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Longitudinal association of infrapatellar fat pad signal intensity alteration with biochemical biomarkers in knee osteoarthritis
Objective
To explore the longitudinal association of quantitative infrapatellar fat pad (IPFP) signal intensity alteration with osteoarthritis (OA)-related biomarkers.
Method
Eighteen OA-related biochemical biomarkers of 600 knee OA participants in the Foundation for the National Institutes of Health OA Biomarkers Consortium (FNIH) study were extracted. The quantitative IPFP signal intensity measures was acquired based on magnetic resonance imaging, including mean value [Mean (IPFP)] and standard deviation [sDev (IPFP)] of the whole IPFP, median value [Median (H)] and upper quartile value [UQ (H)] of high signal intensity, the ratio of volume of high signal intensity to volume of whole IPFP [Percentage (H)] and Clustering factor (H). The linear mixed-effect model was applied to determine the longitudinal associations between IPFP signal intensity alteration and biochemical biomarkers over 2 years.
Results
All IPFP measures except for Clustering factor (H) were positively associated with urine collagenase-cleaved type II collagen neoepitope (uC2C), urine C-terminal cross-linked telopeptide of type II collagen (uCTX-II), urine C-terminal cross-linked telopeptide of type I collagen-α (uCTX-Iα) and urine N-terminal cross-linked telopeptide of type I collagen (uNTX-I). Mean (IPFP), Median (H) and Percentage (H) were positively associated with nitrated form of an epitope located in the triple helix of type II collagen (Coll2-1 NO2). Mean (IPFP), Median (H) and UQ (H) were positively associated with sCTX-I and uCTX-Iβ. Positive associations between sDev (IPFP), Percentage (H) and serum hyaluronic acid (sHA) were found.
Conclusion
Our results suggest a role of IPFP signal intensity alteration in joint tissue remodelling on a molecular level.
History
Publication title
RheumatologyArticle number
keac214Number
keac214ISSN
1462-0324Department/School
Menzies Institute for Medical ResearchPublisher
Oxford Univ PressPlace of publication
Great Clarendon St, Oxford, England, Ox2 6DpRights statement
© The Author(s) 2022. Published by Oxford University Press on behalf of the British Society for Rheumatology.Repository Status
- Restricted