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Editorial

Stress of different types increases the proinflammatory load in rheumatoid arthritis

Rainer H Straub1* and Joachim R Kalden2

Author Affiliations

1 Laboratory of Experimental Rheumatology and Neuroendocrino-Immunology, Division of Rheumatology, Department of Internal Medicine I, University Hospital, 93042 Regensburg, Germany

2 Department of Medicine 3, University of Erlangen-Nuremberg, Nikolaus-Fiebiger-Center, 91054 Erlangen, Germany

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Arthritis Research & Therapy 2009, 11:114  doi:10.1186/ar2712


See related research article by Edwards et al., http://arthritis-research.com/content/11/3/R61

Published: 17 June 2009

Abstract

Stress in patients with chronic inflammatory diseases such as rheumatoid arthritis (RA) stimulates proinflammatory mechanisms due to the defect of stress response systems (for example, the sympathetic nervous system and the hypothalamic–pituitary–adrenal axis). Among other mechanisms, the loss of sympathetic nerve fibers in inflamed tissue and inadequate cortisol secretion in relation to inflammation lead to an enhanced proinflammatory load in RA. Stress and the subsequent stimulation of inflammation (systemic and local) lead to increased sensitization of pain and further defects of stress response systems (vicious cycle of stress, pain, and inflammation).