ORIGINAL ARTICLE

Correlation of Slipped Capital Femoral Epiphysis

With Disk Degeneration
Jason O. Toy, BA,* Zachary L. Gordon, MD,* Jason D. Eubanks, MD,w
Daniel R. Cooperman, MD,* and Nicholas U. Ahn, MD*

Summary of Background Data: Spinal osteoarthritis is greater in

patients with known hip pathology secondary to alterations in
spinopelvic geometry. To our knowledge, no study has investigated the long-term impact of slipped capital femoral epiphysis
(SCFE) on the spine.
Objective: To evaluate the relationship between SCFE and the
presence of degenerative disk disease and facet arthrosis.
Study Design: An anatomic study of disk degeneration in cadaveric lumbar spines with SCFE.
Methods: An observational study was performed on 25 cadaveric specimens with SCFE and 647 controls that were identied
out of 3100 total cadaveric specimens in an osteological collection. The specimens were evaluated for disk degeneration and
facet arthrosis at L1/2 to L5/S1 using the classication of Eubanks and colleagues. Linear regression analyses were then used
to determine the relationship between SCFE and lumbar disk
and facet degeneration at each level, correcting for confounding
factors such as age, sex, and race.
Results: Linear regression demonstrated a signicant association
(P < 0.01) that was found between SCFE and degenerative disk
disease at all levels from L1/2 to L5/S1. In addition, a signicant
association (P < 0.01) was found between SCFE and facet arthrosis at all levels from L1/2 to L5/S1.
Conclusions: The ndings of this study show a relationship between SCFE and lumbar disk degeneration and facet arthrosis.
This relationship may prove useful in predicting the course of
spinal osteoarthritis in patients with SCFE.

Received for publication March 21, 2011; accepted January 6, 2012.

From the *Department of Orthopaedic Surgery, Case Western Reserve
University, University Hospitals Case Medical Center; and wDepartment of Orthopaedic Surgery, Case Western Reserve University,
University Hospitals, Cleveland, OH.
The Hamann-Todd osteological collection at the Cleveland Museum of
Natural History provided all samples for this study. None of the
authors received any nancial support or materials from private or
commercial entities for this research. This study did not require
Institutional Review Board approval due to the exclusive use of
deidentied cadaveric specimens.
The authors declare no conict of interest.
Reprints: Jason O. Toy, BA, Department of Orthopaedic Surgery, Case
Western Reserve University, University Hospitals Case Medical
Center, 11100 Euclid Ave., Cleveland, OH 44106 (e-mails: Jot@
Case.edu; Nicholas.ahn@uhhospitals.org).
Copyright r 2012 by Lippincott Williams & Wilkins

J Spinal Disord Tech

Volume 26, Number 7, October 2013

Key Words: slipped capital femoral epiphysis, spinal osteoarthritis, disk degeneration, facet arthrosis
(J Spinal Disord Tech 2013;26:375378)

lipped capital femoral epiphysis (SCFE) remains the

most common hip disorder in children. It occurs with
failure of the proximal femoral physis, resulting in anterior
and superior displacement of the femoral neck metaphysis
relative to the capital femoral epiphysis.1,2 Ultimately,
shearing forces applied to the femoral head exceed limitations of the capital femoral physis, a process that readily
occurs in the setting of a weakened physeal plate. This
weakness is thought to arise from a multitude of factors,
which include increased mechanical strain on the physis
due to obesity, inammatory changes, endocrine and
metabolic derangement, genetic predisposition, and normal periosteal and physeal changes during adolescence.1
As the femoral neck displaces, a retroversion deformity of the proximal end of the femur occurs, with
subsequent progression of the slip until physeal arrest.1,2
The natural history of this disease is such that many will
display considerable retroversion and loss of hip motion,
the consequences of which may not surface until many
years later. This is of particular concern for those patients
with delayed diagnosis, a forbearer of increased slip severity and poorer long-term outcomes.3 Fortunately, the
majority of slips are mild in severity and stable upon
presentation.4 However, for those who are unable to bear
weight with or without the use of support, the probability
of high morbidity is signicantly increased.5
In recent years, there has been mounting evidence
for the early presence of arthritis and degenerative
changes in patients with SCFE.610 This is thought to be a
direct result of geometric distortion and altered mechanics of the hip that compromise normal wear patterning
and distribution of force.11 However, at the present time,
no studies have investigated the impact of this geometric
distortion on the spine in SCFE. We therefore reviewed
the specimens in the Hamann-Todd osteological collection to determine if any association exists between degenerative disk disease and SCFE.

