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Chronic pain and neuroinflammation.

Authors
  • Vergne-Salle, Pascale1
  • Bertin, Philippe2
  • 1 Service de rhumatologie, CHU de Dupuytren 2, 16, rue Bernard-Descottes, 87042 Limoges, France. Electronic address: [email protected] , (France)
  • 2 Service de rhumatologie, CHU de Dupuytren 2, 16, rue Bernard-Descottes, 87042 Limoges, France. , (France)
Type
Published Article
Journal
Joint bone spine
Publication Date
Dec 01, 2021
Volume
88
Issue
6
Pages
105222–105222
Identifiers
DOI: 10.1016/j.jbspin.2021.105222
PMID: 34022418
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

In rheumatology, chronic pain most often sets in after a musculoskeletal injury. Its persistence is not always due to the progression of the initial injury, but in some cases to the onset of central sensitization. Much scientific data suggests that this central sensitization is caused by multiple complex interactions between the nervous system and immune system. Afferent nerve fibers carrying pain information are responsible for peripheral sensitization partly linked to inflammation molecules. These afferent fibers release neurotransmitters in the dorsal root ganglion and dorsal horn of the spinal cord, capable of activating microglia, which are the local immune cells. The activated microglia will produce pro-inflammatory cytokines, chemokines and neuropeptides capable of interacting with the second-order neuron, but also segmental and descending inhibitory neurons. This is referred to as neuroinflammation, which will amplify the hypersensitivity of second-order neurons, otherwise called central sensitization. This neuroinflammation will be able to reach the higher brain structures, which are involved in pain modulation and the emotional and cognitive aspects of pain. The aim of this update is to describe the pathophysiology of chronic pain, incorporating the latest scientific data on neuroplasticity and neuroinflammation. Copyright © 2021 Société française de rhumatologie. Published by Elsevier Masson SAS. All rights reserved.

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