Longitudinal association of infrapatellar fat pad signal intensity alteration with biochemical biomarkers in knee osteoarthritis

Author:

Cen Han123,Yan Qingran34,Han Weiyu35,Meng Tao6ORCID,Chen Zhongshan37,Ruan Guangfeng35,Wang Tian38,Pan Feng3ORCID,Chen Di9,Kraus Virginia Byers10,Hunter David J511ORCID,Ding Changhai35ORCID

Affiliation:

1. Institute of Geriatrics, the Affiliated Hospital of Medical School

2. Department of Preventive Medicine, School of Medicine, Ningbo University , Ningbo, China

3. Menzies Institute for Medical Research, University of Tasmania , Hobart, Australia

4. Department of Rheumatology, Renji Hospital, School of Medicine, Shanghai Jiaotong University , Shanghai

5. Clinical Research Centre, Zhujiang Hospital, Southern Medical University , Guangzhou

6. Department of Rheumatology and Immunology, The Second Hospital of Anhui Medical University , Hefei

7. School of Mathematics and Information Science, Nanjing Normal University of Special Education , Nanjing

8. Department of Rheumatology and Clinical Immunology, Beijing An Zhen Hospital, Capital Medical University , Beijing

9. Faculty of Pharmaceutical Sciences, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences , Shenzhen, China

10. Duke Molecular Physiology Institute and Division of Rheumatology, Department of Medicine, Duke University School of Medicine , Durham, NC, USA

11. Department of Rheumatology, Royal North Shore Hospital and Institute of Bone and Joint Research, Kolling Institute, University of Sydney , Sydney, Australia

Abstract

Abstract Objective To explore the longitudinal association of quantitative infrapatellar fat pad (IPFP) signal intensity alteration with OA-related biomarkers. Methods 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 were acquired based on magnetic resonance imaging, including mean value [Mean (IPFP)] and standard deviation [sDev (IPFP)] of the whole IPFP signal intensity, 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 signal intensity [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 the 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.

Funder

National Institutes of Health

Merck Research Laboratories

Novartis Pharmaceuticals Corporation

GlaxoSmithKline and Pfizer, Inc

Foundation for the National Institutes of Health

Novartis

Publisher

Oxford University Press (OUP)

Subject

Pharmacology (medical),Rheumatology

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