MATERIALS AND METHODS

The Hamann-Todd osteological collection of the
Cleveland Museum of Natural History consists of over
www.jspinaldisorders.com |

375

J Spinal Disord Tech

Toy et al

3100 individuals who died in Cleveland, Ohio between the

years of 1893 and 1938. The specimens in the collection are
dried and disarticulated. Medical histories, including the
cause of death, are available for most of the specimens.
There were 25 skeletons with femoral heads and neck
abnormalities consistent with the diagnosis of SCFE using
criteria previously dened (Figs. 1AC).12 The lumbar
spines (Figs. 2A, B) and femurs of these individuals were
chosen for examination. Twenty of the 25 skeletons were
identified from previously published work.12 Five additional grossly abnormal specimens were identified in this
study using the same morphologic and radiographic criteria. The present study included 22 men and 3 women.
Nine of these samples were African American with the remaining specimens representing white individuals.
Disk degeneration and facet arthrosis at L1 through
S1 were measured by the classication of Eubanks et al13
In this work, the degenerative disease was graded from no
arthrosis to complete ankylosis on a scale from grade 0 to
grade IV, as suggested by Kettler and Wilke,14 using
previously dened markers of degenerative disease.15,16
The grading scale used was taken from previously published work,13 which describes the osteophytic reaction in
the facets as well as the peripheral rim osteophytes in the
vertebral endplates. We graded the facets and vertebral
endplates from 0 to IV, representing a continuum from no
arthrosis to complete ankylosis: grade 0, normal facet
joints or vertebral endplates; grade I, mild arthrosis, with
evidence of osteophytic reaction involving up to 50% of
the facet joint or vertebral endplates; grade II, moderate
arthrosis, with evidence of osteophytic reaction involving
50% to 100% of facet joint or vertebral endplates; grade
III, severe arthrosis, with evidence of osteophytic reaction
involving 100% of the facet joints or vertebral endplates
and hypertrophic osteophytes bridging the joint space;
and grade IV, complete ankylosis.
Similarly, a control group of 647 specimens without
SCFE defects were evaluated for lumbar endplate and
facet degeneration at all levels from L1/2 to L5/S1.

RESULTS
A total of 25 specimens with SCFE and 647 control
specimens were examined. There were 22 male specimens
and 3 female specimens with a mean age of 57 years at

Volume 26, Number 7, October 2013

FIGURE 2. A, Anterior aspect of the lumbar spine in a slipped

capital femoral epiphysis (SCFE) specimen with considerable
endplate degeneration, displaying grade 3 to 4 endplate degeneration. B, Lateral aspect of the lumbar spine in an SCFE
specimen with grade 3 to 4 facet arthrosis.

death (range, 2685 y). The majority of specimens were

white individuals (N = 16) and the remainder were African
American individuals (N = 9). Linear regression analysis
was performed to study the relationship between the presence of SCFE and disk degeneration at L1S1, correcting
for age, sex, and race. Our analysis demonstrated that a
significant association (P < 0.01) existed between SCFE
and disk degeneration (Fig. 3A). Figure 3B displays this
relationship at each disk level. What becomes evident is an

FIGURE 1. A, Anterior aspect of the right femur in a slipped capital femoral epiphysis (SCFE) specimen. B, Posterior aspect of the
right femur in an SCFE specimen. C, Marked retroversion of the left femur when compared with that of the right femur.

