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
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

100335

Subventions

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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Auteurs

Kosaku Aoyagi (K)

Section of Rheumatology, Boston University School of Medicine, Boston, MA, USA.
Department of Rehabilitation Sciences, University of Texas at El Paso, El Paso, TX, USA.

Laura Frey Law (LF)

University of Iowa, Iowa City, IA, USA.

Lisa Carlesso (L)

McMaster University, ON, Canada.

Michael Nevitt (M)

University of California San Francisco, San Francisco, CA, USA.

Cora E Lewis (CE)

University of Alabama, Birmingham, AL, USA.

Na Wang (N)

Boston University School of Public Health, Boston, MA, USA.

Tuhina Neogi (T)

Section of Rheumatology, Boston University School of Medicine, Boston, MA, USA.

Classifications MeSH