Volume 52, Issue 1 pp. 120-127
Research Article

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

Carl Johan Tiderius

Carl Johan Tiderius

Malmo University Hospital, Lund University, Malmo, Sweden

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Lars Eric Olsson

Lars Eric Olsson

Malmo University Hospital, Lund University, Malmo, Sweden

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Fredrik Nyquist

Fredrik Nyquist

Malmo University Hospital, Lund University, Malmo, Sweden

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Leif Dahlberg

Corresponding Author

Leif Dahlberg

Malmo University Hospital, Lund University, Malmo, Sweden

Department of Orthopedics, Malmo University Hospital, SE-205 02 Malmo, SwedenSearch for more papers by this author
First published: 07 January 2005
Citations: 116

Abstract

Objective

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.

Methods

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.

Results

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).

Conclusion

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.

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