Review Article

Osteonecrosis of the Femoral

Head: Evaluation and Treatment
Abstract
Charalampos G. Zalavras, MD
Jay R. Lieberman, MD

Osteonecrosis of the femoral head may lead to progressive

destruction of the hip joint. Although the etiology of osteonecrosis has
not been definitely delineated, risk factors include corticosteroid use,
alcohol consumption, trauma, and coagulation abnormalities. Size and
location of the lesion are prognostic factors for disease progression and
are best assessed by MRI. The efficacy of medical management of
osteonecrosis with pharmacologic agents and biophysical modalities
requires further investigation. Surgical management is based on patient
factors and lesion characteristics. Preservation of the femoral head may
be attempted in younger patients without head collapse by core
decompression with vascularized bone grafts, avascular grafts, bone
morphogenetic proteins, stem cells, or combinations of the above or
rotational osteotomies. The optimal treatment modality has not been
identified. When the femoral head is collapsed, arthroplasty is the
preferred option.

From the Keck School of Medicine of

the University of Southern California,
Los Angeles, CA.
Dr. Lieberman or an immediate family
member serves as a paid consultant
to or is an employee of DePuy, has
received research or institutional
support from Amgen and Arthrex, and
serves as a board member, owner,
officer, or committee member of the
American Academy of Orthopaedic
Surgeons and the Hip Society. Neither
Dr. Zalavras nor any immediate family
member has received anything of
value from or has stock or stock
options held in a commercial company
or institution related directly or
indirectly to the subject of this chapter.
J Am Acad Orthop Surg 2014;22:
455-464
http://dx.doi.org/10.5435/
JAAOS-22-07-455
Copyright 2014 by the American
Academy of Orthopaedic Surgeons.

July 2014, Vol 22, No 7

steonecrosis of the femoral

head commonly affects patients in the third to fifth decades of
life. In the United States, it is estimated that 20,000 to 30,000 new
patients are diagnosed with osteonecrosis annually, and 5% to 12% of
total hip arthroplasties (THAs) are
performed based on this diagnosis.1,2 Although several risk factors
have been identified, the pathogenesis of osteonecrosis has not been
elucidated. The disease typically follows a progressive course leading to
femoral head collapse and hip joint
destruction. Nonsurgical modalities
have been described, but surgical
intervention is the most prominent
therapeutic regimen. However, the
optimal method to preserve the femoral head remains unclear, and in
many patients, head sparing is not
possible because of the extent of
the pathologic process or the
advanced stage of the disease on
presentation.

Etiology and Pathogenesis

Although risk factors for osteonecrosis have been identified (Table 1),
the etiology and pathogenesis of osteonecrosis remain unclear. Death of
bone cells is the end result of one or
more pathogenic mechanisms, acting
individually or synergistically, that
include ischemia, direct cellular toxicity, and altered differentiation of
mesenchymal stem cells (Table 2).

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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Osteonecrosis of the Femoral Head: Evaluation and Treatment

Table 1
Risk Factors for Osteonecrosis
Trauma
Corticosteroid use
Excessive alcohol consumption
Coagulation disorders
Hemoglobinopathies
Dysbaric phenomena
Autoimmune diseases
Storage diseases
Smoking
Hyperlipidemia

fatty infiltration of the bone marrow

following corticosteroid use or alcohol
overuse. Vasoconstriction of femoral
head epiphyseal arteries may be
enhanced by corticosteroids. Intravascular occlusion may result from
thrombosis, fat or gas embolization, or
sickle cell aggregation.
Thrombosis is the end of result of
several coagulation disorders that
result in an increased tendency for
thrombosis (ie, thrombophilia) or
a reduced ability to lyse thrombi (ie,
hypofibrinolysis).3,4 Zalavras et al3
reported that coagulation abnormalities, such as low protein C, low
protein S, high lipoprotein(a), and
high von Willebrand factor levels,
were present in a significantly higher
proportion of patients with idiopathic
osteonecrosis (10 of 17 patients [59%])
and secondary osteonecrosis (32 of 51
patients [63%]) compared with control
subjects (3 of 36 patients [8%]).
The identification of genetic predisposition to coagulation abnormalities generated interest in the influence
of genetic factors on the development
of osteonecrosis. Thrombophilic and
hypofibrinolytic mutations have been
associated with the disease.4,5 The
thrombophilic G1691A mutation of
factor V Leiden is significantly more
common in patients with osteonecrosis (13 of 72 patients [18%])
compared with controls (14 of 300
patients [5%]).5

