Local innate and adaptive immune processes are of importance during the acute phase of rheumatoid arthritis (RA). In the advanced inflammatory phase alterations of systemic anti-inflammatory feedback mechanisms might be important features which may support chronic inflammation.
Similarly, like in other chronic inflammatory diseases, inadequately low cortisol and androgen serum levels can be detected in RA patients. In addition, there is a marked reduction of anti-inflammatory sympathetic nerve fibers in the inflamed joints paralleled by an enhanced number of pro-inflammatory sensory nerve fibers. Thus, an uncoupling of synergistically acting endocrine and neuronal, anti-inflammatory mechanisms (cortisol, dehydroepiandrosterone, androgens, sympathetic neurotransmitters) and a preponderance of pro-inflammatory mechanisms (estrogens, sensory neurotransmitters) may lead to chronic inflammatory disease.
From this pathogenetic point of view new therapeutic strategies could be developed for the treatment of patients with RA.