• avascular necrosis of the femoral head,
osteonecrosis, osteonecrosis of the
femoral head, ischemic necrosis,
ischemic necrosis of the femoral head,
ischemic bone necrosis, bone necrosis of
the femoral head, bone infarct of the
femoral head, idiopathic bone necrosis of
the femoral head, nontraumatic
avascular necrosis of the femoral head,
traumatic avascular necrosis of the
femoral head, subchondral avascular
necrosis, coronary artery disease of the
femoral head, AVN
are intravascular and
The normal circulation of the femoral head. The posterior-superior
retinacular arteries provide the major blood supply to the epiphysis.
They traverse the femoral neck and are contained within the joint
capsule. They give rise to the lateral epiphyseal vessels at the
junction of the femoral head and neck. From there, they penetrate
the femur and supply the femoral epiphysis.
Intravascular factors Extraosseous vascular
factors - The
femoral head is an end-organ system with
poor collateral development. Trauma to the
hip may lead to contusion or mechanical
interruption to the lateral retinacular vessels,
the main blood supply of the femoral head
Vasculitis, as seen in Raynaud disease, or
vasospasm, as seen in decompression
sickness, can interfere with extraosseous
The blood supply to the femoral head is compromised by
subcapital femoral fractures or slipped capital femoral epiphysis.
As the epiphysis or femoral neck separates from the femoral head,
the femoral metaphysis displaces superolaterally and the femur
rotates externally. This causes the distal posterior-superior
retinacular arteries and proximal lateral epiphyseal vessels to kink
or rotate, compromising the blood flow to the epiphysis.
Intraosseous vascular factors - Arterial
Circulating microemboli that block the
microcirculation of the femoral head.
sickle cell disease (SCD), fat
embolization, or air embolization from
dysbaric phenomena. ed by fat emboli, in
hyperlipidemia associated with alcoholism,
steroid therapy, SCD, and nitrogen bubbles
in decompression sickness.
Intraosseous vascular factors - Venous
Conditions such as Caisson disease and
SCD have a strong tendency to involve the
venous side of the circulation, reducing
venous outflow and causing stasis.
Enlargement of intramedullary fat cells may
be the most significant factor leading to
obstruction of venous drainage.
The bone system within the subchondral region is enclosed within a
rigid shell of cortical bone. This is particularly sensitive to increases in
pressure resulting in a compartment syndrome.
Fat cells, Gaucher cells and inflammatory cells, encroach on
intraosseous capillaries, reducing intramedullary circulation and
resulting in compartment syndrome.
Blood flow normally is poorer in fatty marrow. Transmitted pressure in
the weight bearing region of the femur compresses capillary
circulation, which is already compromised by increased intraosseous
Repeated microfractures in the weightbearing segment of the femur
may cause multiple vascular lesions resulting in ischemia within fragile
and poorly repaired bone.
In cellular cytotoxic factors, such as alcoholism and steroid-related
AVN, there could be a direct toxic metabolic effect on osteogenic
Trabecular deformation, which normally occurs during weight
bearing, also compresses the marrow space to some degree
In idiopathic osteonecrosis, a possible quantitative or qualitative
deficiency in the bone architecture.
Effects of raised pressure are on the sinusoids and the small marrow
capillaries, then on the venous outflow. Reflex spasm can even block
nutrient vessels before they enter the cortex.
Disease processes within the hip joint
that produce effusions, such as
trauma, infection, and arthritis, may
affect the blood supply to the
epiphysis adversely. The mechanism
involves tamponade of the lateral
epiphyseal vessels , which are located
within the synovial membrane,
through increased intracapsular
The cause is multifactorial
The final common pathway may
represent intravascular coagulation
with fibrin-platelet thrombosis
beginning in the vulnerable
(capillary and sinusoidal beds)
resulting in vasoconstriction and
impaired fibrinolysis and infarction.