456

Direct Cellular Toxicity and

Altered Mesenchymal Stem
Cell Differentiation
Direct cellular insult may result from
irradiation, chemotherapy, or oxidative
stress. Lee et al6 observed that osteogenic differentiation of mesenchymal
stem cells derived from the proximal
femur was significantly reduced in
patients with osteonecrosis compared
with patients with osteoarthritis.

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.

Diagnosis and Assessment

Early diagnosis allows for treatment
of the disease at an earlier stage,
thereby potentially improving the
outcome. A high index of suspicion is
required, especially if the patient has
predisposing risk factors.

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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Charalampos G. Zalavras, MD and Jay R. Lieberman, MD

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).

rotation. A considerable loss of internal rotation may be associated with

collapse of the femoral head.

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

a double-density line on T2-weighted

images represents the hypervascular
granulation tissue at the necrotic
viable bone interface (Figure 2).1,9
Transient osteoporosis of the hip
should be included in the differential
diagnosis when osteonecrosis is suspected. Transient osteoporosis of the
hip, commonly affecting pregnant
women and men in the fifth and sixth
decades of life, presents with severe
groin pain and an antalgic gait. MRI
demonstrates bone marrow edema
extending into the femoral neck and
metaphysis. A differentiation between
osteonecrosis and transient osteoporosis is essential because the latter is
a self-limiting condition.

Classification and Staging

Several classification systems have
been developed to stage osteonecrosis
to provide information on prognosis
and assist with treatment decisions
(Table 3). The addition of MRI to the
staging process and consideration of
the extent and location of the necrotic

Coronal T1-weighted magnetic

resonance image of the right hip
demonstrating a single-density line
(arrow) of low signal intensity that
delineates the area of necrotic bone.

area are important advancements reflected in the University of Pennsylvania

(ie, Steinberg) classification staging
system.10

Natural History and

Prognostic Factors
Symptomatic femoral head osteonecrosis typically follows a progressive
course. Prognostic factors for progression include the extent of the osteonecrotic lesion, location of the lesion
within the femoral head, and the presence of bone marrow edema in the
proximal femur. Imaging studies and
particularly MRI are essential for evaluating these factors; these studies may
help assess the risk for femoral head
collapse and clarify the natural history
of the disease.
The extent of the osteonecrotic
lesion is a prognostic factor for femoral head collapse; it can be assessed

457

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Osteonecrosis of the Femoral Head: Evaluation and Treatment

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

as a proportion of the cross-sectional

area of the head or as the combined
angle of the necrotic area in midsagittal and midcoronal MRI cuts (ie,
modified Kerboul method). Ha et al11
prospectively evaluated 37 hips with
precollapse osteonecrosis of the femoral head, of which 23 (62%) were
symptomatic. The combined necrotic

458

angle was determined on MRI using

a modified Kerboul method (Figure 3),
and hips were randomly assigned to
either nonsurgical management or
core decompression. Patient follow-up
continued until collapse or for
a minimum of 5 years when no collapse occurred. None of the 4 hips
with a combined necrotic angle of

