Post-surgical contributors to persistent knee pain following knee replacement: The Multicenter Osteoarthritis Study (MOST).
Central sensitization
Contributors to post-KR pain
Inefficient conditioned pain modulation
The number of painful body sites
Journal
Osteoarthritis and cartilage open
ISSN: 2665-9131
Titre abrégé: Osteoarthr Cartil Open
Pays: England
ID NLM: 101767068
Informations de publication
Date de publication:
Mar 2023
Mar 2023
Historique:
received:
20
09
2022
revised:
06
01
2023
accepted:
12
01
2023
entrez:
17
2
2023
pubmed:
18
2
2023
medline:
18
2
2023
Statut:
epublish
Résumé
Pain persistence following knee replacement (KR) occurs in ∼20-30% of patients. Although several studies have identified preoperative risk factors for persistent post-KR pain, few have focused on post-KR contributing factors. We sought to determine whether altered nociceptive signaling and other peripheral nociceptive drivers present post-operatively contribute to post-KR pain. We included participants from the Multicenter Osteoarthritis Study who were evaluated ∼12 months after KR. We evaluated the relation of measures of pain sensitivity [pressure pain threshold (PPT), temporal summation (TS), and conditioned pain modulation (CPM)] and the number of painful body sites to post-KR WOMAC knee pain, and of the number of painful sites to altered nociceptive signaling using linear or logistic regression models, as appropriate. 171 participants (mean age 69 years, 62% female) were included. TS was associated with worse WOMAC pain post-KR (β = 0.77 95% CI:0.19-1.35) and reduced odds of achieving patient acceptable symptom state (aOR = 0.54 95%CI:0.34-0.88). Inefficient CPM was also associated with worse WOMAC pain post-KR (β = 1.43 95% CI:0.15-2.71). In contrast, PPT was not associated with these outcomes. The number of painful body sites present post-KR was associated with TS (β = 0.05, 95% CI:0.01, 0.05). Post-KR presence of central sensitization and inefficient descending pain modulation was associated with post-KR pain. We also noted that presence of other painful body sites contributes to altered nociceptive signaling, and this may thus also contribute to the experience of knee pain post-KR. Our findings provide novel insights into central pain mechanisms and other peripheral pain sources contributing to post-KR persistent knee pain.
Identifiants
pubmed: 36798734
doi: 10.1016/j.ocarto.2023.100335
pii: S2665-9131(23)00002-X
pmc: PMC9926203
doi:
Types de publication
Journal Article
Langues
eng
Pagination
100335Subventions
Organisme : NIAMS NIH HHS
ID : K24 AR070892
Pays : United States
Organisme : NIAMS NIH HHS
ID : P30 AR072571
Pays : United States
Informations de copyright
© 2023 The Authors.
Déclaration de conflit d'intérêts
None.
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