376 | www.jspinaldisorders.com

2012 Lippincott Williams & Wilkins

Volume 26, Number 7, October 2013

increase in the slope with more caudal disk levels. This

demonstrates an increase in the magnitude of the association of SCFE with lumbar degenerative disease at the lower
levels in the lumbosacral spine as compared with the upper
levels.
Our analysis also demonstrated a signicant association between SCFE (Fig. 4A) and facet arthrosis at
L1S1 (P < 0.01). Likewise, Figure 4 displays analysis of
facet arthrosis at each level as it relates to the presence of
SCFE. The greatest slope appears at the facet level of L5
S1 once again demonstrating that the magnitude of the
association of SCFE with lumbar degenerative disease is
greatest at the lower levels in the lumbosacral spine.

Correlation of Slipped Capital Femoral Epiphysis

Linear Regression:
SCFE vs. Facet Arthrosis at L1-2 to L5-S1
4

Facet Arthrosis

J Spinal Disord Tech

3
2
1
0
0
Non-SCFE

The present study reports a signicant association

between the presence of SCFE and disk degeneration and
facet arthrosis. The observation that a concurrent relationship exists between hip and spine pathology was rst
described as hip-spine syndrome (HSS) by Oerski and
MacNab in 1983.17 In their paper, they classied the syndrome into 4 categories: simple, secondary, complex, and
misdiagnosed HSS. Simple HSS was dened as cases in
which the major cause of the concurrent hip and spine pain
was clearly attributable to either the hip joint or the spine.
Complex HSS described hip and spine pain where the origin of the pain was not necessarily clear after physical examination. In these situations, a nerve root block or joint
injection anesthetic was recommended to diagnose the
cause. Finally, and of most interest to this study, is secondary hip-spine syndrome, a category characterized by

Linear Regression:
SCFE vs. Degenerative Disc Disease at L1-L2 to L5-S1
4

DDD

3
2
Series 1
p < 0.01

1
0

0
Non-SCFE

Linear Regression:
SCFE vs. Degenerative Disc Disease By Level

DDD

1
SCFE

L1-2
p < 0.01

L2-3
p < 0.01

L3-4
p < 0.01

L4-5
p < 0.01

0
0
Non-SCFE

L5-S1
1 p < 0.01
SCFE

FIGURE 3. A, Linear regression of degenerative disk disease

(DDD) at L12 to L5S1 as it relates to the presence of slipped
capital femoral epiphysis (SCFE). B, Breakdown of degenerative disk disease by level.
r

2012 Lippincott Williams & Wilkins

Facet Arthrosis

DISCUSSION

Series 1
p < 0.01

1
SCFE

Linear Regression:
SCFE vs. Facet Arthrosis By Level
L1-2
p < 0.01

L2-3
p < 0.01

L3-4
p < 0.01

L4-5
p < 0.01

0
0
Non-SCFE

1
SCFE

L5-S1
p < 0.01

FIGURE 4. A, Linear regression of facet arthrosis at L12 to

L5S1 as it relates to the presence of slipped capital femoral
epiphysis (SCFE). B, Breakdown of facet arthrosis by level.

changes in the lumbar spine secondary to pathologic

changes in the hip joint. The authors suggested that exion
contracture of the hip resulted in compensatory sagittal
spine changes, a relatively common nding in hip osteoarthritis patients,11,18 A more recent study by Yoshimoto
et al19 investigated the eect of hip pathology on spinal
sagittal alignment by measuring sacropelvic parameters.
They reported signicantly greater values of pelvic incidence, lumbar lordosis, and sharp angles (58.5, 39.6, and
48.0 degrees) in patients with osteoarthrosis of the hip when
compared with the control group (51.9, 35.2, and 40.7 degrees). In fact, the numbers reported for pelvic incidence
and lumbar lordosis are remarkably similar to those seen in
degenerative spondylolisthesis (60 and 40.1 degrees), further corroborating an association between hip and spine
pathology.20
As this study demonstrates, a similar relationship
with spine pathology seems to exist with SCFE. However,
unlike hip osteoarthritis, the inciting mechanism for
secondary hip-spine syndrome is a cam-type femoroacetabular impingement (FAI),21 the consequence of an
anteriorly shifted metaphyseal prominence and an abnormal head-neck oset. Depending upon the severity of the
slip, the metaphyseal prominence will almost invariably
impinge on the anterior acetabulum and result in what is
known as impaction.22 Initially, the unremodeled prominence limits the arc of hip motion and subsequently produces pain. In the chronic state, the femoral head is levered
out of the acetabulum with hip exion, eroding the anterior
acetabular labrum and producing decreased acetabular
coverage. Over time, the metaphyseal prominence is either
www.jspinaldisorders.com |

