Pannus rheumatoid arthritis is nothing but a pannus, which is a phenomenon where immoderate growth of fibro vascular tissue layer occurs. It’s the condition of swollen synovial tissue which mainly raps articular cartilage. The pathologic hallmarks of rheumatoid arthritis include inflammation of the joints particularly the small joints in the hands, wrists and feet, accompanied by cartilage destruction and bone erosion. Underlying inflammation leads to many of the characteristics signs and symptoms of RA, such as pain and swelling of the joints. Inflammation results from abnormal propagation and activation of many types of immune cells resulting in the secretion of cytokines and other mediators that sustain and amplify the inflammatory environment.
As a key pro inflammatory cytokines T N F alpha (tumor necrosis factor alpha) along with other cytokines activate immune cells including macrophages and other cells such as and synovial fibroblasts. In a key step activated macrophages and synovial fibroblasts release pro-inflammatory cytokines including T N F alpha IL 1 and IL 6 and mediator of vascular growth including V E G F (vascular endothelial growth factor), V E G F is essential to the process of blood vessel proliferation or angiogenesis which facilitates the influx of activated cells. These cells contribute the growth of pannus and sustain the inflammatory cycle. The growing vascularised pannus develop villous projections that result in the better access to cartilage and bone and therefore greater opportunity for the activated cells to release damaging inflammatory mediators and enzymes.
In the interface between pannus and cartilage activated synovial fibroblasts and macrophages are resource of enzymes that degrade the cartilage matrix, these include matrix mettaloproteinases (M M Ps) thus activated cells and pannus are key instigators of cartilage destructions, and lead to pannus rheumatoid arthritis. Chondrocytes are the main cellular components of cartilage and normally produces the extra cellular matrix; however in response to stimulation of TN F alpha, I L 1 and other inflammatory mediator’s chondrocyte becomes activated in the rheumatoid joint, activated chondrocyte secrete more inflammatory factors and more M M Ps, which aggravate inflammation and cartilage damage.
The cumulative result is irreversible cartilage damage and joint space narrowing. Under normal conditions bone remodeling evolves also the tightly regulated balance between bone resorption and bone formation. However excessive T N F alpha helps stimulate osteoclastogenesis and bone destructions. In the bone marrow T N F alpha helps stimulate monocyte differentiation into osteoclast precursors, at inflamed joints in the presence of macrophage colony stimulating factor T N F alpha and rank ligand (rank-l). In most cases of rheumatoid arthritis and also arthritis, formation of paanus is quite inevitable. It is due to pannus formation bones and cartilages get destructed. Pannus is directly related to the deterioration of the disease. It is kind of membrane primarily found in vasuclarised tissue.
There is an increased risk of the pannus rheumatoid arthritis to create deterioration into the bone marrow and affect the neighboring body parts like muscle tendons, joint capsule etc. If untreated or neglected for long it can create enormous problem for the patient. Pannus formation not only seen in the joints but it affects the eye which leads to a chronic eye disease known as superficial keratitis.