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death of the bone due to loss of blood supply.
Kumar V, Abbas A,
Fausto N, et al. Robbins
and Cotran Pathologic
Basis of Disease 7th
edition. Philadelphia:
Elsevier, 2005.
Pathology (organ,
cell, system)
AVN is the cellular death of bone due to interruption
of the blood supply and usually involves the
epiphysis of long bones, such as the femoral and
humeral heads and the femoral condyles (the bone
structures collapse). A regenerative process in
surrounding tissues follows necrosis of cortical bone,
and increased osteoclastic activity removes necrotic
bone while increased osteoblastic activity has a
reparative function. Edema, hemorrhage,
fibrilloreticulosis, and hypocellularity may be present
in bone marrow lesions.
Kumar V, Abbas A,
Fausto N, et al. Robbins
and Cotran Pathologic
Basis of Disease 7th
edition. Philadelphia:
Elsevier, 2005.
The pathologic characteristics of bone necrosis are
the same regardless of etiology. The necrosis is
geographic and involves cancellous bone and marrow
in medullary infarcts. The cortex is not typically
affected due to its collateral blood supply. In
subchondral infarcts, necrosis involves a wedgeshaped segment of tissue that has the subchondral
bone plate as its base and the center of the epiphysis
as its apex. Since the overlying articular cartilage
receives nutrition from the synovial fluid, it remains
viable. The dead bone has empty lacunae and is
surrounded by necrotic adipocytes that often rupture
and release their fatty acids. These fatty acids can
bind calcium and form insoluble calcium soaps.
During the healing process, osteoclasts resorb the
necrotic trabeculae, while the remaining ones serve as
scaffolding for the deposition of new bone (i.e.,
creeping substitution). Nevertheless, the pace of
creeping substitution is not fast enough to be
effective, and as a result, the necrotic cancellous bone
collapses and there is distortion, fracture, and
sloughing off of the articular cartilage. These gross
and microscopic findings (necrosis) are all a result of
the underlying problem in AVN – interruption of
blood supply and ischemia.
Pathophysiology
Normal physiology involves the production of bone
by osteoblasts and the resorption of bone by
osteoclasts. Whereas osteoblasts secrete an organic
matrix and mineralize the matrix, osteoclasts secrete
acid and proteolytic enzymes to digest the bone
matrix. The process of bone resorption releases
calcium and other ions and leads to deposition of
newer, better bone. In AVN, the remodeling process
is aborted due to interruption of blood supply to the
bone (ischemia), and the lack of bone remodeling
leads to the accumulation of micro-damage, collapse
of subchondral bone, rough joint surfaces, and
mechanical failure. This mechanical failure in
subchondral bone can result in arthritis.
Mont, MA, Hungerford,
DS. Non-traumatic
avascular necrosis of the
femoral head. J Bone
Joint Surg Am 1995;
77:459.
Avascular necrosis is specifically caused by loss of
blood supply and ischemia, but common diseases that
could conceivably have a similar presentation include
osteoarthritis (deterioration of cartilage and
overgrowth of bone that often occurs due to the “wear
and tear” of aging) and osteoporosis (decreased bone
mass with a normal ratio of mineral to matrix). Other
diseases on the differential include inflammatory
synovitis, complex regional pain syndrome, labral
tears, osteomyelitis, and neoplastic bone conditions.
AVN is also associated with trauma, systemic
corticosteroid use or Cushing disease, alcohol abuse,
SLE (and other connective tissue disorders),
antiphospholipid syndrome, sickle cell
Jackson SM. Pathologic
conditions mimicking
osteonecrosis. Orthop
Clin North Am 2004;
35(3): 315-20.
Mankin, HJ.
Nontraumatic necrosis of
bone. N Engl J Med 1992;
326:1473.
Chang, C, Greenspan, A,
Gershwin, M.
Osteonecrosis: Current
It is important to note that the exact pathophysiology perspectives on
of AVN is somewhat controversial, but most would pathogenesis and
argue that it is caused by a combination of metabolic treatment. Semin Arthritis
Rheum 1993; 23:47.
factors, local factors that affect blood supply (e.g.,
vascular damage), increased intraosseous pressure,
and mechanical stresses. The sequence likely begins
with an interrupted blood circulation within the bone
and leads to an adjacent hyperemic area,
demineralization, trabecular thinning, and collapse.
The collapse of bone structures leads to bone
destruction, pain, and loss of joint function.
Differential
Diagnosis
Chang, C, Greenspan, A,
Gershwin, M.
