Osteoarthritis hip spur
This destructive effect is further compounded by IL1 (and TNF) which suppresses synthesis of these matrix molecules. osteoarthritis hip spur How do you treat arthritis in dogs. Thus, IL1 provides a "double insult" to connective tissue by both promoting its degradation (by inducing synthesis of proteases) and preventing its repair (by suppressing synthesis of collagen and proteoglycans). (top of section) Other Contributors to the Inflammatory Process Soluble mediators of inflammation that may diffuse in from blood and/or be formed locally within the joint cavity include kinins and complement. Kinins cause release of prostaglandins from synovial fibroblasts, and are also potent algesic (pain-producing) agents. osteoarthritis hip spur Lupus arthritis. Complement may be available for interaction with immune complexes to generate additional chemotactic stimuli. Chondrocytes, like synovial fibroblasts, are activated by IL1 and TNF to secrete proteolytic enzymes. They may, therefore, contribute to the dissolution of their own cartilage matrix, thus explaining the progressive narrowing of joint spaces seen radiographically in this disease. osteoarthritis hip spur Forearm pain. Finally, the neuropeptide substance P is a potent vasoactive, proinflammatory peptide that is likely to contribute to joint destruction and probably explains the remarkable symmetry of this disease. (top of section) Unanswered questions Two pieces in the middle of the puzzle remain inadequately explained in this theory of self-sustained inflammation, however. The first is the macrophage. What is the stimulus for its initial and continued recruitment to the joint? And what causes its initial activation? Immune complex deposition (containing a bacterial or viral antigen or rheumatoid factor) in blood vessel walls may lead to local induction of endothelial and monocyte adhesion molecules which, in turn, allows for migration of monocytes into the synovium. Once in the synovium, initial activation of monocytes/macrophages may be induced by g-IFN secreted by activated CD4+ cells. Chronic maintenance in the activated state, however, is presumably independent of g-IFN, but may be promoted by immune complexes (again containing a bacterial or viral antigen or rheumatoid factor itself). Support for this concept comes from synovial biopsies of RA synovium in which IgG, IgM and C3 can be demonstrated by immuno-fluorescence. GM-CSF, elaborated by the synovial fibroblast, may also feedback to sustain the macrophages in a mature, activated state, as already noted.
Osteoarthritis hip spur
Symptoms || Facial pain || Lupus arthritis || Pain assessment