377

J Spinal Disord Tech

Toy et al

reduced and rounded or signicantly remodeled, shifting

impaction to inclusion forces.22 The end result is a nonspherical femoral head and abnormal femoroacetabular
articulation, setting the stage for gait alteration, sagittal
imbalance, and early osteoarthritis.
Gait analysis in patients with FAI reveals signicantly lower peak hip abduction, hip extension, and
total sagittal pelvic range of motion when compared with
controls.23 Similarly, a study of SCFE patients treated
with in situ xation demonstrated reduction of internal
rotation and abduction in the aected versus the normal
hip, with no signicant dierence in hip exion.24 Given
the mechanism of FAI, we suspect that these ndings may
be a result of signicant alteration to sacropelvic and
sagittal geometry. To our knowledge, no studies have
evaluated sacropelvic or lumbosacral parameters in
SCFE. However, it has been suggested that FAI may
result in a compensatory decrease in pelvic tilt, and thus
decrease acetabular retroversion to minimize contact between the acetabular rim and femoral head-neck junction.23,25 In this setting, we would predict a decrease in
lumbar lordosis. Similar alterations of sagittal balance
have been shown to signicantly impact load bearing and
the distribution of lumbar disk degeneration.26 Although
this may explain the ndings in this study, future research
is expected to further clarify the relationship between
sagittal geometry and spinal pathology in SCFE.
Another explanation for the observed correlations
in this study could be an inherent defect in cartilage integrity, which may hinder the ability of cartilage to resist
mechanical shear forces.1 Therefore, it is conceivable that
hip deforming forces in combination with a cartilaginous
defect may both contribute to early spinal arthritis.
In conclusion, we report a signicant correlation
between SCFE and the presence of degenerative disk
disease and facet arthrosis. To our knowledge, no other
study has reported on this subject matter. This study rearms the signicant contribution of hip geometric distortion to osteoarthritis of the spine, highlighting another
potential long-term consequence in SCFE.
An obvious limitation of this study is that all
measurements were based on osteologic specimens only,
and thus dierences in soft tissue structures could not be
studied. That said, assuming that changes in the skeletal
anatomy of the adjacent vertebrae represent the latter
stages of underlying soft tissue derangement, our conclusions would seem to accurately reect alterations in the
soft tissues that make up the intervertebral spaces.

CONCLUSIONS
The ndings of this study show an association between SCFE and disk degeneration as well as facet arthrosis. This relationship may prove useful in predicting the
course of osteoarthritis of the spine in patients with SCFE.
REFERENCES
1. Loder RT, Aronsson DD, Dobbs MB, et al. Slipped capital femoral
epiphysis. Instr Course Lect. 2001;50:555570.

