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Ischemia
Ischemia may result from vascular
disruption, compression, constriction,
or intravascular occlusion. Disruption
of the vascular network around the
femoral head results in traumatic osteonecrosis, thus causing complications in 15% to 50% of displaced
femoral neck fractures and 10% to
25% of hip dislocations.1 Vascular
compression may result from intraosseous hypertension secondary to
455
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Table 1
Risk Factors for Osteonecrosis
Trauma
Corticosteroid use
Excessive alcohol consumption
Coagulation disorders
Hemoglobinopathies
Dysbaric phenomena
Autoimmune diseases
Storage diseases
Smoking
Hyperlipidemia
456
Multifactorial Process
Predisposing risk factors may not be
identified in every patient. Moreover,
out of all patients exposed to a specific
risk factor, only a small percentage
develop the disease.
For example, in two separate studies
by Lieberman and colleagues7,8 that
assessed the development of osteonecrosis after exposure to large corticosteroid doses, osteonecrosis was
infrequently identified. In the first
study, symptomatic hip osteonecrosis
developed in only 3 of 203 patients
(2%) who underwent liver transplantation. Similarly, in the second
study, osteonecrosis of the hip or
knee developed in only 6 of 204 patients (3%) following cardiac transplantation. This finding may be
explained by the multifactorial process of osteonecrosis and suggests
that additional genetic factors are
necessary for a patient to develop
symptomatic disease.
Clinical Presentation
Osteonecrosis may be asymptomatic
in its early stages. When the disease
becomes symptomatic, deep pain in
Table 2
Pathogenic Mechanisms for
Osteonecrosis
Ischemia
Vascular disruption
Femoral head fracture
Hip dislocation
Surgery
Vascular compression or
constriction
Increased intraosseous pressure
due to marrow fatty infiltration
Corticosteroids, alcohol
Vasoconstriction of arteries
perfusing femoral head
Corticosteroids, eNOS
polymorphisms
Intravascular occlusion
Thrombosis
Thrombophilia
Low protein C and S
Activated protein
C resistance, factor
V mutation
High homocysteine
eNOS polymorphisms
Hypofibrinolysis
High PAI activity, PAI-1
polymorphisms
High lipoprotein(a)
Embolization
Fat, air
Sickle cell occlusion
Direct cellular toxicity
Pharmacologic agents
Irradiation
Oxidative stress
Altered differentiation of
mesenchymal stem cells
Increased adipogenesis and
decreased osteogenesis
Corticosteroids, alcohol
eNOS = endothelial nitric oxide synthase,
PAI = plasminogen activator inhibitor
the groin is the most common symptom, and pain may be referred to the
ipsilateral buttock or knee. A detailed
history may reveal the presence of risk
factors. Physical examination may be
normal or may reveal painful and
limited hip motion, especially internal
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Figure 1
Figure 2
Lateral radiograph of the left hip (A) demonstrating presence of the crescent sign
(arrows) and AP radiograph (B) demonstrating mild flattening of the femoral head
(arrow).
Imaging Studies
The diagnosis of osteonecrosis is
based on plain AP and lateral frog-leg
radiographs and MRI. Plain radiographs may be normal in the early
stages. The first radiographic findings consist of cystic and sclerotic
changes in the femoral head. The
crescent sign most likely represents
early delamination of the cartilage
from the underlying bone and is a poor
prognostic sign (Figure 1, A). Flattening of the femoral head initially is
subtle and may be visible in only one
view (Figure 1, B). Progressive flattening of the femoral head and
degenerative changes of the hip joint
are subsequently observed.
