Ulcer pain
Since synovial fibroblasts line the joint cavity, their elaboration of this cytokine into the joint cavity is likely to explain the selective recruitment of neutrophils to the synovial cavity. ulcer pain Inflamatory arthritis. Neutrophils in the synovial fluid are in an activated state, releasing oxygen-derived free radicals that depolymerize hyaluronic acid and inactivate endogenous inhibitors of proteases, thus promoting damage to the joint. Prostaglandins and proteases are also secreted from synovial fibroblasts as the pannus invades contiguous bone and cartilage. PGE2 resorbs bone and contributes to the radiographically demonstrable erosions at the site of synovial-bone attachment. ulcer pain Pictures of rheumatoid arthritis. The proteases (collagenase, stromelysin and gelatinase) act enzymatically to degrade the collagen and proteoglycan matrix of bone and cartilage. This destructive effect is further compounded by IL1 (and TNF) which suppresses synthesis of these matrix molecules. 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). ulcer pain Cortisone injections arthritis. (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. Complement may be available for interaction with immune complexes to generate additional chemotactic stimuli.
Ulcer pain
Herb || Caprine arthritis encephalitis || Juvenille-rheumatoid-arthritis || Rhuematiod-arthritis