An ultrastructural study of slipped capital femoral epiphysis: Pathogenetic considerations

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.

Slipped capital femoral epiphysis and its association with endocrine, metabolic and chronic diseases: A systematic review of the literature

“…The resting zones of the epiphysis appeared to be relatively normal in SCFE [3][4][5][6], although some tissue samples showed clusters of numerous chondrocytes cells [5].…”

“…The proliferative and hypertrophic zones of the epiphysis in SCFE were widened compared with normal physis, and showed irregular columnar organisation with gradual loss of longitudinal septa and diminished number of chondrocytes in each column [3][4][5][6][7]. Interestingly, Adamczyk et al showed that apoptosis was increased throughout the physis in SCFE, in contrast with controls, where apoptosis was found only in the hypertrophic zone [8].…”

Slipped capital femoral epiphysis: an ultrastructural study before and after osteosynthesis

“…In the PGs, another component of the extracellular matrix, we did not find any abnormalities—either in the morphology or in the distribution. Ippolito et al (1989) believed that the floccular electron-dense material present in the chondrocytes and in the matrix is caused by an altered production of PGs. However, our observations did not confirm this supposition.…”

“…Various authors have reported histological alterations of the growth plate in slipped capital femoral epiphysis (SCFE) (Kleinberg and Buchman 1936, Howorth 1941, 1949, Harris 1950, Lacroix and Verbrugge 1951, Ponseti and McClintock 1956, Wagner 1961, Taillard et al 1964, Consolo and Randelli 1971, Ippolito et al 1981, Agamanolis et al 1985a, Portigliatti Barbos et al 1985, Guzzanti et al 2003). To our knowledge, however, there have only been 3 ultrastructural studies that have considered the pathology of the slippage in SCFE (Mickelson et al 1977, Agamanolis et al 1985b, Ippolito et al 1989). …”

“…Ippolito et al (1989) found the characteristic alterations of the growth plate in 2 cases of pre-slipping; they believed that the pathology is present before the slippage occurs and that it may have been caused by a change in chondrocyte metabolism. The consequent modifications of the matrix, due to altered synthesis of collagen and PGs, would predispose to slippage.…”