#190 collapsed; 4 of the 8 hips with

a combined necrotic angle of between
190 and 240 collapsed; and all 25
hips with a combined necrotic angle of
.240 collapsed. No difference was
noted between untreated hips and hips
undergoing core decompression.11
Nishii et al12 evaluated 54 osteonecrotic hips without collapse in 35
patients at a minimum follow-up of 5
years. Hips with extensive osteonecrotic lesions (ie, occupying more
than two thirds of the weight-bearing
area of the femoral head), compared
with hips with smaller lesions, had
a significantly higher rate of collapse
and collapse progression to .2 mm.
Interestingly, lack of collapse progression and improvement of symptoms were observed in eight of nine
hips that had lesions occupying less
than two thirds of the weight-bearing
area of the femoral head.12
Bone marrow edema in the proximal femur appears to be a risk factor
for collapse of the femoral head. Ito
et al9 identified 83 asymptomatic
or minimally symptomatic hips with
MRI evidence of osteonecrosis and
prospectively followed them until the
hip became symptomatic or for
a minimum of 2 years. Thirty-six of
83 hips (43%) became symptomatic
and developed femoral head collapse.
The presence of bone marrow edema
on initial diagnostic MRI was significantly associated with progression to
symptomatic disease with collapse of
the head. All 21 hips with bone
marrow edema on diagnosis were
symptomatic at final follow-up,
compared with 15 of 62 hips (24%)
without bone marrow edema.9
Few studies with long-term followup have evaluated the fate of asymptomatic osteonecrosis. In a prospective
study of 40 asymptomatic hips with
small (,10% of femoral head volume)
lesions, Hernigou et al13 reported that,
after a minimum 10-year follow-up,
35 of 40 hips (88%) became symptomatic, and 29 of 40 hips (73%)
collapsed. In contrast, Nam et al14

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Charalampos G. Zalavras, MD and Jay R. Lieberman, MD

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.)

reported that after a minimum 5-year

follow-up, 43 of 105 hips (41%)
remained asymptomatic, whereas 62
of 105 hips (59%) became painful
and collapsed. The collapse rate was
5% in small lesions (,30% of the
area of the femoral head) versus
46% in medium lesions (30% to
50%), and 83% in large (.50%)
lesions.14 In both studies, pain consistently preceded the development
of head collapse.13,14 A systematic
review of nonsurgical management
outcomes showed that at a mean
follow-up of 53 months, only 28%
of hips did not have radiographic
progression, and 33% of hips did
not require reoperation.15

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

Treatment With Biophysical

Modalities and
Pharmacologic Agents
Biophysical modalities, such as extracorporeal shock waves and pulsed
electromagnetic fields, have been used
for treatment of osteonecrosis, but there
is limited information in the literature.
In a randomized trial, Wang et al16
compared extracorporeal shock waves
to core decompression with nonvascularized fibula grafting; at a mean
25-month follow-up, both pain and
Harris hip scores were significantly
improved in the shock wave group.
Pharmacologic agents, such as anticoagulants, lipid-lowering agents,
diphosphonates, growth factors, antioxidants, vasoactive substances, and
hormones, have been investigated for
prevention and treatment of osteonecrosis; however, the few clinical
studies of pharmacologic treatment of
osteonecrosis have not yet established
the usefulness of this approach.17-19
Enoxaparin may prevent progression of primary hip osteonecrosis
in patients with thrombophilic or
hypofibrinolytic disorders, but this

was not the case in osteonecrosis

secondary to corticosteroid use.17
Alendronate for treatment of earlystage osteonecrosis was evaluated in
two randomized trials, with conflicting
results. Lai et al18 reported that, at
a minimum follow-up of 24 months,
alendronate significantly reduced disease progression and femoral head
collapse (collapse of 2 of 29 hips [7%])
compared with the control group
(collapse of 19 of 25 hips [76%]). In
a study by Chen et al,19 these results
were not corroborated; these authors
reported no differences between the
alendronate and placebo groups with
respect to disease progression, the
need for THA, and clinical outcome
after 24 months.
Successful pharmacologic treatment is complicated by our lack of
understanding of the pathogenesis of
osteonecrosis and the multifactorial
nature of the disease.

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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Osteonecrosis of the Femoral Head: Evaluation and Treatment

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.

