epiphysis allowing displacement of the femoral head on the neck and is also
called ‘epiphyseolysis’. Weiner [23] has described the different etiologic theories
very well and presents a concept of pathogenesis, which includes recent
histomorphological as well as clinical data: A delicate imbalance of puberty
hormones weakens the physis by negatively impacting on the collagenous
framework of physis and perichondral ring as demonstrated by severe morphologic
changes at all metabolically active levels of the growth plate. Constant
shear forces acting on this weakened physis exceed its ability to resist displacement.
Main mechanical risk factors for a progressive displacement are an
increasingly oblique physis lying in a relative degree of retroversion and a large
body mass.
The commonly encountered large body mass seems to play a significant
role in the disease process. Many investigators discussed that risk factor and
even described study populations with SCFE where most involved children and
adolescents are overweight or obese [20, 23–26].
Whether obesity is simply a matter of excess body mass or a biochemical
disorder, with as yet unknown hormonal alterations is not known [23]. Wilcox
et al. [24] presented a group of SCFE patients with body weights above the 80th
percentile, thyroid levels below the 25th percentile, and markedly decreased
testosterone levels. Due to the anabolic effect of testosterone versus estrogen
the mechanical strength of the growth plate in females seems to be stronger
than in males, which could explain a male preponderance of SCFE. If relative
hypothyroidism exists, the growth plate strength probably also is weakened.
At present it is unclear if mechanical overload alone, alterations in the
hormonal balance alone or both risk factors together are needed to cause the
specific pathology of the growth plate. Obesity, however, seems to play a major
role in the probably multifactorial disease process.
Apart from the different classification types of SCFE, which all lead to
hip or thigh pain with weight-bearing (stable slip) or even inability to walk
(unstable slip), there is probably another entity, which shows a subclinical
course: Murray [27, 28] has described a ‘tilt deformity’ of the femoral head as
a consequence of excessive physical activity during the growth period, which
does not cause remarkable pain and is therefore often not recognized. Like the
painful slip in classical SCFE, however, this more or less mild deformation
of the epiphysis can cause hip OA in the long term. Segesser [29] for example
analyzed a patient cohort with hip OA and found an association between tilt
deformities and a history of professional sports activity.
The different entities of a clinically painful slip (stable or unstable), which
requires surgical treatment, and a mild subclinical deformation of the growing
hip (always stable and obviously painless) are probably a major reason for
differing reports in the literature regarding the incidence of SCFE. Kelsey et al.
[30] estimated an incidence of approximately three per 100,000 per year in the
southwestern US general population, while Jerre et al. [31] found an incidence
of 0.08% in a Scandinavian survey. The definition of SCFE (with or without
inclusion of subclinical findings like a mild tilt deformity) and the design of
the study (e.g. hospital- or population-based, type and extent of radiographic
investigation) will influence the results of prevalence and incidence studies to a
certain degree. From hospital-based cohorts with advanced hip osteoarthritis
(OA) we know, however, that the incidence of symptomatic and asymptomatic
slips together must be higher: In a meta-analysis of published studies which
evaluate morphological changes of the hip as risk factor for OA (‘secondary
osteoarthritis’) 5–50% of arthritic hips are attributed to former SCFE [32]. In
the ‘Ulm Osteoarthritis Study’ [33], for example, we could radiographically
detect a tilt deformity as underlying hip pathology in 7.1% of all 420 participants
with advanced hip OA (220 females and 200 males with a mean age of
63.3 years).
The prevalence of hip OA in Caucasian populations in the age group of
60–70 years is around 10–20% [34]. If in 7% or even more of all hip OA
patients a tilt deformity would be a main risk factor, the incidence of SCFE
must be substantially higher as proposed.
When we consider obesity as a main risk factor for epiphyseal slips, it
would be important to estimate the prevalence or incidence of radiographic
changes in a patient cohort with elevated body weight. In a recent investigation
of the Pediatric and Orthopedic Departments at the University of Ulm 411 children
and adolescents (215 girls and 196 boys, mean age 14.5 years) necessitating
treatment for marked obesity (BMI 2.8 standard deviations) were screened
for hip pathology [3]. All participants underwent a clinical examination of
both hips and in case of an abnormal range of motion (e.g. diminished internal
rotation) hip radiographs were obtained consecutively. In 54 patients a radiographic
examination (a.p. pelvis and axial view) was performed and the
‘femoral-head-ratio’ according to Murray [27] as a measure of epiphyseal tilt
determined: The centre points between the most lateral part of the greater
trochanter and of the narrowest portion of the femoral neck are joined and the
line extended proximally to traverse the femoral head. The greatest width on
each side of this line to the edge of the femoral head is then measured. Division
of the figure for the lateral portion into the figure for the medial portion
produces a coefficient designated as the femoral-head-ratio. Values greater than
1.35 indicate the presence of a tilt deformity. In the radiographically investigated
subgroup of 54 obese patients, we identified 11 individuals with an
elevated femoral-head ratio (5 boys and 6 girls). The mean body weight in these
patients was 99.8 kg, the mean BMI was 36.8 kg/m2. Only one third of these
patients reported minor and occasional complaints in hip and/or knee joints.
No study participant had undergone surgical treatment of SCFE prior to entry
and no patient showed clinical or radiographic signs of SCFE at examination.
Due to ethical considerations we did not perform radiographic investigations
in the total cohort of 411 obese children. The study design implicates
other methodological problems as well (sensitivity, specificity, and reliability of
measurement techniques not assessed) and we are faced with a considerable
selection bias, as only patients involved in treatment programs due to severe
obesity were included. The results indicate, however, a higher prevalence of
SCFE-like tilt deformities in the patient cohort of severely obese children as
would be expected in the normal population. As the deformities are relatively
mild and the natural history with regard to development of hip OA is somewhat
unclear in these cases, we would not perform surgical interventions.
If the elevated body weight as a general risk factor for the development
and progression of OA will not be reduced over time in the patients, however, a
negative influence on their future hip situation cannot be excluded and they
should be carefully watched.
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