Osteonecrosis: Current
perspectives on
pathogenesis and
treatment. Semin Arthritis
Epidemiology
Etiology
disease/hemoglobinopathies, metabolic diseases
(hyperlipidemia, gout, renal failure), orthopedic
disorders (SCFE, DDH, Legg-Calve-Perthes disease),
infection (HIV), renal transplantation, radiation
therapy, and bisphosphonate use in malignant disease.
Rheum 1993; 23:47.
In the United States, approximately 10,000 to 20,000
new patients are diagnosed per year, and AVN
accounts for more than 10% of the total hip
replacement surgeries that are performed. AVN is a
disease of middle-age that often occurs during the
fourth or fifth decade. The male-to-female ratio is
8:1 but differs depending on the co-morbidities (e.g.,
an important exception to this male-to-female ratio is
SLE). AVN is bilateral in about 55% of cases, and
the most common site is the hip.
Mont, MA, Hungerford,
DS. Non-traumatic
avascular necrosis of the
femoral head. J Bone
Joint Surg Am 1995;
77:459.
AVN is caused by interruption of blood supply and
ischemia. Glucocorticoid use and excessive alcohol
intake have been reported to be associated with more
than 90% of AVN cases. The other causes can be
traumatic, such as femoral neck fracture,
dislocation/fracture, minor trauma, or non-traumatic,
such as sickle cell hemoglobinopathies, Caisson
disease, SLE, Gaucher’s disease, chronic renal failure
or hemodialysis, pancreatitis, pregnancy,
hyperlipidemia, radiation, organ transplantation,
intravascular coagulation, thrombophlebitis, cigarette
smoking, hyperuricemia/gout, and HIV infection. We
understand the pathogenesis of several of these causes
of AVN. Vascular occlusion is one possible factor in
pathogenesis; direct trauma, non-traumatic stress, and
stress fractures can interrupt the extraosseous blood
supply and lead to vascular occlusion. Another
possible factor in pathogenesis is primary cell death;
examples include isolated osteocyte death in renal
transplant patients and in patients who receive
steroids and drink excessive amounts of alcohol.
Increased lipid deposition in the femoral head caused
Chang, C, Greenspan, A,
Gershwin, M.
Osteonecrosis: Current
perspectives on
pathogenesis and
treatment. Semin Arthritis
Rheum 1993; 23:47.
Jones, L. Osteonecrosis
(avascular necrosis of
bone). In: UpToDate,
Basow, DS (Ed),
UpToDate, Waltham,
MA, 2010.
Mankin, HJ.
Nontraumatic necrosis of
bone. N Engl J Med 1992;
326:1473.
Kawai K, Tamaki A,
Hirohata K. Steroidinduced accumulation of
lipid in the osteocytes of
the rabbit femoral head. A
histochemical and
electron microscopic
study. J Bone Joint Surg
Am. Jun 1985;67(5):75563.
Wang GJ, Sweet DE,
Reger SI, et al. Fat-cell
changes as a mechanism
of avascular necrosis of
by increased serum lipids can lead to femoral
hypertension and ischemia and eventually AVN.
Another issue in the pathogenesis of AVN is the
healing process; the repair of necrotic bone can
produce a thick scar that prevents revascularization
and leads to abnormal joint remodeling.
the femoral head in
cortisone-treated rabbits. J
Bone Joint Surg
Am. Sep 1977;59(6):72935.
Jones, L. Osteonecrosis
(avascular necrosis of
bone). In: UpToDate,
Basow, DS (Ed),
UpToDate, Waltham,
MA, 2010.
Clinical
manifestations
AVN can be asymptomatic and found incidentally on
imaging, but infarcts of the small bones of the hands
and feet often produce symptoms. Unfortunately,
most patients present late in the course of disease. A
high index of suspicion is necessary for patients with
risk factors. Pain in the affected joint (although nonspecific) is usually the presenting symptom; patients
with AVN of the femoral head often complain of
groin pain that worsens with weight-bearing and
motion and less commonly complain of thigh and
buttock pain. Rest pain occurs in about two-thirds of
patients, while night pain occurs in about one-third of
patients. The initial physical exam findings may not
be useful and are often non-specific, but after AVN
progresses, joint function deteriorates and the patient
may walk with a limp, have tenderness around the
affected bone, have painful, restricted active and
passive joint movements, have joint deformity and
muscle wasting, and may even have a neurologic
deficit if a nerve is compressed due to necrosis and
deformity of the affected bones. Limitation in range
of motion that may eventually develop is seen
particularly with forced internal rotation and
abduction. The signs and symptoms at the joint are
clearly related to the absence of remodeling,
accumulation of micro-damage, collapse of
subchondral bone, and development of rough joint
surfaces that ultimately lead to mechanical failure.
