The role of obesity and adipose tissue dysfunction in osteoarthritis pain.


Journal

Nature reviews. Rheumatology
ISSN: 1759-4804
Titre abrégé: Nat Rev Rheumatol
Pays: United States
ID NLM: 101500080

Informations de publication

Date de publication:
07 Aug 2024
Historique:
accepted: 05 07 2024
medline: 8 8 2024
pubmed: 8 8 2024
entrez: 7 8 2024
Statut: aheadofprint

Résumé

Obesity has a pivotal and multifaceted role in pain associated with osteoarthritis (OA), extending beyond the mechanistic influence of BMI. It exerts its effects both directly and indirectly through various modifiable risk factors associated with OA-related pain. Adipose tissue dysfunction is highly involved in OA-related pain through local and systemic inflammation, immune dysfunction, and the production of pro-inflammatory cytokines and adipokines. Adipose tissue dysfunction is intricately connected with metabolic syndrome, which independently exerts specific effects on OA-related pain, distinct from its association with BMI. The interplay among obesity, adipose tissue dysfunction and metabolic syndrome influences OA-related pain through diverse pain mechanisms, including nociceptive pain, peripheral sensitization and central sensitization. These complex interactions contribute to the heightened pain experience observed in individuals with OA and obesity. In addition, pain management strategies are less efficient in individuals with obesity. Importantly, therapeutic interventions targeting obesity and metabolic syndrome hold promise in managing OA-related pain. A deeper understanding of the intricate relationship between obesity, metabolic syndrome and OA-related pain is crucial and could have important implications for improving pain management and developing innovative therapeutic options in OA.

Identifiants

pubmed: 39112603
doi: 10.1038/s41584-024-01143-3
pii: 10.1038/s41584-024-01143-3
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© 2024. Springer Nature Limited.

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Auteurs

Marie Binvignat (M)

Department of Rheumatology, Sorbonne University, AP-HP Saint-Antoine hospital, Paris, France.
Sorbonne University, INSERM UMRS_938, Centre de Recherche Saint-Antoine (CRSA), Paris Center for Microbiome Medicine (PaCeMM) FHU, Paris, France.
Sorbonne University, INSERM UMRS_959, I3 Lab Immunology Immunopathology Immunotherapy, Paris, France.

Jérémie Sellam (J)

Department of Rheumatology, Sorbonne University, AP-HP Saint-Antoine hospital, Paris, France. jeremie.sellam@aphp.fr.
Sorbonne University, INSERM UMRS_938, Centre de Recherche Saint-Antoine (CRSA), Paris Center for Microbiome Medicine (PaCeMM) FHU, Paris, France. jeremie.sellam@aphp.fr.

Francis Berenbaum (F)

Department of Rheumatology, Sorbonne University, AP-HP Saint-Antoine hospital, Paris, France.
Sorbonne University, INSERM UMRS_938, Centre de Recherche Saint-Antoine (CRSA), Paris Center for Microbiome Medicine (PaCeMM) FHU, Paris, France.

David T Felson (DT)

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

Classifications MeSH