Encouraging results have been reported when core decompression is

performed at a precollapse stage in
small lesions. Israelite et al20 conducted a study of core decompression with bone grafting in 276 hips
with a minimum follow-up of 2 years
and reported that THA was required
in 38% of hips. In precollapse stages,
small lesions (,15% of the femoral
head) had a significantly better outcome (14% required arthroplasty)
compared with intermediate lesions
(15% to 30% of the femoral head)
and large lesions (.30% of the femoral head), which required arthroplasty in 48% and 42% of hips,
respectively.20 A systematic review by
Marker et al15 showed that, of 1,268
hips treated since 1992, 70% did
not require additional surgery and
63% had a successful radiographic
outcome.
Core Decompression With
Nonvascularized Grafts, Stem
Cells, or Biologic Adjuncts
Core decompression has been supplemented with the insertion of allografts and nonvascularized autografts
to provide mechanical support of the
osteonecrotic lesion and prevent collapse. Grafting can be performed with
the Phemister technique (ie, through
the core tract), the light bulb technique
(ie, through a cortical window at the

460

junction of cartilage and the femoral

neck), or the trap door technique (ie,
through a cartilage window). Given
the decreased osteogenic differentiation ability of mesenchymal stem cells
from the proximal femur of patients
with osteonecrosis,6 recent studies
have focused on the promotion of
bone formation and enhancement of
the repair process by introducing
bone morphogenetic proteins or bone
marrow cells.21-23
Lieberman et al21 treated 17 hips in
15 patients with core decompression,
autogenous bone graft, and a fibular
allograft perfused with human bone
morphogenetic protein and noncollagenous proteins. At a mean
follow-up of 53 months, 14 of 15
hips (93%) with Ficat-Arlet stage
IIA disease had relief of pain and no
radiographic progression.
Hernigou and Beaujean22 prospectively evaluated core decompression and injection of concentrated
autologous bone marrow cells in 189
hips of 116 patients. At a minimum
follow-up of 5 years, arthroplasty was
required in only 9 of the 145 Steinberg
stage I and II hips (6%), compared
with 25 of the 44 hips (57%) that
were in stages III and IV. A lower
number of progenitor cells were harvested from patients with steroid- or
alcohol-induced osteonecrosis, and
these patients had a greater risk of

failure than did patients with other

diagnoses.
A recent small prospective study
conducted by Gangji et al23 compared
core decompression with implantation of autogenous bone marrow cells
with core decompression alone. Bone
marrow implantation significantly
reduced pain and disease progression
at a 5-year follow-up. In the bone
marrow group, 3 of 13 hips (23%)
progressed, compared with 8 of 11
hips (73%) in the control core
decompression group. However, the
need for THA was not significantly
reduced in the bone marrow group
(2 of 13 hips [15%]) versus the control group (3 of 11 hips [27%]).
In the future, bone grafting procedures combined with systemic agents
that promote bone repair may be the
best regimen to optimize results.
Vascularized Bone Grafting
The goal of vascularized bone grafting
using fibula or iliac crest grafts is to
support the subchondral bone with
a viable strong bone strut and enhance
revascularization of the femoral head
(Figure 5). A comparison of vascularized to nonvascularized fibula grafting
demonstrated that vascularized fibular
graft (VFG) significantly improved
survival of precollapse hips (86% versus 30%) at 7 years postoperatively.24
Soucacos et al25 reported that, at

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Charalampos G. Zalavras, MD and Jay R. Lieberman, MD

Figure 5

Vascularized fibula graft. The fibular

graft is inserted into the core tract
and stabilized with a Kirschner wire
(K). The peroneal veins and artery
are anastomosed to the ascending
branches of the lateral femoral
circumflex artery (LFCA) and vein.

a mean follow-up of 4.7 years, osteonecrosis progressed radiographically in

only 5% of Steinberg stage II hips
treated with VFG compared with 44%
of stage IV hips. Berend et al26 evaluated VFG for postcollapse osteonecrosis of the femoral head and found
that, despite the advanced stage of
the disease, 64.5% of hips with
a minimum follow-up of 5 years did
not require conversion to THA.
Unfortunately, no level I studies are
available to compare the efficacy of
vascularized and nonvascularized
grafts.
The long-term outcome of VFG has
been investigated.27,28 Yoo et al27
reported that, at a mean follow-up of
13.9 years, 13 of 124 hips (11%)
failed and underwent THA. No difference in hip survival was observed
between Ficat-Arlet stage II and III
hips. Hip survival was significantly
associated with patient age and size
and with location of the lesion.27
Edward et al28 followed 65 FicatArlet stage I and II hips for a mean of
14.4 years. The survival rate was
60% (39 of 65 hips), and the 39
July 2014, Vol 22, No 7

surviving hips had a mean Harris hip

score of 89.
Free vascularized bone grafting is
technically demanding, requires expertise in microsurgery, and is associated
with donor site morbidity (ie, motor
weakness, contracture of the flexor
hallucis longus, sensory abnormalities)
in approximately 20% of patients. In
general, this procedure should be
reserved for patients without collapse
of the femoral head.