Sequelae of AVN
Minimal disease: Small vascular area not adjacent to an articular
surface -- asymptomatic and it could heal spontaneously –
severe disease: AVN develops, repair starts at the interface
between viable and necrotic bone. Dead bone is reabsorbed
Reactive and reparative bone is laid down on dead trabeculae
resulting in a sclerotic margin of thickened trabeculae . The
incomplete resorption of dead bone results in a mixed sclerotic and
cystic appearance . Mechanical failure: subchondral region,
microfractures do not heal because they occur within an area of
dead bone. Progression of the microfractures results in a diffuse
subchondral fracture, the crescent sign Following subchondral
fracture and progressive weightbearing, collapse of the articular
cartilage occurs . Continued fracture, necrosis, and further
weightbearing can progress to degenerative joint disease (DJD) and
Anteroposterior view of the pelvis shows flattening of
the outer portion of the right femoral head from
avascular necrosis (arrow), with adjacent joint space
narrowing, juxta-articular sclerosis, and osteophytes
representing degenerative joint disease.
flattening of the right femoral head
Trauma is the most common cause of AVN. AVN can
occur within 8 hours after traumatic disruption of the
blood supply. The superior retinacular vessels and the
nutrient artery can be damaged as they enter the
femur. The artery of the ligamentum teres (ALT) also
may be damaged. Intracapsular hematoma
increases intracapsular pressure, which can cause
tamponade of the vessels within the joint capsule.
Intertrochanteric and extracapsular fractures of the
femur rarely develop AVN. Following hip dislocation,
circulation is interrupted because of tears of the
ligamentum teres, tearing the ALT. Tearing of the joint
capsule compromises the vessels within the capsular
Alcohol may have a toxic effect on
osteogenic cells. The direct toxic effect of
alcohol results in fat deposition in the liver.
Livers with fat deposits are a constant
source of low-grade asymptomatic fat
emboli. Intraosseous fat emboli become
hydrolyzed to free fatty acids, which cause
endothelial damage. Alcohol intake
exceeding 40 mL per week increases the
risk of AVN more than 11 times compared
to the risk in nondrinkers. A clear dose-
response relationship exists.
1.Occlusion of small vessels occurs related to fat
emboli from the liver.
2. Increased intraosseous pressure results from a
steroid-related increase in the size of the
intramedullary fat cells without an equivalent
compensatory loss of trabecular and cortical bone.
3. Fat emboli become hydrolyzed to free fatty acids,
which are toxic to vascular endothelium, causing
4. Angiogenesis is inhibited by a reduction of
proteolytic activity by the synthesis of polyclonal
antithyroid hormone receptor alpha-1 antibody
5. A direct toxic effect occurs on osteogenic cells.
6. Steroid use causes conversion of hematopoietic
marrow to fatty marrow, a prerequisite for the
development of AVN.
Decompression sickness (Caisson disease)
Workers in underwater enclosures requiring
compressed air to prevent water seepage are at risk.
AVN occurs as a result of exposure to pressure
greater than 17 lb per square inch. These infarcts
tend to be large. Undersea divers are at risk. Key risk
factors are the depth of the dive, the number of
dives, uncontrolled decompression, and low oxygen
concentrations. The presence of intravascular
bubbles of nitrogen obstructs capillaries.
Extravascular nitrogen within the fatty marrow,
encased within the bone, compresses intramedullary
vessels. Arteriolar spasm also may occur. Fat cells
have a 5-fold ability to absorb dissolved nitrogen.
Such absorption increases their volume within the
nonexpandable confines of the bony trabeculae
and cortex, increasing intraosseous marrow pressure
and causing venous stasis.
Metastatic cells can pack the
marrow, resulting in increased
intramedullary pressure obstructing
the intramedullary vessels. Patients are
at higher risk if they are receiving
steroid therapy and/or are
undergoing local radiation therapy to
The release of lipolytic enzymes into the
bloodstream results in breakdown of the fat
within the marrow cells into free fatty acids,
which are toxic to endothelium, causing
intravascular coagulation. Upon entering
the portal venous radicals in patients with
pancreatitis, pancreatic enzymes can
cause release of intracellular fat from fat-
laden hepatic cells.
