Abstract

Dysplasia of the cruciate ligaments has been found in many patients with congenital fibular deficiency. A recent classification system has shown that radiographic tibial spine changes can predict the hypoplasia and aplasia of the cruciate ligaments. We used this radiographic classification to determine the frequency of these abnormalities and how they correlate with the severity of fibular deficiency and lateral femoral condylar hypoplasia. Using a hospital database search for fibular deficiency, 99 patients ≥6 years with unilateral fibular deficiency were identified. Existing radiographs of both knees were available for 75 patients and reviewed for the tibial spine changes and Achterman and Kalamchi classification of the fibular deficiency. Measurements of femoral condyle heights in 74 of 75 patients were recorded before any surgery to the distal femoral physis to assess lateral femoral condylar hypoplasia. Twenty-two patients had hypoplasia of the lateral tibial spine+normal medial spine, 29 had absence of the lateral tibial spine+hypoplastic medial spine, and 11 had absence of both tibial spines. Five tibial spines were normal and 8 were unclassifiable. The severity of the tibial spine dysplasia, particularly absence of the lateral tibial spine, correlated with the severity of the fibular deficiency. (P<0.0001) The mean lateral femoral condylar hypoplasia, measured by involved: uninvolved lateral condyle heights, was 0.85±0.11. Those with some preservation of the lateral tibial spine had less lateral femoral condylar hypoplasia (P=0.0009). This lateral femoral condylar hypoplasia was positively associated with the severity of the fibular absence (P=0.039) and foot ray deficiency (P=0.036). The severity of cruciate ligament dysplasia in fibular deficiency is directly correlated with the severity of fibular absence, lateral femoral condylar hypoplasia, and the absence of foot rays. This suggests that the embryological factors involved have a complex interplay for all of these clinical findings. Level III.

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