Obesity – Inflammation – PsA

  • Sponsored by Lilly Medical Affairs
 Oct 01, 2026 9:00 am

Developed under the direction and sponsorship of Lilly Medical Affairs and is intended for US healthcare professionals only

Obesity May Impact PsA Burden and Outcomes 1

Despite advances in PsA treatment, obesity remains a key modifiable risk factor impacting disease severity, cardiometabolic risk, treatment response, and patient outcomes
 
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Obese Adipose Tissue Is an Active Endocrine Driver of Inflammation1

 

 

 

Two Paths from Obesity to Joint Damage in PsA

  • Increased mechanical load from excess adipose tissue adds stress to entheses of weight-bearing joints, resulting in microtrauma associated with the pathology of PsA2,3
  • Pro-inflammatory adipokines and cytokines (e.g. TNF-α, IL-17, IL-6) stimulate osteoclast differentiation and bone resorption via RANKL-mediated and RANKL-independent mechanisms.1,4
 

 

 

Obesity Activates Immune Pathways Relevant to PsA Pathogenesis

  • PsA and obesity share intertwined pathogenic pathways built on common inflammatory mediators, lymphocyte and macrophage polarization, and overlapping signaling cascades.1
  • This overlap positions excess adiposity as an active contributor to the PsA inflammatory milieu, not merely a comorbidity.1
 

 

 

 

PsA and Obesity Have Mutually Reinforcing Mechanisms2,3

Click below to watch a short animation on the obesity–PsA connection and the underlying mechanisms driving disease

Clinical Implications1

  • Obesity is increasingly recognized as an active contributor to the inflammatory biology of PsA rather than a passive comorbidity
  • Understanding this shared pathophysiology reinforces the value of considering adiposity in the comprehensive assessment and care of patients with PsA

Abbreviations

AMPK=adenosine monophosphate-activated protein kinase; IFN-γ=Interferon gamma; IL=Interleukin; JAK-STAT=Janus kinase–signal transducer and activator of transcription; M1/M2=Macrophage polarization phenotypes 1 and 2; MAPK=Mitogen-activated protein kinase; MCP-1=Monocyte chemoattractant protein-1; NF-κB=Nuclear factor kappa B; PI3K-AKT=Phosphoinositide 3-kinase–AKT; PsA=Psoriatic arthritis; RANKL=Receptor activator of nuclear factor kappa-B ligand; TGF-β=Transforming growth factor beta; Th1/Th17/Th22=T-helper cell subsets 1, 17, and 22; TNF-α=Tumor necrosis factor alpha; Wnt/β-catenin=Wingless-related integration site/beta-catenin signaling pathway.

References
  1. Madsen N, et al. RMD Open. 2026;12:e006577. 
  2. Porta S, et al. Front Immunol. 2021;11:590749.
  3. Kumthekar A, Ogdie A. Rheumatol Ther. 2020;7:447-456.
  4. Paine A, Ritchlin C. Calcif Tissue Int. 2018 May;102(5):559-574.
 
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