Find Out More About Pathogenesis Of Rheumatoid Arthritis

Pathogenesis of rheumatoid arthritis means the alterations taking place in the tissues suffering from rheumatoid arthritis. The alterations particularly occur in the synovium. Synovium is the covering layer of the joints. Amongst these alterations, the foremost to be seen is a rise in the quantity of cells in the synovium. And among these, the mononuclear cells are the first to be elevated. They are a category of WBCs having a single oval or round shaped nucleus. They pile up around the blood vessels in the synovium.

Due to the addition in the cells, an addition in the remaining matters within the tissue also arises, due to which the synovium becomes swollen and thinck. This thick and inflated synovium enters the space in the joint. It looks like a tiny finger and is known as villi.

After a period, the mononuclear cells are replaced by T lymphocytes, which are WBCs given out by the gland termed as Thymus and play a major part in immune mechanism. It is at this phase that the symptoms of the condition are seen.

With the progress of RA, the synovium manifests a specific form of chronic inflammatory arthritis. When scrutinized under a laboratory microscope, it is visible that there is an augmentation in the amount as well as size of cells of synovial lining at this step. There is also an amplification in the amount of seeping blood vessels in the synovium, which develop blood clots at many areas. There is a risen number of WBCs, that too T cells particularly, close to these blood vessels. Additionally, B cells, which are responsible for humoral immune mechanism, mast cells and fibroblasts are observed. Edema too occurs owing to the growth of fluid within synovium. CD4 subset of T cells is accumulated in the vicinity of the small veins and CD8 subset also is present in a small quantity right through the synovium.   

In the pathogenesis of rheumatoid arthritis, mast cells play a role by releasing histamine whereas fibroblast cells participate by giving out enzymes which kill cartilage. Different cells in the synovium secrete cytokines and chemokines. They are the factors which play a role in the inflammatory process and ultimately end in destruction of bone as well as cartilage. They are of two categories. One of the kinds boosts inflammation while the other decreases it. The previous one is found in higher quantity than the inflammation-reducing one in pathogenesis of rheumatoid arthritis.

Some particular cytokines are given out by T cells and they stimulate B cells to release more number of antibodies to harm synovium. These antibodies stimulate the complement system. Complement system is a group of proteins forming a part of the blood, which when induced, damage cells.

Concurrently with the chronic inflammation in the synovium, an acute inflammation also begins growing inside the synovial fluid, i.e. the fluid present in the joints. The synovial fluid is created by synovium in very small quantities in healthy conditions, while during inflammation, the synovium leaks and creates high quanities of synovial fluid. This fluid is composed of neutrophils in large amounts which are primarily responsible for acute inflammation.

Cartilage destruction starts at a place, closest to the synovium. A flap of tissue, known as pannus is developed from the synovium which creeps steadily over the cartilage. Pannus comprises of mononuclear cells, fibroblasts and blood vessels in a large number. The pannus cells are activated by cytokines to create large quanity of hazardous enzymes.