Abstract
Introduction: Shortening of the affected limb has frequently been observed in children with Legg-Calvé-Perthes disease (LCPD). Many factors have been thought as the cause of this residual shortening after LCPD. There has been no clear answer regarding which is more responsible for the residual shortening between coxa plana and the disturbed physeal growth. To clarify the main cause of residual shortening, clinical and experimental studies were conducted.
Materials and Methods: For clinical study, 40 LCPD children with definite shortening were evaluated. This included 20 children with active disease and 20 children at skeletal maturity. Teleoroentgenograms were obtained for all children. For the experimental study, LCPD simulation in 30 piglets was achieved by disrupting the blood supply to the capital femoral epiphysis.
Results: In the clinical study, total shortening in the skeletal maturity group was 14.6 mm, which consisted of 3.2 mm (16%) shortening by decreased epiphyseal height and 11.5 mm (84%) shortening by physeal growth disturbance. Total shortening in the active disease group was 7.9 mm, which consisted of 6.4 mm (84%) decrease of epiphyseal height and 1.5 mm (16%) shortening by physeal growth disturbance. In the experimental study, overall shortening (13.6 mm) in the piglet model showed a predominance of disturbed physeal growth. The proportions were 3.2 mm (24%) by epiphyseal height decrease and 10.4 mm (76%) by physeal growth disturbance.
Conclusion: Physeal growth disturbance was mostly responsible for the residual shortening following LCPD. However, in the stages of active disease, the shortening of the extremity was mainly caused by a decrease of epiphyseal height.
The abstracts were prepared by Michael A. Mont, M.D. and Lynne C. Jones, Ph.D. Correspondence should be addressed to L. Jones at Good Samaritan Prof. Bldg., Suite 201, 5601 Loch Raven Blvd., Baltimore, MD 21239