Zizic, TM, Marcoux, DS,
Hungerford, DS, Stevens,
MB. The early diagnosis
of ischemic necrosis of
bone. Arthritis Rheum
1986; 29:1177.
LaPorte, DM, Mont, MA,
Mohan, V, et al.
Multifocal osteonecrosis.
J Rheumatol 1998;
25:1968.
Jones, L. Osteonecrosis
(avascular necrosis of
bone). In: UpToDate,
Basow, DS (Ed),
UpToDate, Waltham,
MA, 2010.
Late presentation,
complications
In the late stages of AVN, you would be more likely
to see highly deteriorated joint function (sclerosis and
total destruction) and a significant limp during
walking in lower extremity disease. Without
treatment, the patient would be more likely to present
with severe pain at rest and at night and would have
more restriction and pain with joint movements. Joint
deformity, muscle wasting, and nonunion of fracture
are also more common with advanced AVN that has
not been treated. It is important to note that
medullary infarcts usually remain stable over time,
while subchondral infarcts often collapse and may
predispose to severe secondary osteoarthritis.
Zizic, TM, Marcoux, DS,
Hungerford, DS, Stevens,
MB. The early diagnosis
of ischemic necrosis of
bone. Arthritis Rheum
1986; 29:1177.
LaPorte, DM, Mont, MA,
Mohan, V, et al.
Multifocal osteonecrosis.
J Rheumatol 1998;
25:1968.
Kumar V, Abbas A,
Fausto N, et al. Robbins
and Cotran Pathologic
Basis of Disease 7th
edition. Philadelphia:
Elsevier, 2005.
Jones, L. Osteonecrosis
(avascular necrosis of
bone). In: UpToDate,
Basow, DS (Ed),
UpToDate, Waltham,
MA, 2010.
Nutritional factors
Nutrition does play an important role in this
condition. Alcohol abuse should be avoided, and a
healthy, balanced diet (with low lipids) should be
adopted because excessive alcohol use and
hyperlipidemia/gout are associated with AVN. In
general, the patient should also have normal intake of
calcium and vitamin D to maintain normal bone
density.
Jackson SM. Pathologic
conditions mimicking
osteonecrosis. Orthop
Clin North Am 2004;
35(3): 315-20.
Jones, L. Osteonecrosis
(avascular necrosis of
bone). In: UpToDate,
Basow, DS (Ed),
UpToDate, Waltham,
MA, 2010.
Kawai K, Tamaki A,
Hirohata K. Steroidinduced accumulation of
lipid in the osteocytes of
the rabbit femoral head. A
histochemical and
electron microscopic
study. J Bone Joint Surg
Am. Jun 1985;67(5):75563.
Wang GJ, Sweet DE,
Reger SI, et al. Fat-cell
changes as a mechanism
of avascular necrosis of
the femoral head in
cortisone-treated rabbits. J
Bone Joint Surg
Am. Sep 1977;59(6):72935.
Radiographic
evidence
Plain radiograph may be normal for months after the
onset of symptoms of osteonecrosis, but early
findings may include mild density changes followed
by sclerosis and cysts as AVN progresses. The
pathognomonic crescent sign (subchondral
radiolucency) indicates subchondral collapse. In late
stages of AVN, loss of sphericity and collapse of the
femoral head and joint-space narrowing and
degenerative changes in the acetabulum can be seen.
Bone scanning can show increased bone turnover at
the junction of dead and reactive bone (increased
uptake around a cold area – doughnut sign), but it is
significantly less sensitive than MRI in diagnosing
osteonecrosis (56% versus 100% in 1 study of 48
patients). MRI has been reported to have a sensitivity
of 91%, and changes can often be seen on MRI early
in the course of disease (unlike on plain radiograph
and bone scanning). On T-1 weighted imaging, focal
lesions are well-demarcated and inhomogeneous; in
early stages of AVN, you may see a single density
line that reflects the separation of normal and
ischemic bone. On T-2 weighted imaging, you may
see a second high intensity line that reflects
hypervascular granulation tissue (i.e., the
pathognomonic double-line sign). CT scanning may
be used to determine the extent of the disease and
calcification, but it is not as sensitive as MRI. There
is a direct relationship between the radiographic
Chang, C, Greenspan, A,
Gershwin, M.
