Two normal proximal femoral growth plates and core biopsies from six patients with slipped capital femoral epiphysis (SCFE) were studied by electron microscopy. In these SCFE patients, chondrocytes from all the zones of the plate were frequently smaller than normal, more irregular in shape, and many of them were degenerating, with formation of matrix vesicles and cellular debris. Floccular electron-dense material, most likely abnormal proteoglycan, was present in the hypertrophic rough-surfaced endoplasmic reticulum and Golgi apparatus as well as in the extracellular matrix, intermingled with collagen fibrils thinner than normal and loosely arranged. Mineralization of the abnormal matrix of the longitudinal septa of the degenerating zone was either scanty or absent, with scanty formation of irregular and thin bone trabeculae. The abnormalities observed in SCFE seem to be caused by a change in chondrocyte metabolism with consequent altered synthesis and/or extracellular aggregation of both collagen and proteoglycan, and scanty mineralization of the abnormal cartilage matrix.
Ippolito, E., Bellocci, M., Farsetti, P., Tudisco, C., Perugia, D. (1989). An ultrastructural study of slipped capital femoral epiphysis: pathogenetic considerations. JOURNAL OF ORTHOPAEDIC RESEARCH, 7(2), 252-259 [10.1002/jor.1100070213].
An ultrastructural study of slipped capital femoral epiphysis: pathogenetic considerations
IPPOLITO, ERNESTO;FARSETTI, PASQUALE;TUDISCO, COSIMO;PERUGIA, DARIO
1989-01-01
Abstract
Two normal proximal femoral growth plates and core biopsies from six patients with slipped capital femoral epiphysis (SCFE) were studied by electron microscopy. In these SCFE patients, chondrocytes from all the zones of the plate were frequently smaller than normal, more irregular in shape, and many of them were degenerating, with formation of matrix vesicles and cellular debris. Floccular electron-dense material, most likely abnormal proteoglycan, was present in the hypertrophic rough-surfaced endoplasmic reticulum and Golgi apparatus as well as in the extracellular matrix, intermingled with collagen fibrils thinner than normal and loosely arranged. Mineralization of the abnormal matrix of the longitudinal septa of the degenerating zone was either scanty or absent, with scanty formation of irregular and thin bone trabeculae. The abnormalities observed in SCFE seem to be caused by a change in chondrocyte metabolism with consequent altered synthesis and/or extracellular aggregation of both collagen and proteoglycan, and scanty mineralization of the abnormal cartilage matrix.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.