Tantalum Rod Insertion

A tantalum implant has been used as
an alternative to bone grafting following core decompression. The tantalum
implant aims to provide mechanical
structural support to the necrotic area
and may enhance bone ingrowth
because of its high porosity and osteoconductive microtexture. In a study by
Veillete et al,29 early results at a mean
follow-up of 24 months showed
radiographic progression in 16 of
58 hips (28%) and conversion to
arthroplasty in 9 of 58 hips (16%). In
a study by Tanzer et al30 of 113
osteonecrotic hips treated with a tantalum rod, the failure rate was 15%
(17 hips), and the mean interval
between implantation and failure was
13.4 months. Histologic analysis of
specimens retrieved at the time of
conversion to a THA demonstrated
little bone ingrowth and insufficient
mechanical support of the subchondral bone.30 Based on the available data, we cannot recommend that
this technology be used until longterm follow-up results are published.

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-

tional osteotomies (anterior or posterior) and intertrochanteric varus or

valgus osteotomies (usually combined
with flexion or extension).
Transtrochanteric rotational osteotomies have been popularized in
Japan. Sugioka and Yamamoto31 reported survival of 43 of 46 hips
(93%) at a mean 12-year follow-up
after a posterior rotational osteotomy. However, these results have not
been replicated in the United States or
Europe, and intertrochanteric varus
or valgus osteotomies have been
preferred instead. Mont et al32 reported good or excellent clinical
outcomes without need for arthroplasty in 28 of 37 hips (76%) at
a mean follow-up of 11.5 years
following intertrochanteric varus
osteotomy.
Success of an osteotomy procedure
depends on the size of the osteonecrotic lesion and requires careful preoperative evaluation to assess whether
a sufficiently large area of healthy
bone can be transposed to the weightbearing area of the acetabulum. The
outcome is improved when the intact
area of the transposed femoral head is
at least one third of the weight-bearing
area of the acetabulum and the combined necrotic angle is ,200. Osteotomies are technically demanding,
and conversion of failed cases to
THA may be difficult.
Total Hip Arthroplasty
Collapse of the femoral head or the
presence of a large osteonecrotic
lesion in the precollapse stages
compromises the outcome of headsparing procedures. THA is the surgical treatment that can most reliably
achieve pain relief and provide
prompt functional return with a single procedure in patients with femoral head collapse, especially when
painful degenerative changes of the
hip joint are present.
The durability of THA in patients
with osteonecrosis compared with
that in patients with osteoarthritis has

461

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Osteonecrosis of the Femoral Head: Evaluation and Treatment

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)

Chrome-cobaltcoated stem: all

Issa et al36

42 (32)a

37 (18-58)

N/A

Hydroxyapatitecoated stem: all

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%

Metal on poly: all

Ceramic on ceramic:
all
Kim et al38

94 (94)c

47 (26-58)

N/A

Anatomic
metaphysealfitting stem: all
Metal on poly: all

HHS = Harris hip score, ON = osteonecrosis, N/A = nonavailable, poly = polyethylene

a
Forty-two hips with ON due to sickle cell anemia were compared with 102 hips with ON due to other etiologies.
b
Osteonecrosis was the diagnosis in 69 of 127 hips in this study. Patient data and outcome data are derived from all 127 hips in 96 patients.
c
Noncemented THA was performed in 94 of 142 hips in this study. Patient data and outcome data are derived from these 94 hips in 94 patients.

been questioned based on the younger

age and increased activity of patients
with osteonecrosis. Ortiguera et al33
reported that, at a mean follow-up of
17.8 years, patients with osteonecrosis had a significantly higher dislocation rate than did patients with
osteoarthritis. Patients with osteonecrosis may have higher dislocation
rates because, in many cases, the
patient has better preoperative range
of motion compared with a patient
who has long-standing osteoarthritis.
In addition, the revision rate in patients younger than 50 years with
osteonecrosis was significantly higher
compared with that in patients in the
same age group with osteoarthritis.33
Over the past 15 years, the results of
THA have considerably improved.
Noncemented fixation can reliably be
achieved in most patients with osteonecrosis of the hip; recent studies have

