Histological, histochemical and ultrastructural study of slipped capital femoral epiphysis.

PURPOSE: The purpose of our study was to investigate the histological, histochemical and ultrastructural aspects of the proximal femoral growth plate in slipped capital femoral epiphysis (SCFE). METHODS: Eight core biopsies of the proximal femoral growth plate were performed during in situ epiphysiodesis in patients with SCFE that was at the pre-slipping stage in two cases and at the mild slipping stage (Southwick angle < 30°) in six cases. After fixation, the specimens were processed for either histological or histochemical or ultrastructural studies. RESULTS: The proximal femoral growth plate was thicker than normal in the SCFE cases, and the 3:1 ratio between the thickness of the resting zone and the other zones of the plate was reversed. Chondrocytes of the proliferating, maturation, hypertrophic and degenerating zones were arranged in large clusters rather than in columns, which were separated by loose fibrillary septae that appeared moderately alcian blue positive and metachromatic. The collagen fibrils of the longitudinal septae were uniformly thin, measuring about 200 Å, whereas in the normal plate collagen fibrils were in the range of 300 to 1200 Å in thickness. Chondrocytes were elongated and smaller than normal, with a dark cytoplasm. In the degenerating zone, mineralisation of the longitudinal and transversal septae was scanty and enchondral ossification was impaired, with a few small osteoblasts forming thin bone trabeculae on the cartilage septae of the degenerating zone. CONCLUSION: In SCFE, the proximal femoral growth plate undergoes several histological, histochemical and ultrastructural changes that precede slipping of the epiphysis since they are already present at a pre-slipping stage of the disease. The loss of solidity of the extracellular matrix and the disarrangement of the normal architecture of the physis very likely cause the consequent slipping of the proximal femoral epiphysis. SCFE aetiology remains unknown.

Stable fault sliding and earthquake nucleation

The process of earthquake nucleation is studied assuming that faults are rupture surfaces on which sliding is controlled by friction. Earthquakes are assumed to arise through an instability of frictional sliding. Empirical slip laws indicate that, under constant ambient conditions, friction depends on time, slip rate and slip history. Regular stick-slip behaviour is induced by velocity weakening, a negative dependence of friction on slip rate. Velocity weakening is introduced into a model for a propagating Somigliana dislocation under slowly increasing ambient shear stress. The instability occurs when the rate at which friction decreases becomes greater than the rate at which the applied stress must increase to produce an advance of fault slip. The possibility that this condition is fullfilled depends on the velocity dependence and on the spatial distribution of friction on the fault. A critical nucleation width of the dislocation is associated with the instability and is controlled by the friction distribution, which determines the size of the initial slipping patch. Depending on the stress drop and the characteristics slip distance, the critical nucleation width may be greater for small earthquakes than for large earthquakes, with respect to the initial slipping patch