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In particular, macrophages and T cells in their activated form in the synovial membrane produce proinflammatory cytokines such as IL-1 and TNF- that have the ability to induce ROS production which activate NF-B [127,128,129], thus causing the increased production of proinflammatory cytokines that positively feedback this same route through canonical pathway and by H 2 O 2 as an alternative pathway, which causes an oxidative and an inflammatory environment characterized by synovitis and eventual joint destruction [123,130]

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A treatment strategy designed to significantly delay the symptoms and pathology of this disease could maintain the patients quality of life and reduce health care costs