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2013 ; 7
(3
): 213-23
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Slipped capital femoral epiphysis and its association with endocrine, metabolic
and chronic diseases: a systematic review of the literature
#MMPMID24432080
Witbreuk M
; van Kemenade FJ
; van der Sluijs JA
; Jansma EP
; Rotteveel J
; van Royen BJ
J Child Orthop
2013[Jun]; 7
(3
): 213-23
PMID24432080
show ga
PURPOSE: Puberty, obesity, endocrine and chronic systemic diseases are known to
be associated with slipped capital femoral epiphysis (SCFE). The mechanical
insufficiency of the physis in SCFE is thought to be the result of an abnormal
weakening of the physis. However, the mechanism at the cellular level has not
been unravelled up to now. METHODS: To understand the pathophysiology of
endocrine and metabolic factors acting on the physis, we performed a systematic
review focussing on published studies reporting on hormonal, morphological and
cellular abnormalities of the physis in children with SCFE. In addition, we
looked for studies of the effects of endocrinopathies on the human physis which
can lead to cause SCFE and focussed in detail on hormonal signalling, hormone
receptor expression and extracellular matrix (ECM) composition of the physis. We
searched in the PubMed, EMBASE.com and The Cochrane Library (via Wiley) databases
from inception to 11th September 2012. The search generated a total of 689
references: 382 in PubMed, 232 in EMBASE.com and 75 in The Cochrane Library.
After removing duplicate papers, 525 papers remained. Of these, 119 were selected
based on titles and abstracts. After excluding 63 papers not related to the human
physis, 56 papers were included in this review. RESULTS: Activation of the
gonadal axis and the subsequent augmentation of the activity of the growth
hormone-insulin-like growth factor 1 (GH-IGF-1) axis are important for the
pubertal growth spurt, as well as for cessation of the physis at the end of
puberty. The effects of leptin, thyroid hormone and corticosteroids on linear
growth and on the physis are also discussed. Children with chronic diseases
suffer from inflammation, acidosis and malnutrition. These consequences of
chronic diseases affect the GH-IGF-1 axis, thereby, increasing the risk of the
development of SCFE. The risk of SCFE and avascular necrosis in children with
chronic renal insufficiency, growth hormone treatment and renal osteodystrophy
remains equivocal. CONCLUSIONS: SCFE is most likely the result of a
multi-factorial event during adolescence when height and weight increase
dramatically and the delicate balance between the various hormonal equilibria can
be disturbed. Up to now, there are no screening or diagnostic tests available to
predict patients at risk.