Osteonecrosis: Current
perspectives on
pathogenesis and
treatment. Semin Arthritis
Rheum 1993; 23:47.
Mazieres, B.
Osteonecrosis. In:
Rheumatology, Hochberg,
MC, Silman, AJ, Smolen,
JS, et al. (Eds), Mosby,
London 2003. p.1877.
Dumont, M, Danais, S,
Taillefer, R. "Doughnut"
sign in avascular necrosis
of the bone. Clin Nucl
Med 1984; 9:44.
Mont, MA, Ulrich, SD,
Seyler, TM, et al. Bone
scanning of limited value
for diagnosis of
symptomatic oligofocal
and multifocal
osteonecrosis. J
Rheumatol 2008;
findings and the pathophysiology because the lesions 35:1629.
seen on imaging reflect the joint surface damage and
Guerra, JJ, Steinberg, ME.
bone collapse that ultimately result from ischemia.
Distinguishing transient
osteoporosis from
avascular necrosis of the
hip. J Bone Joint Surg Am
1995; 77:616.
Laboratory
evidence
No laboratory test findings specifically suggest or
confirm the presence of AVN.
Jones, L. Osteonecrosis
(avascular necrosis of
bone). In: UpToDate,
Basow, DS (Ed),
UpToDate, Waltham,
MA, 2010.
Psychosocial
impact of disease
Given the high morbidity rates and the significant
prevalence of long-term disability with AVN,
psychosocial factors are a key consideration in this
patient population. The pain and difficulty with
weight bearing can prevent these patients from
working and from socializing to the extent that they
usually do. This can certainly lead to depression and
anxiety. In addition, the psychological distress can
affect these patients’ relationships with their partners
and families because they are less independent ; they
may often experience pain and cannot ambulate and
weight-bear as they did prior to progression of the
disease, so they may require assistance from loved
ones. Another important issue to consider is that
many patients with advanced AVN require more than
one hemiarthroplasty or total hip replacement during
their lifetime. These patients may become more
apathetic and may feel as though they are a burden to
their friends and families because they cannot control
their disease.
Chang, C, Greenspan, A,
Gershwin, M.
Osteonecrosis: Current
perspectives on
pathogenesis and
treatment. Semin Arthritis
Rheum 1993; 23:47.
Risk factors
Risk factors for AVN include increased rates of
trauma, systemic corticosteroid use or Cushing
disease, alcohol abuse, SLE (with or without
antiphosopholipid syndrome), other connective tissue
diseases, sickle cell disease/hemoglobinopathies,
metabolic diseases (hyperlipidemia, gout, renal
Chang, C, Greenspan, A,
Gershwin, M.
Osteonecrosis: Current
perspectives on
pathogenesis and
treatment. Semin Arthritis
failure), orthopedic disorders (SCFE, DDH, LeggCalve-Perthes disease), osteomyelitis, HIV infection,
renal transplantation, radiation therapy, pancreatitis,
Gaucher disease, malignancy (marrow infiltration,
malignant fibrous histiocytoma), Caisson disease,
pregnancy, and bisphosphonate use.
Rheum 1993; 23:47.
Kawai K, Tamaki A,
Hirohata K. Steroidinduced accumulation of
lipid in the osteocytes of
the rabbit femoral head. A
histochemical and
electron microscopic
study. J Bone Joint Surg
Am. Jun 1985;67(5):75563.
Wang GJ, Sweet DE,
Reger SI, et al. Fat-cell
changes as a mechanism
of avascular necrosis of
the femoral head in
cortisone-treated rabbits. J
Bone Joint Surg
Am. Sep 1977;59(6):72935.
Jones, L. Osteonecrosis
(avascular necrosis of
bone). In: UpToDate,
Basow, DS (Ed),
UpToDate, Waltham,
MA, 2010.
Prevention
To prevent AVN, the minimum effective dose of
systemic corticosteroids should be used and if
possible, steroid-sparing agents should be used.
Statins may reduce AVN incidence with long-term
corticosteroid use. AVN should be detected as early
as possible so that treatment can be initiated
immediately and less invasive options are still
available. Patients at high risk of AVN (e.g., with
prolonged corticosteroid use, hemoglobinopathies,
renal transplant) should be educated about AVN and
advised to report symptoms as soon as possible to
facilitate treatment. Patient education and
minimizing corticosteroid doses are both very cost-
Musso, ES, Mitchell, SN,
Schink-Ascani, M,
Bassett, CA. Results of
conservative management
of osteonecrosis of the
femoral head. A
retrospective review. Clin
Orthop 1986; 207:209.
