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MOVEMENT OF THE SAGITTAL PLANE AXIS IN NORMAL AND ANTERIOR CRUCIATE LIGAMENT DEFICIENT KNEES



Abstract

Purpose: Femoral roll causes the sagittal plane axis of the knee to move posteriorly and anteriorly with flexion and extension. The aim of this study was to measure this movement with a surface marker imaging system and assess the effect of Anterior Cruciate Ligament (ACL) deficiency on the Sagittal Axis Pathway (SAP) of the knee.

Method: Twelve normal and fourteen unilateral ACL deficient subjects were video recorded as they flexed and extended their knees in the sagittal plane. Video stills were captured at 150 intervals from 90o flexion to full extension. An imaging system was then used to extract the co-ordinates of leg markers from each still. These co-ordinates were then processed to derive the SAP for each knee throughout its range of movement.

Results: Pooling all the normal results together (24 bilateral + 14 unilateral = 38 knees), it was found that a 90° knee extension caused the sagittal axis to displace anteriorly with a mean value of 20.0mm (SD=7.8). In comparison the 14 ACL deficient knees were found to have a mean anterior displacement of 9.2 mm (SD=8.0). A bilateral comparison of the 12 pairs of normal knees showed no significant difference between left and right sides (paired-t, p=0.99). However, a bilateral comparison of the 14 unilateral ACL deficient patients showed a significant difference between normal and injured sides (paired-t, p=0.00025). In this group, the normal knees axis at full extension had a mean location 28.9mm (SD=8.8) posterior to the front of the tibial plateau. In comparison the injured knees axis has a mean location 37.8 mm (SD=8.5) posterior to the front of the tibial plateau. Again, this was highly significant (paired-t, p=0.0001).

Conclusion: These results indicate that normal knees have a mean forward roll of 20 mm for a 90° knee extension. In comparison ACL deficient knees have a reduced roll of 9.2 mm which occurs at the rear of the joint. This reduction in roll is consistent with the abnormal ligament biomechanics.

The abstracts were prepared by Mr Roger Smith. Correspondence should be addressed to him care of the British Orthopaedic Association, Royal College of Surgeons, 35-43 Lincoln’s Inn Fields, London WC2A 3PN.