Obesity—a key driver in osteoarthritis

Abstract

Purpose: Obesity causes mechanical stress and metabolic dysfunction. However, the relationship between obesity and osteoarthritis (OA) pain still needs further investigation. This study aims to examine the effect of weight loss on pain and function through a secondary analysis of a randomized, double-blind, multicenter OA trial and to evaluate obesity's impact on OA pain using a rat model.

Methods: In a post hoc analysis of a randomized controlled trial (RCT; NCT00486434), we evaluated baseline body mass index and Western Ontario and McMaster Universities Osteoarthritis (WOMAC) scores (n = 1175) and examined the impact of 5% weight loss on WOMAC scores after 2 years using a factorial analysis of covariance (n = 674). In a preclinical model of metabolic OA induced by meniscectomy, pain-like behavior was assessed with the von Frey and cold plate tests.

Results: Participants who lost >5% of weight within 2 years experienced a mean decrease of −567.1 (95% CI −666.7 to −467.6) and −399.2 (−505.8 to −292.5) in total WOMAC scores for their target and nontarget knees, respectively, whereas individuals who gained >5% in weight had a smaller decrease of −364.6 (−496.5 to −232.7) and −135 (−277.4 to −6.3), respectively. Additionally, the high-fat diet–fed rat model showed more pain-like behavior than the lean model.

Main conclusion: These studies indicate that weight loss could decrease OA pain in both target and nontarget knees of patients with obesity, supporting the inclusion of obesity in OA animal models to improve the translatability of OA treatments.

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Cite

BibTeX RIS

BibTeX

@article{mohamed2026obesitya,
  title = {{Obesity—a key driver in osteoarthritis}},
  author = {Khaled Elhady Mohamed and Christian S Thudium and Asger Reinstrup Bihlet and Mette Sørensen Iken and Morten Asser Karsdal and Kim Henriksen and Anne-Christine Bay-Jensen},
  journal = {Journal of the Endocrine Society},
  year = {2026},
  month = oct,
  doi = {10.1210/jendso/bvag245},
  url = {https://europepmc.org/article/PMC/PMC13724259},
  note = {CC BY},
}

RIS

TY  - JOUR
TI  - Obesity—a key driver in osteoarthritis
AU  - Khaled Elhady Mohamed
AU  - Christian S Thudium
AU  - Asger Reinstrup Bihlet
AU  - Mette Sørensen Iken
AU  - Morten Asser Karsdal
AU  - Kim Henriksen
AU  - Anne-Christine Bay-Jensen
PY  - 2026
DA  - 2026/10/22
JO  - Journal of the Endocrine Society
DO  - 10.1210/jendso/bvag245
UR  - https://europepmc.org/article/PMC/PMC13724259
AB  - Purpose: Obesity causes mechanical stress and metabolic dysfunction. However, the relationship between obesity and osteoarthritis (OA) pain still needs further investigation. This study aims to examine the effect of weight loss on pain and function through a secondary analysis of a randomized, double-blind, multicenter OA trial and to evaluate obesity's impact on OA pain using a rat model.  Methods: In a post hoc analysis of a randomized controlled trial (RCT; NCT00486434), we evaluated baseline body mass index and Western Ontario and McMaster Universities Osteoarthritis (WOMAC) scores (n = 1175) and examined the impact of 5% weight loss on WOMAC scores after 2 years using a factorial analysis of covariance (n = 674). In a preclinical model of metabolic OA induced by meniscectomy, pain-like behavior was assessed with the von Frey and cold plate tests.  Results: Participants who lost >5% of weight within 2 years experienced a mean decrease of −567.1 (95% CI −666.7 to −467.6) and −399.2 (−505.8 to −292.5) in total WOMAC scores for their target and nontarget knees, respectively, whereas individuals who gained >5% in weight had a smaller decrease of −364.6 (−496.5 to −232.7) and −135 (−277.4 to −6.3), respectively. Additionally, the high-fat diet–fed rat model showed more pain-like behavior than the lean model.  Main conclusion: These studies indicate that weight loss could decrease OA pain in both target and nontarget knees of patients with obesity, supporting the inclusion of obesity in OA animal models to improve the translatability of OA treatments.
SN  - 2472-1972
ER  -

Abstract

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