Mont, MA, Carbone, JJ,
Fairbank, AC. Core
decompression versus
non-operative
effective ways to reduce the incidence of AVN, and
even though they may not always prevent AVN, they
would allow patients to be treated earlier in the course
of disease. Two uncontrolled studies showed that
bisphosphonates may delay collapse of the femoral
head and delay the need for surgical intervention, but
further studies are required. Conservative therapy
will be discussed in the “treatment options” section,
but it should be noted here that this approach is
typically ineffective at halting the progression of
disease.
management for
osteonecrosis of the hip.
Clin Orthop 1996;
324:169.
Agarwala, S, Shah, S,
Joshi, VR. The use of
alendronate in the
treatment of avascular
necrosis of the femoral
head: follow-up to eight
years. J Bone Joint Surg
Br 2009; 91:1013.
Lai, KA, Shen, WJ, Yang,
CY, et al. The use of
alendronate to prevent
early collapse of the
femoral head in patients
with nontraumatic
osteonecrosis. A
randomized clinical study.
J Bone Joint Surg Am
2005; 87:2155.
Wang GJ, Rawles JG,
Hubbard SL, et
al. Steroid-induced
femoral head pressure
changes and their
response to lipid-clearing
agents. Clin Orthop Relat
Res. Apr 1983;298-302.
Treatment options
Options for treatment include conservative
management, joint-preserving procedures, and joint
replacement. Conservative management includes bed
rest, limited weight bearing with crutches, and pain
medications. The goal is to minimize mechanical
stress, but most studies show that conservative
management is usually ineffective at halting
progression of disease (one exception may be AVN
of the shoulder). In advanced AVN, activity does not
affect the disease course and surgery is required.
Musso, ES, Mitchell, SN,
Schink-Ascani, M,
Bassett, CA. Results of
conservative management
of osteonecrosis of the
femoral head. A
retrospective review. Clin
Orthop 1986; 207:209.
Mont, MA, Carbone, JJ,
Two uncontrolled studies showed that
bisphosphonates may delay collapse of the femoral
head and delay the need for surgical intervention, but
further studies are required to assess long-term
results. Although there is no consensus on the best
surgical procedure for AVN, core decompression
with or without bone graft is appropriate in early
stages of AVN and total hip arthroplasty is
appropriate in the late stages (collapse, femoral head
deformity, secondary osteoarthritis). Core
decompression may enhance circulation by
decreasing intramedullary pressure and preventing
more ischemia. This treatment is evidence-based
(primarily case series and retrospective studies
though) and has better results than conservative
management. It is often useful for pain relief and is
especially effective in the early stages of disease.
Bone grafts (especially free vascularized bone grafts)
are another evidence-based option that can provide
structural support to the subchondral bone and can be
a source of mesenchymal stem cells and a vascular
supply to the necrotic tissue. Osteotomy can be used
to move the area of necrosis away from the major
load-transmitting area of the acetabulum and
redistribute the weight-bearing to the articular
cartilage, but the results are variable. Total joint
replacement is an evidence-based option for patients
with advanced disease. Total hip arthroplasty
provides significant pain relief for several years,
though revision rates are often high.
Fairbank, AC. Core
decompression versus
non-operative
management for
osteonecrosis of the hip.
Clin Orthop 1996;
324:169.
Agarwala, S, Shah, S,
Joshi, VR. The use of
alendronate in the
treatment of avascular
necrosis of the femoral
head: follow-up to eight
years. J Bone Joint Surg
Br 2009; 91:1013.
Lai, KA, Shen, WJ, Yang,
CY, et al. The use of
alendronate to prevent
early collapse of the
femoral head in patients
with nontraumatic
osteonecrosis. A
randomized clinical study.
J Bone Joint Surg Am
2005; 87:2155.
Urbaniak, JR, Coogan,
PG, Gunneson, EB,
Nunley, JA. Treatment of
osteonecrosis of the
femoral head with free
vascularized fibular
grafting. A long-term
follow-up of one hundred
and three hips. J Bone and
Joint Surg 1995; 78A:681.
Sugioka, Y, Katsuki, I,
Hotokebuchi, T.