378 | www.jspinaldisorders.com

Volume 26, Number 7, October 2013

2. Loder RT, Aronsson DD, Weinstein SL, et al. Slipped capital

femoral epiphysis. Instr Course Lect. 2008;57:473498.
3. Kocher MS, Bishop JA, Weed B, et al. Delay in diagnosis of slipped
capital femoral epiphysis. Pediatrics. 2004;113:e322e325.
4. Carney BT, Weinstein SL, Noble J. Long-term follow-up of slipped
capital femoral epiphysis. J Bone Joint Surg Am. 1991;73:667674.
5. Aronsson DD, Karol LA. Stable slipped capital femoral epiphysis:
evaluation and management. J Am Acad Orthop Surg. 1996;4:173181.
6. Goodman DA, Feighan JE, Smith AD, et al. Subclinical slipped
capital femoral epiphysis. relationship to osteoarthrosis of the hip.
J Bone Joint Surg Am. 1997;79:14891497.
7. Aronson J. Osteoarthritis of the young adult hip: etiology and
treatment. Instr Course Lect. 1986;35:119128.
8. Croft P, Cooper C, Wickham C, et al. Osteoarthritis of the hip and
acetabular dysplasia. Ann Rheum Dis. 1991;50:308310.
9. Harris WH. Etiology of osteoarthritis of the hip. Clin Orthop Relat
Res. 1986;213:2033.
10. Solomon L. Patterns of osteoarthritis of the hip. J Bone Joint Surg
Br. 1976;58:176183.
11. Abraham E, Gonzalez MH, Pratap S, et al. Clinical implications of
anatomical wear characteristics in slipped capital femoral epiphysis
and primary osteoarthritis. J Pediatr Orthop. 2007;27:788795.
12. Cooperman DR, Charles LM, Pathria M, et al. Post-mortem
description of slipped capital femoral epiphysis. J Bone Joint Surg Br.
1992;74:595599.
13. Eubanks JD, Lee MJ, Cassinelli E, et al. Prevalence of lumbar facet
arthrosis and its relationship to age, sex, and race: an anatomic
study of cadaveric specimens. Spine (Phila Pa 1976). 2007;32:
20582062.
14. Kettler A, Wilke HJ. Review of existing grading systems for cervical
or lumbar disc and facet joint degeneration. Eur Spine J. 2006;
15:705718.
15. Miller JA, Schmatz C, Schultz AB. Lumbar disc degeneration:
correlation with age, sex, and spine level in 600 autopsy specimens.
Spine (Phila Pa 1976). 1988;13:173178.
16. Nathan H. Spondylolysis; its anatomy and mechanism of development. J Bone Joint Surg Am. 1959;41-A:303320.
17. Offierski CM, MacNab I. Hip-spine syndrome. Spine (Phila Pa
1976). 1983;8:316321.
18. Spencer S, Millis MB, Kim YJ. Early results of treatment of hip
impingement syndrome in slipped capital femoral epiphysis and
pistol grip deformity of the femoral head-neck junction using the
surgical dislocation technique. J Pediatr Orthop. 2006;26:281285.
19. Yoshimoto H, Sato S, Masuda T, et al. Spinopelvic alignment in
patients with osteoarthrosis of the hip: a radiographic comparison
to patients with low back pain. Spine (Phila Pa 1976). 2005;30:
16501657.
20. Barrey C, Jund J, Noseda O, et al. Sagittal balance of the pelvisspine complex and lumbar degenerative diseases. A comparative
study about 85 cases. Eur Spine J. 2007;16:14591467.
21. Kordelle J, Richolt JA, Millis M, et al. Development of the
acetabulum in patients with slipped capital femoral epiphysis:
a three-dimensional analysis based on computed tomography.
J Pediatr Orthop. 2001;21:174178.
22. Rab GT. The geometry of slipped capital femoral epiphysis:
Implications for movement, impingement, and corrective osteotomy. J Pediatr Orthop. 1999;19:419424.
23. Kennedy MJ, Lamontagne M, Beaule PE. Femoroacetabular
impingement alters hip and pelvic biomechanics during gait walking
biomechanics of FAI. Gait Posture. 2009;30:4144.
24. Fraitzl CR, Kafer W, Nelitz M, et al. Radiological evidence of
femoroacetabular impingement in mild slipped capital femoral
epiphysis: a mean follow-up of 14.4 years after pinning in situ.
J Bone Joint Surg Br. 2007;89:15921596.
25. Konishi N, Mieno T. Determination of acetabular coverage of the
femoral head with use of a single anteroposterior radiograph. A new
computerized technique. J Bone Joint Surg Am. 1993;75:13181333.
26. Keorochana G, Taghavi CE, Lee KB, et al. Effect of sagittal
alignment on kinematic changes and degree of disc degeneration in
the lumbar spine: an analysis using positional MRI. Spine (Phila Pa
1976). 2011;36:893898.

2012 Lippincott Williams & Wilkins