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Differential expression of cerebrospinal fluid neuroinflammatory mediators depending on osteoarthritis pain phenotype

Flores Bjurström, Martin LU ; Bodelsson, Mikael LU ; Montgomery, Agneta LU ; Harsten, Andreas LU ; Waldén, Markus ; Janelidze, Shorena LU ; Hall, Sara LU ; Hansson, Oskar LU orcid ; Irwin, Michael R. and Mattsson-Carlgren, Niklas LU orcid (2020) In Pain 161(9). p.2142-2154
Abstract

ABSTRACT: Neuroinflammation is implicated in the development and maintenance of persistent pain states, but there are limited data linking cerebrospinal fluid (CSF) inflammatory mediators with neurophysiological pain processes in humans. In a prospective observational study, CSF inflammatory mediators were compared between patients with osteoarthritis (OA) who were undergoing total hip arthroplasty due to disabling pain symptoms (n = 52) and pain-free comparison controls (n = 30). In OA patients only, detailed clinical examination and quantitative sensory testing were completed. Cerebrospinal fluid samples were analyzed for 10 proinflammatory mediators using Meso Scale Discovery platform. Compared to controls, OA patients had higher CSF... (More)

ABSTRACT: Neuroinflammation is implicated in the development and maintenance of persistent pain states, but there are limited data linking cerebrospinal fluid (CSF) inflammatory mediators with neurophysiological pain processes in humans. In a prospective observational study, CSF inflammatory mediators were compared between patients with osteoarthritis (OA) who were undergoing total hip arthroplasty due to disabling pain symptoms (n = 52) and pain-free comparison controls (n = 30). In OA patients only, detailed clinical examination and quantitative sensory testing were completed. Cerebrospinal fluid samples were analyzed for 10 proinflammatory mediators using Meso Scale Discovery platform. Compared to controls, OA patients had higher CSF levels of interleukin 8 (IL-8) (P = 0.002), intercellular adhesion molecule 1 (P = 0.007), and vascular cell adhesion molecule 1 (P = 0.006). Osteoarthritis patients with central sensitization possibly indicated by arm pressure pain detection threshold <250 kPa showed significantly higher CSF levels of Fms-related tyrosine kinase 1 (Flt-1) (P = 0.044) and interferon gamma-induced protein 10 (IP-10) (P = 0.024), as compared to subjects with PPDT above that threshold. In patients reporting pain numerical rating scale score ≥3/10 during peripheral venous cannulation, Flt-1 was elevated (P = 0.025), and in patients with punctate stimulus wind-up ratio ≥2, CSF monocyte chemoattractant protein 1 was higher (P = 0.011). Multiple logistic regression models showed that increased Flt-1 was associated with central sensitization, assessed by remote-site PPDT and peripheral venous cannulation pain, and monocyte chemoattractant protein-1 with temporal summation in the area of maximum pain. Multiple proinflammatory mediators measured in CSF are associated with persistent hip OA-related pain. Pain phenotype may be influenced by specific CSF neuroinflammatory profiles.

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author
; ; ; ; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Pain
volume
161
issue
9
pages
13 pages
publisher
Elsevier
external identifiers
  • scopus:85100070257
  • pmid:32384383
ISSN
1872-6623
DOI
10.1097/j.pain.0000000000001903
language
English
LU publication?
yes
id
80eac7f3-0ae1-4573-8e80-7dea0520f9ef
date added to LUP
2021-02-10 11:14:52
date last changed
2024-05-02 03:02:14
@article{80eac7f3-0ae1-4573-8e80-7dea0520f9ef,
  abstract     = {{<p>ABSTRACT: Neuroinflammation is implicated in the development and maintenance of persistent pain states, but there are limited data linking cerebrospinal fluid (CSF) inflammatory mediators with neurophysiological pain processes in humans. In a prospective observational study, CSF inflammatory mediators were compared between patients with osteoarthritis (OA) who were undergoing total hip arthroplasty due to disabling pain symptoms (n = 52) and pain-free comparison controls (n = 30). In OA patients only, detailed clinical examination and quantitative sensory testing were completed. Cerebrospinal fluid samples were analyzed for 10 proinflammatory mediators using Meso Scale Discovery platform. Compared to controls, OA patients had higher CSF levels of interleukin 8 (IL-8) (P = 0.002), intercellular adhesion molecule 1 (P = 0.007), and vascular cell adhesion molecule 1 (P = 0.006). Osteoarthritis patients with central sensitization possibly indicated by arm pressure pain detection threshold &lt;250 kPa showed significantly higher CSF levels of Fms-related tyrosine kinase 1 (Flt-1) (P = 0.044) and interferon gamma-induced protein 10 (IP-10) (P = 0.024), as compared to subjects with PPDT above that threshold. In patients reporting pain numerical rating scale score ≥3/10 during peripheral venous cannulation, Flt-1 was elevated (P = 0.025), and in patients with punctate stimulus wind-up ratio ≥2, CSF monocyte chemoattractant protein 1 was higher (P = 0.011). Multiple logistic regression models showed that increased Flt-1 was associated with central sensitization, assessed by remote-site PPDT and peripheral venous cannulation pain, and monocyte chemoattractant protein-1 with temporal summation in the area of maximum pain. Multiple proinflammatory mediators measured in CSF are associated with persistent hip OA-related pain. Pain phenotype may be influenced by specific CSF neuroinflammatory profiles.</p>}},
  author       = {{Flores Bjurström, Martin and Bodelsson, Mikael and Montgomery, Agneta and Harsten, Andreas and Waldén, Markus and Janelidze, Shorena and Hall, Sara and Hansson, Oskar and Irwin, Michael R. and Mattsson-Carlgren, Niklas}},
  issn         = {{1872-6623}},
  language     = {{eng}},
  number       = {{9}},
  pages        = {{2142--2154}},
  publisher    = {{Elsevier}},
  series       = {{Pain}},
  title        = {{Differential expression of cerebrospinal fluid neuroinflammatory mediators depending on osteoarthritis pain phenotype}},
  url          = {{http://dx.doi.org/10.1097/j.pain.0000000000001903}},
  doi          = {{10.1097/j.pain.0000000000001903}},
  volume       = {{161}},
  year         = {{2020}},
}