Page 64 - Slipped Capital Femoral Epiphysis Pathogenetic and Clinical aspects

Chapter 4
Introduction
Slipped capital femoral epiphysis (SCFE) is a disorder of the proximal femur in adolescents. SCFE is defined as the displacement of the femoral head relative to the femoral neck and shaft in the physis. The proximal femoral neck and shaft move anteriorly and rotate externally relative to the femoral head, leaving the femoral head stabilized in the acetabulum. SCFE is most often diagnosed in obese adolescents and in children with endocrinopathies or chronic systemic diseases. The pathogenesis of SCFE has not been unravelled fully so far. A precise insight into the pathogenesis of SCFE is important for understanding the disease and possible development of rational therapy.
It is thought that SCFE is the result of mechanical insufficiency of the proximal femoral physis. The slip is a result of either an abnormally high load across a normal physis or a physiological load across an abnormally weak physis, or a combination of these two. Mechanical factors for an abnormally high load include obesity, femoral retroversion and increased physeal obliquity [1]. The majority of adolescents with SCFE might not have hormonal metabolic or chronic diseases, but they are obese and fast growing. However, it seems unlikely that mechanical overload of the proximal femur epiphysis, by, for example, high body weight only, can lead to SCFE. Many children in their growing age are exposed to high mechanical loads of their hip joints during normal activities and sports activities for example. Conditions that weaken the physis include endocrine or systemic diseases, for example, hypothyroidism, growth hormone suppletion and hypogonadal abnormalities [1].
The underlying mechanisms that are involved in the development of abnormal weakening of the physis may originate from the cellular level and include dysregulation of chondrocytes in the hypertrophic layer of the physis, as well as disturbances in the extracellular matrix (ECM) turnover. In addition, these phenomena may result from improper or dysregulated signaling through the several pathways involved, for instance, hormonal receptors or its second messengers.
However, how metabolic and endocrine factors can cause a weak physis is unclear. In order to obtain insight into the available data on the role of metabolic and endocrine factors in physis weakening and the pathogenesis of SCFE, we performed a systematic review with emphasis on the pathogenetic mechanisms. In this review, we will only discuss the association of endocrine, metabolic and
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