MRI is 99% sensitive and specific
and is the benchmark for diagnosing
osteonecrosis.1 A single-density line
on T1-weighted images delineates the
necroticviable bone interface, and
July 2014, Vol 22, No 7
457
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Table 3
Classification and Staging Systems for Osteonecrosis
Ficat and Arlet
Stage I
Stage II
Normal
Sclerotic or cystic lesions
A No crescent sign
B Subchondral collapse (crescent sign)
without flattening of the femoral head
Stage III
Flattening of femoral head
Stage IV
Osteoarthritis with decreased joint space with
articular collapse
Steinberg University of Pennsylvania
Stage 0
Normal or nondiagnostic radiograph, bone
scan, and magnetic resonance imaging
Stage I
Normal radiograph; abnormal bone scan and/or
magnetic resonance imaging
A Mild (,15% of head affected)
B Moderate (15% to 30% of head affected)
C Severe (.30% of head affected)
Stage II
Lucent and sclerotic changes in femoral head
A Mild (,15% of head affected)
B Moderate (15% to 30% of head affected)
C Severe (.30% of head affected)
Stage III
Subchondral collapse (crescent sign) without
flattening of femoral head
A Mild (,15% of articular surface)
B Moderate (15% to 30% of articular
surface)
C Severe (.30% of articular surface)
Stage IV
Flattening of femoral head
A Mild (,15% of surface and ,2-mm
depression)
B Moderate (15% to 30% of surface or 2- to
4-mm depression)
C Severe (.30% of surface or .4-mm
depression)
Stage V
Joint narrowing and/or acetabular changes
A Mild
B Moderate
C Severe
Stage VI
Advanced degenerative changes
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Figure 3
Modified Kerboul method. The arc of the necrotic portion of the femoral head on
both midcoronal (A) and midsagittal (B) magnetic resonance images is measured,
and the sum of the two angles is then calculated. (Reproduced with permission
from Ha YC, Jung WH, Kim JR, Seong NH, Kim SY, Koo KH: Prediction of
collapse in femoral head osteonecrosis: A modified Kerboul method with use of
magnetic resonance images. J Bone Joint Surg Am 2006;88[suppl 3]:35-40.)
Treatment
Nonsurgical Management
Nonsurgical management with observation or protected weight bearing has
a very limited role in the treatment of
femoral head osteonecrosis.13-15 The
exception is follow-up of a small
asymptomatic lesion until it becomes
symptomatic.
July 2014, Vol 22, No 7
Surgical Treatment
Surgical treatment of osteonecrosis
can be broadly divided into femoral
headpreserving procedures and hip
arthroplasty. Unfortunately, the optimal surgical treatment of osteonecrosis of the femoral head has not been
identified. Femoral headpreserving
procedures include core decompression; core decompression combined
with supplemental nonvascularized
bone grafting, vascularized bone
grafting, concentrated stem cells, biologic adjuncts, or tantalum rods; and
rotational osteotomies. Hip arthroplasty procedures include THA and
resurfacing arthroplasty.
Core Decompression
Core decompression has been widely
used for treatment of early-stage osteonecrosis intended to reduce intraosseous
pressure in the femoral head, restore
vascular flow, and improve pain. The
procedure can be performed with a single core tract of varying size or with
multiple small core tracts (Figure 4).
459
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Figure 4
Core decompression for a small osteonecrotic lesion seen on a coronal T1-weighted magnetic resonance image of the right hip
(A). AP fluoroscopic images of the right hip show directing and centering the guidewire at the lesion (B), drilling over the guidewire
to create a core tract (C), and removal of the necrotic bone with a burr (D). The femoral head is bone grafted with concentrated
stem cells harvested from the iliac crest. The core tract is sealed with demineralized matrix.
