Physiopathology of pain in rheumatology

Abstract

summary Pain is the main manifestation of many rheumatic diseases (be they overtly inflammatory such as rheumatoid arthritis or dysfunctional such as fibromyalgia) but, at least initially, the mechanisms involved in the genesis, amplification and chronicisation of the persistent pain characterising the various conditions can be very different. The main peripheral mechanism underlying acute nociceptive pain is a change in the activity of the nociceptors located in the affected anatomical structures (joints, tendons and ligaments), which makes them more sensitive to normally painful stimuli (hyperalgesia) or normally non-painful stimuli (allodynia). This physiopathological mechanism of peripheral sensitisation plays a primary role in rheumatic diseases characterised by acute inflammation, such as the arthritides due to microcrystals. In the case of chronic rheumatic diseases that do not regress spontaneously, functional and structural central nervous system changes cause a generalised reduction in the pain threshold that is not limited to the anatomical structures involved, thus leading to the appearance of hyperalgesia and allodynia in many, if not all body districts. This is the physiopathological basis of chronic, widespread musculoskeletal pain.

Vitamin D in Fibromyalgia: A Causative or Confounding Biological Interplay?

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Subjective health complaints and illness perception amongst adults with Joint Hypermobility Syndrome/Ehlers–Danlos Syndrome-HypermobilityType – a cross-sectional study

“…Neurophysiological changes compatible with central sensitization are now recognized in understanding chronic pain in rheumatoid conditions, such as rheumatoid arthritis, osteoarthritis and fibromyalgia (38). Several studies have found EDS to have close resemblance with fibromyalgia as both conditions are characterized by pain, fatigue and physical disability (4,9).…”

“…In addition to the total score for each of the five subscales of SHC, a mean score was calculated (38). For each of the eight items of B-IPQ a mean group value was calculated.…”

Pain in systemic connective tissue diseases

“…Until a few years ago, the pain associated with many rheumatic diseases was considered to be peripheral in origin and induced by the well-known mechanisms of acute or chronic inflammation, or morpho-structural alterations in the involved joints [37,38]. However, the mechanisms underlying chronic widespread pain (the prototype of which is FM) have only recently been identified as neurophysiological modifications in the perception, transmission and, above all, processing of nociceptive afferents at the level of the CNS, which seem to be caused by what has come to be called "sensitisation": i.e.…”