[ETIOLOGY AND PATHOGENESIS OF PAIN IN RHEUMATIC DISEASES].

Abstract

Rheumatic diseases are chronic inflammatory disorders with ongoing inflammation that causes tissue damage. Inflammatory and damaged cells synthetize and release many diff erent intracellular substances which can activate highly specialized subsets of primary sensory neurons called nociceptors. Some of these proinflammatory mediators directly activate the nociceptor terminal and produce pain (such as hydrogen ion, adenosine triphosphate, and bradykinin), and others sensitize the terminal so that it becomes hypersensitive to subsequent and non-noxious stimuli (such as prostaglandin E2 and bradykinin). Acute pain has a protective role since it induces behavior that promotes healing and recovery, such as immobilization which limits tissue damage. Chronic pain is unhelpful pain that tends to be out of proportion to the actual tissue damage and persists long after the tissues have healed, so that the pain becomes the problem rather than the tissues of origin. Chronic pain affects the physical and mental status and causes impairment of quality of life as well as work disability. For rheumatologists the assessment and treatment of pain is a very important integral part of patient care, and understanding the etiology and pathogenesis of pain is necessary to fi nd adequate modalities of treatment to prevent suffering.