Proinflammatory cytokines
are induced during OA, particularly interleukin-
1beta (IL-1beta), tumor necrosis factor-a, and matrix
metalloproteinase, and these cytokines disrupt the
anabolic/catabolic balance to the detriment of growth
factors such as insulin-like growth factor-1, transforming
growth factor beta (TGF-beta), and basic fibroblast growth
factor, provoking a chronic degenerative process of the
subchondral bone, cartilage, and/or synovial membrane
[2,4,5]. Therefore, applying a successful treatment can be
a real challenge, particularly in the long term.
Proinflammatory cytokinesare induced during OA, particularly interleukin-1beta (IL-1beta), tumor necrosis factor-a, and matrixmetalloproteinase, and these cytokines disrupt theanabolic/catabolic balance to the detriment of growthfactors such as insulin-like growth factor-1, transforminggrowth factor beta (TGF-beta), and basic fibroblast growthfactor, provoking a chronic degenerative process of thesubchondral bone, cartilage, and/or synovial membrane[2,4,5]. Therefore, applying a successful treatment can bea real challenge, particularly in the long term.
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