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. 2003 Mar;19(3):262-8.
doi: 10.1053/jars.2003.50037.

Arthroscopic Evaluation of Articular Cartilage Lesions in Posterior-Cruciate-Ligament-Deficient Knees


Arthroscopic Evaluation of Articular Cartilage Lesions in Posterior-Cruciate-Ligament-Deficient Knees

Michael J Strobel et al. Arthroscopy. .


Purpose: The goal of this study was to gain more information on the likelihood of developing cartilage lesions in posterior cruciate ligament (PCL)-deficient knees.

Type of study: Retrospective clinical study.

Methods: Standardized arthroscopy records of 181 patients with a nonsurgically treated acute or chronic PCL injury were analyzed with respect to cartilage degeneration. Subgroups with different duration of PCL insufficiency, the influence of isolated PCL or combined PCL/posterolateral instability, and the grade of posterior laxity was analyzed.

Results: PCL insufficiency significantly increased the risk of developing medial femoral condyle and patellar cartilage degeneration over time. Of patients whose PCL deficiency was present for more than 5 years, 77.8% showed degenerative cartilage lesions of the medial femoral condyle and 46.7% showed cartilage degeneration of the patella. After 1 year of PCL insufficiency, the number of medial femoral cartilage lesions increased threefold (13.6% v 39.1%). With the presence of combined PCL/posterolateral insufficiency the amount of medial femoral degeneration was significantly increased (36.6% v 60.6%).

Conclusions: We found that PCL insufficiency is not a benign injury with respect to the development of degenerative articular cartilage lesions. The early and continuous increase in cartilage degeneration at the medial femoral condyle and the patella should be considered when discussing operative versus conservative treatment for a PCL-deficient knee. The rapid development of medial arthritis should also be considered during decision making, particularly in patients with combined PCL/posterolateral instability or those who underwent previous partial medial menisectomy.

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