Transtrochanteric
rotational osteotomy of
the femoral head for the
treatment of
osteonecrosis. Follow-up
statistics. Clin Orthop
1982; 169:115.
Saito, S, Saito, M,
Nishina, T, Ohzono, K, et.
al. Long-term results of
total hip arthroplasty for
osteonecrosis of the
femoral head. Clin Orthop
1989; 244:198.
Kim, YH, Oh, SH, Kim,
JS, Koo, KH.
Contemporary total hip
arthroplasty with and
without cement in patients
with osteonecrosis of the
femoral head. J Bone
Joint Surg Am 2003; 85A:675.
Outcomes of
treatment
Outcomes of treatment directly correlate with the
stage of disease. No medical treatment has been
demonstrated to be effective in preventing the disease
process, and half of patients with subchondral
collapse of the femoral head develop AVN in the
contralateral hip. Total hip replacement may seem
like the ideal treatment, but some studies have
showed that revision rates in patients with avascular
necrosis are significantly higher than revision rates in
patients with other disorders. For example, one
retrospective review compared total hip replacement
of hips in patients with osteonecrosis with
replacement of hips in patients with osteoarthritis and
found that the revision rate was higher in patients in
the osteonecrosis group (28 percent compared with 6
percent) and that the time of revision was an average
of 5 years less in osteonecrosis patients. Patients do
not do as well if they are older than 50 years of age,
have advanced disease at the time of diagnosis, have
necrosis of more than one third of the weight-bearing
area of the femoral head on MRI, or have lateral
Musso, ES, Mitchell, SN,
Schink-Ascani, M,
Bassett, CA. Results of
conservative management
of osteonecrosis of the
femoral head. A
retrospective review. Clin
Orthop 1986; 207:209.
Saito, S, Saito, M,
Nishina, T, Ohzono, K, et.
al. Long-term results of
total hip arthroplasty for
osteonecrosis of the
femoral head. Clin Orthop
1989; 244:198.
Kim, YH, Oh, SH, Kim,
JS, Koo, KH.
Contemporary total hip
arthroplasty with and
without cement in patients
Potential
Complications of
treatment
involvement of the femoral head.
with osteonecrosis of the
femoral head. J Bone
Joint Surg Am 2003; 85A:675.
Disadvantages of free vascularized bone grafts
include longer recovery, less complete analgesia,
variable success rate, and decreased effectiveness in
advanced AVN. As was mentioned earlier, total hip
arthroplasty has high revision rates. It also carries the
risks of infection, dislocation, bleeding, deep vein
thrombosis, damage to nerves or blood vessels,
wound irritation, leg length inequality, wear and tear,
scars, inadequate pain relief, limping due to muscle
weakness, and fractures of the femur or pelvis. The
patient can also have allergic reactions to medications
and is at risk of heart attack, stroke, kidney failure,
bladder infection, and pneumonia with a surgical
procedure.
Hasegawa Y, Iwata H,
Torii S, et
al. Vascularized pedicle
bone-grafting for
nontraumatic avascular
necrosis of the femoral
head. A 5- to 11-year
follow-up. Arch Orthop
Trauma
Surg. 1997;116(5):251-8.
Urbaniak JR, Coogan PG,
Gunneson EB, et
al. Treatment of
osteonecrosis of the
femoral head with free
vascularized fibular
grafting. A long-term
follow-up study of one
hundred and three hips. J
Bone Joint Surg
Am. May 1995;77(5):68194.
Saito, S, Saito, M,
Nishina, T, Ohzono, K, et.
al. Long-term results of
total hip arthroplasty for
osteonecrosis of the
femoral head. Clin Orthop
1989; 244:198.
Kim, YH, Oh, SH, Kim,
JS, Koo, KH.
Contemporary total hip
arthroplasty with and
without cement in patients
with osteonecrosis of the
femoral head. J Bone
Joint Surg Am 2003; 85A:675.
Misc
The athlete Bo Jackson had avascular necrosis of his Almeida A, Roberts I. Br
left hip. He had a hip replacement and returned to the J Haematol. 2006
Chicago White Sox in 1991.
Apr;133(2):212-4.
Total hip replacement fails in almost 60% of patients
with AVN due to sickle cell disease. Bone
involvement is a common clinical manifestation of
sickle cell disease; it occurs in the acute setting with
painful vaso-occlusive crises and in a more chronic
setting with AVN and progressive disability.
Thinking of sickle cell disease and AVN together is a
good way to remember AVN because it underscores
the importance of loss of blood supply in the
pathogenesis of the disease.