Cartilage glycosaminoglycan loss in the acute phase after an anterior cruciate ligament injury: Delayed gadolinium-enhanced magnetic resonance imaging of cartilage and synovial fluid analysis
Article first published online: 7 JAN 2005
Copyright © 2005 by the American College of Rheumatology
Arthritis & Rheumatism
Volume 52, Issue 1, pages 120–127, January 2005
How to Cite
Tiderius, C. J., Olsson, L. E., Nyquist, F. and Dahlberg, L. (2005), Cartilage glycosaminoglycan loss in the acute phase after an anterior cruciate ligament injury: Delayed gadolinium-enhanced magnetic resonance imaging of cartilage and synovial fluid analysis. Arthritis & Rheumatism, 52: 120–127. doi: 10.1002/art.20795
- Issue published online: 7 JAN 2005
- Article first published online: 7 JAN 2005
- Manuscript Accepted: 15 OCT 2004
- Manuscript Received: 9 DEC 2003
- Swedish Medical Research Council. Grant Number: K99-73X
- Swedish Center for Research in Sports
- Medical Faculty of Lund University
To examine the glycosaminoglycan (GAG) content in cartilage and that in synovial fluid and determine whether they are associated, in patients with an acute anterior cruciate ligament (ACL) injury.
Twenty-four patients (14 of whom were male) with a mean age of 27 years (range 17–40 years) were assessed with delayed gadolinium-enhanced magnetic resonance imaging (MRI) of cartilage an average of 3 weeks after an ACL rupture and compared with 24 healthy volunteers. Two hours after an intravenous injection of Gd-DTPA2− (0.3 mmoles/kg body weight), quantitative measurements of the T1 relaxation time (T1Gd [T1 relaxation time in the presence of Gd-DTPA]) were made in lateral and medial femoral weight-bearing cartilage. In the patients, synovial fluid was aspirated immediately before the MRI, and GAG was analyzed using dye precipitation with Alcian blue.
Fifteen of the 24 patients had an isolated bone bruise in the lateral femoral condyle, where the cartilage T1Gd was shorter than that in the controls (mean ± SD 385 ± 83 msec and 445 ± 41 msec, respectively; P = 0.004), consistent with decreased GAG content. However, the T1Gd was also decreased in the medial femoral cartilage, where bone bruises were rare (376 ± 76 msec in patients versus 428 ± 38 msec in controls; P = 0.006). The mean ± SD synovial fluid GAG concentration in patients was 157 ± 86 μg/ml and showed a positive correlation with the T1Gd (r = 0.49, P = 0.02).
This study indicates that an ACL injury causes posttraumatic edema of the lateral femoral cartilage but initializes a generalized biochemical change within the knee that leads to GAG loss from both lateral and medial femoral cartilage. In cartilage with a high GAG content (long T1Gd), more GAG is released into the synovial fluid, suggesting that cartilage quality is a factor to consider when interpreting cartilage biomarkers of metabolism.