Article Text

SAT0337 Adipokines related to biochemical and radiographic measures of burden, incidence, and progression in early-stage knee osteoarthritis: Data from check
  1. W.E. van Spil,
  2. P.M. Welsing,
  3. F.P. Lafeber
  1. Rheumatology & Clinical Immunology, University Medical Center Utrecht, Utrecht, Netherlands


Background The association between obesity and knee OA has classically been attributed to biomechanical mechanisms, but more recently also metabolic mechanisms have been implied to be involved. Key mediators in this metabolic link between obesity and OA could be the adipokines (leptin, adiponectin, resistin, and others) that are mainly secreted by adipose tissue.

Objectives To investigate cross-sectional and predictive associations between plasma adipokines and biochemical and radiographic measures of (very) early-stage knee osteoarthritis (OA).

Methods Baseline pLeptin, pAdiponectin, and pResistin, and uCTX-II, sPIIANP, sCS846, sCOMP, sHA, and sPIIINP were assessed by ELISA or RIA in CHECK (Cohort Hip and Cohort Knee), a cohort of 1002 participants with symptoms related to (very) early-stage knee and/or hip OA. Knee radiography was performed at baseline and after 2 and 5 years. Knee OA burden was defined as the summed Kellgren & Lawrence (K&L) grade of both knees at baseline. Five-year knee OA incidence and progression were defined as the area under the curve (AUC) of summed K&L grade progression.

Results pLeptin showed positive associations with uCTX-II, sCOMP, sPIIANP, sHA, and sPIIINP. Furthermore, pLeptin was positively associated with knee OA burden and progression. Associations largely disappeared after adjustment for BMI. pAdiponectin showed positive associations with uCTX-II and sCOMP, but no association with any radiographic OA measure. pResistin was positively associated with sPIIINP and with knee OA burden and incidence. Although statistically significant, all associations were weak.

Conclusions Especially leptin and resistin showed positive associations with multiple biomarkers of synovial and cartilage metabolism and with radiographic knee OA burden, incidence, and progression. This might indicate that these adipokines play aggravating roles in knee OA, possibly (also) mediated through synovitis. However, since associations were only weak, another conclusion should be that these systemic adipokines generally do not play a major role in early-stage knee OA.

Acknowledgements This study was funded by CHECK, an initiative of the Dutch Arthritis Association.

Disclosure of Interest None Declared

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