U Heilmeier1, K Mamoto2, K Amano3, B Eck4, M Tanaka5, J A Bullen6, B J Schwaiger7, J L Huebner8, T V Stabler9, V B Kraus10, C B Ma11, T M Link12, X Li13. 1. Department of Radiology and Biomedical Imaging, Musculoskeletal Quantitative Imaging Research, University of California San Francisco, San Francisco, CA, USA. Electronic address: ursula.heilmeier@ucsf.edu. 2. Department of Radiology and Biomedical Imaging, Musculoskeletal Quantitative Imaging Research, University of California San Francisco, San Francisco, CA, USA; Department of Biomedical Engineering, Program of Advanced Musculoskeletal Imaging (PAMI), Cleveland Clinic, Cleveland, OH, USA; Department of Orthopaedic Surgery, Osaka City University Medical School, Osaka, Japan. Electronic address: mamoto7@hotmail.com. 3. Department of Radiology and Biomedical Imaging, Musculoskeletal Quantitative Imaging Research, University of California San Francisco, San Francisco, CA, USA. Electronic address: amanokeiko@gmail.com. 4. Department of Biomedical Engineering, Program of Advanced Musculoskeletal Imaging (PAMI), Cleveland Clinic, Cleveland, OH, USA. Electronic address: eckb@ccf.org. 5. Department of Radiology and Biomedical Imaging, Musculoskeletal Quantitative Imaging Research, University of California San Francisco, San Francisco, CA, USA. Electronic address: matthew.tanaka@ucsf.edu. 6. Department of Quantitative Health Sciences, Cleveland Clinic, Cleveland, OH, USA. Electronic address: bullenj@ccf.org. 7. Department of Radiology and Biomedical Imaging, Musculoskeletal Quantitative Imaging Research, University of California San Francisco, San Francisco, CA, USA. Electronic address: benedikt.schwaiger@tum.de. 8. Duke Molecular Physiology Institute, Duke University School of Medicine, Durham, NC, USA. Electronic address: janet.huebner@duke.edu. 9. Duke Molecular Physiology Institute, Duke University School of Medicine, Durham, NC, USA. Electronic address: stablert@hotmail.com. 10. Duke Molecular Physiology Institute, Duke University School of Medicine, Durham, NC, USA. Electronic address: kraus004@duke.edu. 11. Department of Orthopaedic Surgery, University of California San Francisco, San Francisco, CA, USA. Electronic address: maben@ucsf.edu. 12. Department of Radiology and Biomedical Imaging, Musculoskeletal Quantitative Imaging Research, University of California San Francisco, San Francisco, CA, USA. Electronic address: thomas.link@ucsf.edu. 13. Department of Radiology and Biomedical Imaging, Musculoskeletal Quantitative Imaging Research, University of California San Francisco, San Francisco, CA, USA; Department of Biomedical Engineering, Program of Advanced Musculoskeletal Imaging (PAMI), Cleveland Clinic, Cleveland, OH, USA. Electronic address: lix6@ccf.org.
