A Histological and Ultrastructural Study of the Iliac Crest Apophysis in Legg-Calve-Perthes Disease

Abstract

Legg-Calve-Perthes disease (LCPD) is a common hip disorder in children characterized by avascular necrosis of the proximal capital femoral epiphysis. The underlying etiology of the vascular disturbance is still unknown, but it is suggested that LCPD may be a part of a generalized constitutional disorder associated with growth disturbance of bone and cartilage tissue. In this study, the biopsy specimens of the iliac crest apophysis from LCPD patients were examined histologically and ultrastructurally to determine preexisting generalized abnormalities of endochondral ossification. Iliac crest apophysis cartilage was taken during Salter innominate osteotomy from 11 children (8 boys and 3 girls) with LCPD at an average age of 7.8 years. As controls, the samples were also obtained from 10 children (2 boys and 8 girls) at an average age of 6.3 years undergoing Salter osteotomy due to residual acetabular dysplasia after reduction of developmental dysplasia of the hip. Each iliac crest apophysis specimen was examined histologically (Toluidine blue staining and Sudan III staining) and ultrastructurally. Although there were no obvious differences in Toluidine blue-stained sections of the iliac crest cartilage between LCPD and control patients, the Sudan III-positive chondrocytes in the resting cartilage were more prominent in the LCPD specimens than in the control specimens. These sudanophilic granules were confirmed to be lipid droplets by electron microscopic examinations. Ultrastructural examinations of the resting chondrocytes from 3 LCPD patients demonstrated numerous cytoplasmic inclusion bodies with electron dense materials, which were similar to those seen in some of the mucopolysaccharidoses. Increased lipid droplets and numerous cytoplasmic inclusions filled with fibrillar materials were suggestive of the initial metabolic changes of the chondrocytes, which may have a pivotal role in degenerating matrix and lead to vulnerability of the cartilage tissue. Our results indicated that generalized insufficiency in growth cartilage metabolism may be related to the onset of the disease in some LCPD patients.