- Chronic inflammatory and destructive disease of the joints.
- Erosion of the articular cartilage and destruction of the subjacent bone.
- Initial events is the activation of CD4 cells by undetermined antigen.
- Activated CD4 stimulate the production of tumor necrosis factors-α (IL-2) and IL-6, and secretion of collagenase and mettaloproteinases by monocytes, macrophages and fibroblasts like synovial cells.
- Activated CD4 stimulate B cells to differentiate into plasma cells to produce Ig and Rheumatoid factor.
- TNF- α, IL-1, and IL-6 are key cytokines in driving inflammation in rheumatoid arthritis. TNF- α can be detected in the synovial fluid of the rheumatoid arthritis patients.
- TNF- α, IL-1 stimulate fibroblast-like synovial cells, osteoblasts and chondrocytes to release cartilage and bone-destroying matrix and metalloproteinases.
- The synovial membrane normally consists of a lining of one or two cell layers of synovial cells and underlying loose connective tissue. The synovial-lining cells are designated type A (macrophage-like synovial cells) and type B (fibroblast-like synovial cells).
- In rheumatoid arthritis, the synovial membrane becomes thickened by the proliferation (hyperplasia) and enlargement (hypertrophy) of the synovial lining cells. A synovial membrane with abundant villi develops. T and B cells and plasma cells infiltrate the connective tissue of the synovial membrane. T cells and macrophages can be found in the synovial fluid.
- Binding of tumor necrosis factor- α and interleukin-1 or -6 to their receptors triggers the production of inflammatory effector molecules by synovial cells. Proinflammatory effectors determine progressive damage of the joint (cartilage and bone erosion).
- When there's no proinflammatory effector, Proinflammatory cytokines cannot bind to the cytokine receptor because receptor antagonists or a monoclonal antibody occupies binding sites for proinflammatory cytokines produced by synovial cells. No proinflammatory effector is produced by synovial cells.
- When there's no proinflammatory effector, soluble cytokine receptor (etanercept) or a monoclonal antibody targeting a proinflammatory cytokine (infliximab) prevents cytokine bind to the cytokine receptor. No proinflammatory effector is produced by synovial cells.
- When there's no proinflammatory effector, anti-inflammatory cytokinds bind to the cytokine receptor and inhibit the expression of proinflammatory effectors.
- Erythrocyte Sedimentation Rate is increased in patients with rheumatoid arthritis.
- Damage to the ligaments controlling stability of the column may occur in the absence of evident bony pathology. This is particularly prevalent in inflammatory disease of the upper cervical spine, where rheumatoid arthritis may weaken or destroy the ligaments on which atlanto-axial stability depends.
- Rheumatoid arthritis is a chronic inflammatory disease that affects primarily the joints but may involve extra-articular tissues such as the skin, blood vessels, lungs, and heart. Abundant evidence supports the autoimmune nature of the disease
- is a chronic inflammatory condition that can be complicated by amyloidosis of the reactive systemic variety with SAA protein contributing to amyloid deposition in a variety of organs.
References:
1. Kumar, Raminder et al. Robbins and Cotran Pathologic Basis of Disease 8th Ed. Sander Elsevier. 2010.
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