Facial pain

The stimulus for maturation of B cells to immunoglobulin-secreting plasma cells has classically been ascribed to CD4+ T cells; however, as already noted, CD4+ T cells are not activated in the chronic phase of rheumatoid arthritis. facial pain Abbott labs and rheumatoid arthritis. IL-6, however, is a potent stimulus for maturation of B cells to plasma cells. Thus, synovial fibroblasts are likely providing the "T cell independent" stimulus for continuous plasma cell activation and rheumatoid factor production. IL-6 also suppresses albumin synthesis by the liver and stimulates acute phase protein synthesis (slide). facial pain Prosorba-column-therapy-for-rheumatoid-arthritis. IL-6, therefore, contributes significantly to ESR elevation. Neutrophils are recruited in very large numbers to the rheumatoid cavity where they can be aspirated in the synovial fluid. Complement activation is not a prominent feature of RA. facial pain Abbott labs and rheumatoid arthritis. Therefore, C5a is unlikely to contribute significantly to the recruitment of neutrophils to the joint. IL-8, however, is also a potent and specific chemotactic stimulus for neutrophils (slide). 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. 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. 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). (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.

Facial pain



Symptoms || Pain assessment || Human-body-joints || Lupus-arthritis
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