Abstract
OBJECTIVE: To evaluate the degree of knee fat pad abnormalities after acute anterior cruciate ligament (ACL) tear via magnetic resonance fat pad scoring and to assess cross-sectionally its association with synovial fluid biomarkers and with early cartilage damage as quantified via T1ρ and T2 relaxation time measurements. DESIGN: 26 patients with acute ACL tears underwent 3T MR scanning of the injured knee prior to ACL reconstruction. The presence and degree of abnormalities of the infrapatellar (IPFP) and the suprapatellar (SPFP) fat pads were scored on MR images along with grading of effusion-synovitis and synovial proliferations. Knee cartilage composition was assessed by 3T MR T1ρ and T2 mapping in six knee compartments. We quantified concentrations of 20 biomarkers in synovial fluid aspirated at the time of ACL reconstruction. Spearman rank partial correlations with adjustments for age and gender were employed to evaluate correlations of MR, particularly cartilage composition and fat pad abnormalities, and biomarker data. RESULTS: The degree of IPFP abnormality correlated positively with the synovial levels of the inflammatory cytokine markers IFN-γ (ρpartial = 0.64, 95% CI (0.26-0.85)), IL-10 (ρpartial = 0.47, 95% CI (0.04-0.75)), IL-6 (ρpartial = 0.56, 95% CI (0.16-0.81)), IL-8 (ρpartial = 0.49, 95% CI (0.06-0.76)), TNF-α (ρpartial = 0.55, 95% CI (0.14-0.80)) and of the chondrodestructive markers MMP-1 and -3 (MMP-1: ρpartial = 0.57, 95% CI (0.17-0.81); MMP-3: ρpartial = 0.60, 95% CI (0.21-0.83)). IPFP abnormalities were significantly associated with higher T1ρ and T2 values in the trochlear cartilage (T1ρ: ρpartial = 0.55, 95% CI (0.15-0.80); T2: ρpartial = 0.58, 95% CI (0.18-0.81)) and with higher T2 values in the medial femoral, medial tibial as well as in patellar cartilage (0.45 ≤ ρpartial ≤ 0.59). Correlations between SPFP abnormalities and synovial markers were not significant except for IL-6 (ρpartial = 0.57, 95% CI (0.17-0.81)). CONCLUSIONS: This exploratory study suggests that acute ACL rupture can be associated with damage to knee tissues such as the inferior fat pad of the knee. Such fat pad injury could be partially responsible for the apparent post-injury pro-inflammatory response noted in ACL-injured individuals. However, future longitudinal studies are needed to link ACL-rupture associated fat pad injury with important patient outcomes such as the development of posttraumatic osteoarthritis.
OBJECTIVE: To evaluate the degree of knee fat pad abnormalities after acute anterior cruciate ligament (ACL) tear via magnetic resonance fat pad scoring and to assess cross-sectionally its association with synovial fluid biomarkers and with early cartilage damage as quantified via T1ρ and T2 relaxation time measurements. DESIGN: 26 patients with acute ACL tears underwent 3T MR scanning of the injured knee prior to ACL reconstruction. The presence and degree of abnormalities of the infrapatellar (IPFP) and the suprapatellar (SPFP) fat pads were scored on MR images along with grading of effusion-synovitis and synovial proliferations. Knee cartilage composition was assessed by 3T MR T1ρ and T2 mapping in six knee compartments. We quantified concentrations of 20 biomarkers in synovial fluid aspirated at the time of ACL reconstruction. Spearman rank partial correlations with adjustments for age and gender were employed to evaluate correlations of MR, particularly cartilage composition and fat pad abnormalities, and biomarker data. RESULTS: The degree of IPFP abnormality correlated positively with the synovial levels of the inflammatory cytokine markers IFN-γ (ρpartial = 0.64, 95% CI (0.26-0.85)), IL-10 (ρpartial = 0.47, 95% CI (0.04-0.75)), IL-6 (ρpartial = 0.56, 95% CI (0.16-0.81)), IL-8 (ρpartial = 0.49, 95% CI (0.06-0.76)), TNF-α (ρpartial = 0.55, 95% CI (0.14-0.80)) and of the chondrodestructive markers MMP-1 and -3 (MMP-1: ρpartial = 0.57, 95% CI (0.17-0.81); MMP-3: ρpartial = 0.60, 95% CI (0.21-0.83)). IPFP abnormalities were significantly associated with higher T1ρ and T2 values in the trochlear cartilage (T1ρ: ρpartial = 0.55, 95% CI (0.15-0.80); T2: ρpartial = 0.58, 95% CI (0.18-0.81)) and with higher T2 values in the medial femoral, medial tibial as well as in patellar cartilage (0.45 ≤ ρpartial ≤ 0.59). Correlations between SPFP abnormalities and synovial markers were not significant except for IL-6 (ρpartial = 0.57, 95% CI (0.17-0.81)). CONCLUSIONS: This exploratory study suggests that acute ACL rupture can be associated with damage to knee tissues such as the inferior fat pad of the knee. Such fat pad injury could be partially responsible for the apparent post-injury pro-inflammatory response noted in ACL-injured individuals. However, future longitudinal studies are needed to link ACL-rupture associated fat pad injury with important patient outcomes such as the development of posttraumatic osteoarthritis.
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