460
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Figure 5
Rotational Osteotomies
Osteotomies aim to prevent femoral
head collapse by transposing the osteonecrotic area from a weight-bearing
to a nonweight-bearing area of the
hip joint, thereby diverting mechanical stress from the lesion to healthy
bone. Two types of osteotomies have
been used: transtrochanteric rota-
461
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Table 4
Outcome of Noncemented Total Hip Arthroplasty in Patients with Osteonecrosis
Study
Kim et al34
Hips With
ON
(patients)
Patient Age
in Years:
Mean
(range)
Body Mass
Index in kg/
m2: Mean
(range)
64 (55)
40.2 (25-49)
23.1 (17-32)
Noncemented
Arthroplasty
Details
Modular stem: all
Femoral
Stem
Acetabular
Revision
Cup
Rate
Revision
due to
Rate due to
Aseptic
Aseptic
Loosening Loosening
Follow-up in
Years: Mean
(range)
HHS: Mean
(range)
15.8 (15-16.8)
92.7 (72-100)
0%
14%
12.6 (10-16)
80.3 (5-100)
2%
0%
5%
5%
Ceramic on poly: 45
Metal on poly: 19
Bedard
et al35
60 (50)
43.3 (22-63)
30.6 (18-51)
Issa et al36
42 (32)a
37 (18-58)
N/A
7.5 (5-11)
87 (78-100)
Issa et al36
102 (87)a
43 (18-71)
N/A
N/A
7 (3-10.5)
88 (70-100)
3%
3%
Kim et al37
69 (N/A)b
24 (19-30)
26 (22-36)
Anatomic
metaphysealfitting stem: all
14.6 (10-16)
95(71-100)
0%
0%
17.3 (16-18)
93 (75-100)
0%
0%
Ceramic on ceramic:
all
Kim et al38
94 (94)c
47 (26-58)
N/A
Anatomic
metaphysealfitting stem: all
Metal on poly: all
462
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Summary
Osteonecrosis of the femoral head
commonly affects patients in the
third to fifth decades of life and follows a progressive course resulting
in femoral head collapse and hip
joint degeneration. The major risk
factors include corticosteroid use,
excessive alcohol intake, trauma, and
coagulation abnormalities. Diagnosis
is based on radiographs and MRI.
Imaging findings, such as head
collapse and the size and location of
the lesion, should be considered in
the selection of a treatment method.
Pharmacologic agents and biophysical modalities require further
study. Surgical treatment consists of
either femoral head-sparing procedures or arthroplasty. Preservation of
the femoral head is preferable in
younger patients without head collapse. In the presence of collapse,
arthroplasty reliably achieves prompt
pain relief and functional return with
a single procedure.
References
Evidence-based Medicine: Levels of
evidence are described in the table of
contents. In this article, references 11,
13, 16, and 18 are level I studies.
Reference 14 is a level II study. Reference 24 is a level III study. References 29, 30, 37, and 38 are level IV
studies.
References printed in bold type are
those published within the past 5 years.
1. Lieberman JR, Berry DJ, Mont MA, et al:
Osteonecrosis of the hip: Management in
the 21st century. Instr Course Lect 2003;
52:337-355.
2. Petrigliano FA, Lieberman JR:
Osteonecrosis of the hip: Novel approaches
to evaluation and treatment. Clin Orthop
Relat Res 2007;465(465):53-62.
3. Zalavras C, Dailiana Z, Elisaf M, et al:
Potential aetiological factors concerning the
development of osteonecrosis of the femoral
head. Eur J Clin Invest 2000;30(3):215-221.
4. Glueck CJ, Freiberg RA, Wang P: Heritable
thrombophilia-hypofibrinolysis and
osteonecrosis of the femoral head. Clin
Orthop Relat Res 2008;466(5):1034-1040.
5. Zalavras CG, Vartholomatos G, Dokou E,
Malizos KN: Genetic background of
osteonecrosis: Associated with
thrombophilic mutations? Clin Orthop
Relat Res 2004;422:251-255.
6. Lee JS, Lee JS, Roh HL, Kim CH, Jung JS,
Suh KT: Alterations in the differentiation
ability of mesenchymal stem cells in patients
with nontraumatic osteonecrosis of the
femoral head: Comparative analysis
according to the risk factor. J Orthop Res
2006;24(4):604-609.
7. Lieberman JR, Scaduto AA, Wellmeyer E:
Symptomatic osteonecrosis of the hip after
orthotopic liver transplantation.
J Arthroplasty 2000;15(6):767-771.
8. Lieberman JR, Roth KM, Elsissy P,
Dorey FJ, Kobashigawa JA: Symptomatic
osteonecrosis of the hip and knee after
cardiac transplantation. J Arthroplasty
2008;23(1):90-96.
9. Ito H, Matsuno T, Minami A: Relationship
between bone marrow edema and
development of symptoms in patients with
osteonecrosis of the femoral head. AJR Am
J Roentgenol 2006;186(6):1761-1770.
10. Steinberg ME, Hayken GD, Steinberg DR:
A quantitative system for staging avascular
necrosis. J Bone Joint Surg Br 1995;77(1):
34-41.
11. Ha YC, Jung WH, Kim JR, Seong NH,
Kim SY, Koo KH: Prediction of collapse in
463
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35.
36.
37.
38.
464
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