Page 87 - Slipped Capital Femoral Epiphysis Pathogenetic and Clinical aspects

Introduction
Slipped Capital Femoral Epiphysis (SCFE) is one of the most common hip disorders in adolescence [13]. The condition is radiological characterized by displacement of the femoral neck through the physis, whilst the femoral head stays in the acetabulum. Clinical diagnosis is often based on pain in the groin or upper leg and the development of a limp. Treatment is usually through percutaneous single screw epiphysiodesis with or without gentle reposition depending on timing and stability. Prognosis is generally dependent on whether the SCFE is classified as stable or unstable and the degree of slippage on the Lauenstein radiological view [13].
The literature focuses on known risk factors and diagnostic features of SCFE but the
pathogenesis of SCFE remains obscure and appears multifactorial. Little is known
about the natural history of slippage of the epiphysis. Biomechanical factors, such
as obesity, femoral retroversion and increased obliquity seem to play a role in
SCFE[13]. 5 SCFE occurs during puberty, so biochemical factors may also take part. In puberty,
transient hormonal changes could possibly influence the physis and might be crucial in creating a weak physis of the hip that cannot resist the load-applying pressure [21]. In addition, there is an increased incidence of SCFE in children with endocrine diseases such as hypothyroidism, renal osteodystrophy, growth hormone supplements, and hypogonadal states [5, 18].
It is hypothesized that improper or dysregulated signaling, through one or more of the several hormonal pathways, leads to altered expression of hormonal receptors or its second messengers in the physes. This may result in perturbed regulation of the hypertrophic chondrocytes and altered extracellular matrix (ECM) turnover. Earlier studies of the human SCFE physis have found a marked distortion of architecture and diminished cellularity on a microscopical and ultrastructural level. Collagen fibrils were fewer and randomly oriented [2, 3, 9, 11]. Another feature was an increased frequency and distribution of chondrocytes undergoing apoptosis, which resulted in diminished numbers of chondrocytes in the human SCFE physis [1]. Evidently, the perturbed orientation of chondrocytes and the diminished collagen observed are not necessarily causal related to development of a slip and given the insidious nature of slippage, this may also represent an effect of slippage. In general, little is known about the histomorphological changes in SCFE in humans. In this study we compared chondrocytes in physes of 27 children with SCFE to
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