients with rheumatoid arthritis with HLA DR4, identified local synthesis of antibodies to type II collagen, and the liquid content in the synovial collagen degradation products significantly increased. It is possible that local synthesis of antibodies directed against cartilage collagen degradation products.

Interaction with aggregated IgG rheumatoid factors leads to the formation of immune complexes which are phagocytosed by neutrophils and macrophages synovium. The process is accompanied by damage neutrophil phagocytosis, release of lysosomal enzymes, inflammatory mediators (histamine, serotonin, kinins, prostaglandins, leukotrienes, etc.), Which causes the development of inflammatory, proliferative and destructive changes in the synovium and cartilage. Development of immune complexes also promotes platelet aggregation, formation mikrotrombov, disturbances in the microcirculation system. Damage to the immune complexes joint tissue leads to further autoantiteloobrazovaniyu and chronic inflammation. The lesions of the connective tissue, and other organ systems (systemic manifestations of rheumatoid arthritis) associated with the development of immune vasculitis.

The pathogenesis of rheumatoid arthritis cytokines play a huge role - low molecular weight protein cell regulators, which are mediators of growth and differentiation of hematopoietic, mesenchymal and lymphoid cells, immune responses and inflammation. They are produced primarily by cells of the immune system, bone marrow, fibroblasts, platelets, monocytes, macrophages. Cytokines include colony stimulating factors, interleukins, interferons, growth factors. The tissues and synovial fluid of joints in rheumatoid arthritis are in excess cytokines interleukin-1, tumor necrosis factor (TNF), granulocyte-macrophage colony stimulating factor, interleukin-6. These cytokines are produced by cells lining the synovium, macrophages and fibroblasts and located underneath (Wenblatt, Gravallese, 1997), and have the ability to greatly stimulate the inflammatory process.

Rheumatoid arthritis step

There are several criteria by which to classify the stage of development of rheumatoid arthritis, but the most informative ones, which are based on the testimony of radiographs.

They can be divided into four categories:

Initially seen the first signs of thinning bones, it is practically the only manifestation of which can be seen in the picture. The soft tissue around the joints of the fingers are sealed, and are slightly thicker. Sometimes there are noticeable bright space available on the bone - is formed cysts. When the joint spaces are narrow, then we can talk about that the disease is progressing and will soon move to the next stage. A characteristic feature of this stage of development of the disease is that it can occur at any age and proceed quite a long time, almost did not prove itself. Sometimes such states are found even in childhood, but the disease first manifests itself after many years.

The second stage is characterized by the fact that in addition to the intricacies of bones, localized mainly around the joint begins to be affected and the very bone by erosive type. The first to suffer in the hands of the elbows and wrists. If the erosion is located close to the cartilage, in this case, a limitation of mobility. This cartilage tissue itself can not be deformed, but the muscles begin to atrophy, primarily those surrounding the affected joint itself. Bursa swollen and slightly sore. During exacerbation they can be hot, and the patients in the second stage of the disease complain of pain and aches. The more bone erosions, the closer the third stage of disease progression.

At this stage, not only visible damage to the bone and its refinement, here in the picture is clearly seen atrophy of muscles, wearing a broad character, he has exposed the joint deformation. If salt deposits begin more in the first stage, then the third calcification becomes visible on x-ray. In this deposition can be of various sizes and shapes. Their structures can vary from a dense to a rather loose. Joints already at this stage is significantly limited in movement.

The fourth stage - this is the stage at which visible bone disorders. X-ray examination detects osteoporosis, visible and erosion, and cysts that are multiple, cracks can grow together, or have an extremely narrow gaps. The joint is completely deformed, muscles and soft tissues around it atrophied. The disease affects all the limbs, and patients complain of severe persistent pain.