462

reported satisfactory midterm outcomes of noncemented arthroplasty

in patients with osteonecrosis34-38
(Table 4). Kim et al34 demonstrated
that, after a minimum 15-year followup in patients with osteonecrosis
younger than 50 years, no noncemented femoral stems and 14% of
noncemented acetabular cups required
revision because of aseptic loosening.
Bedard et al35 reported that, after
a minimum 10-year follow-up, the
reoperation rate for aseptic loosening
was 2% and zero for noncemented
femoral and acetabular components,
respectively.
When preparing an acetabulum in
an osteonecrotic hip, the surgeon
must remember that the bone quality
may be poor secondary to corticosteroid use, lack of weight bearing, or the
underlying disease (ie, rheumatoid
arthritis). In addition, the subchondral

sclerosis typically associated with

osteoarthritis may not be present, so it
is prudent to gently ream the acetabulum and use care when impacting the
acetabular component. The surgeon
should be aware of any alterations of
femoral anatomy resulting from previous osteotomy, core decompression,
or bone graft. An intraoperative plain
radiograph may be useful to help verify
appropriate seating and alignment of
the femoral broach. Moreover, careful
perioperative management and optimization of the patients medical conditions may reduce complications and
improve outcomes.
Hip Resurfacing Arthroplasty
Resurfacing arthroplasty preserves
bone and does not compromise subsequent conversion to THA; therefore, it has been considered a viable
option in the management of

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Charalampos G. Zalavras, MD and Jay R. Lieberman, MD

postcollapse osteonecrosis in young

patients with good bone stock.
However, a femoral neck fracture
may complicate the procedure, and
the outcome may be compromised in
women, obese patients, and patients
with extensive necrotic lesions, poor
bone stock, or narrow femoral necks.
In a series of 550 resurfacing procedures, 71 of which were performed for
osteonecrosis, the prevalence of femoral neck fractures was 2.5% (14 of
550).39 Obesity, female gender, and
femoral head/neck cysts were significantly associated with this complication. Interestingly, the prevalence of
femoral neck fractures was 17% in
the first 69 procedures compared
with 0.4% in the 481 subsequent
procedures, indicating the importance
of patient selection and surgical technique in the early learning curve of this
technically difficult procedure.39 Furthermore, concerns with the generation of metallic wear debris associated
with the metal-on-metal bearing and
the quality of bone in the femoral head
have limited the use of hip resurfacing
in patients with osteonecrosis of
the hip.
Selection of Treatment Options
Because there is no level I evidence
with long-term follow-up, it is difficult to identify the optimal treatment
protocol to manage patients with precollapse lesions. Moreover, the existing retrospective studies use different
staging systems and report on patients
with different underlying diagnoses. In
a recent systematic review, Lieberman
et al40 concluded that the optimal
head-sparing procedure is difficult to
determine because of limitations in
the current literature. These authors
also found that the outcome of headsparing procedures is compromised
when collapse has already occurred.
Radiographic progression of the disease was observed in 31% of precollapse hips (264 of 864 hips with
available data) treated with a headsparing procedure compared with
July 2014, Vol 22, No 7

49% of postcollapse hips (419 of 850

hips). Conversion to THA was
required in 19% of precollapse hips
(409 of 2,163) compared with 30% of
postcollapse hips (442 of 1,463).40
In the absence of level I evidence, it
is not possible to make definitive
treatment recommendations. However, based on the available data, our
treatment recommendations can be
summarized as follows: patients with
symptomatic osteonecrosis with
small lesions in precollapse hips
should be treated with a head-sparing
procedure; large lesions in precollapse hips may be treated with
a head-sparing procedure in younger
patients, but it is reasonable to consider THA in older patients; and the
great majority of patients with collapse of the femoral head should
not have a femoral head-saving procedure. THA is the most reliable
option for these patients.

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.

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