Hemoglobinopathies (SCD, thalassemia,
hemoglobin C disease, hemoglobin D disease,
hemoglobin E disease)
Hemoglobinopathies are the principal cause of
AVN . Infarcts in hemoglobinopathies tend to be
large. AVN only occurs when a sickle gene is
present to cause the sickling phenomena. Sickling
of abnormal red blood cells occurs in
intramedullary capillaries and venules, causing
hyperviscosity and vascular occlusion.
Bone marrow hyperplasia resulting from chronic
anemia may pack the marrow, placing it at
increased risk for developing AVN from elevated
Gaucher disease is a metabolic disorder
consisting of a deficiency of the enzyme b-
glucosidase, which normally catalyzes the
removal of glucose from glucocerebroside.
Glucocerebroside accumulates in the
reticuloendothelial cells within the bone
marrow, resulting in packing of marrow,
compression of interosseous sinusoids, and
elevation of interosseous pressure. Infarcts
tend to be large.
Elevated levels of parathormone may cause increased
subchondral bone turnover with replacement by
disorganized bone matrix unable to support normal
weightbearing, resulting in microfractures and
increased intramedullary pressure.
Fibrosis and endothelial proliferation resulting from
radiation-induced arteritis cause underlying vascular
compromise. Patients with metastatic lymphoma or
carcinoma to the femoral head who are treated with
steroids and chemotherapy are at increased risk of
developing AVN. AVN occurs with doses exceeding 30
Repeated microhemorrhages within the confines of the
marrow result in increased intramedullary pressure.
Capsular distension from hemorrhage may compress
the retinacular vessels within the synovial capsule.
Hypercoagulable states - Inherited
Hypercoagulable states - Acquired
Legg-Calvé-Perthes (LCP) disease
Slipped capital femoral epiphysis
Congenital dislocation of the hip
Femoral head fracture
Femoral head dislocation
Sickle cell disease
Gross pathology Cancellous bone in the femoral head
shows irregular areas of yellow necrosis extending up to
several millimeters of articular cartilage. With progression,
a patchy zone of softening develops in the necrotic
cancellous bone, adjacent to viable bone, representing
resorption of the necrotic segment. With further
weightbearing and bone resorption, structural support is
lost in the subarticular region with resultant microfractures
and subsequent creation of an articular sequestrum.
A line of trabecular fractures extends across the dead
bone, which creates and separates an articular
sequestrum. Following trabecular fracture, the load-
bearing segment of the femoral head collapses. Breaks in
the smooth contour of the femoral head become visible,
most often at the superior margin of the fovea and
beneath the acetabular lip. After collapse of the femoral
head, progressive destruction of the articular cartilage
and underlying bone occurs, loose bodies appear, and
marginal osteophytes develop, heralding the
development of DJD
of the Hematopoietic elements ,the bone
cells, eg, osteocytes, osteoclasts, and
osteoblasts and marrow fat cells is seen.
Bone infarcts can be divided into 4 zones,
ie, a central zone of cell death surrounded
by successive zones of ischemia,
hyperemia, and normal tissue.
Bone resorption occurs first, followed by
new bone formation.
Repair begins along the outer perimeter at
the junction between the dead area and
the viable area containing an intact
Sex: disease affects males 4 times
more frequently than it affects
Age: AVN usually occurs in
patients in the third-to-fifth
decades unless predisposing
conditions exist that place
different age groups at risk, ie,
LCP and slipped capital femoral
Clinical Details: Patients may be asymptomatic or may
develop pain gradually , experience a decreased range of motion
(ROM), and walk with a limp. Pain can be
excruciating and of sudden onset.
Pain can be focal, over the groin or hip, or it can radiate to the
buttocks, anteromedial thigh, or knee.
Pain can be induced mechanically by standing and walking and
can be eased by rest.
Pain can be very intense, especially in the large infarcts When the
disease is chronic, pain can be vague.
Following treatment of a traumatic hip fracture, AVN may manifest
as worsening pain.
A click may be heard when the patient rises from a sitting position.
A click may be elicited by external rotation of an abducted hip.
Range of motion
ROM may be diminished, especially after collapse of the femoral
ROM may be limited, especially in flexion, abduction, and internal
Gait: Patients may walk with a limp.
Stage 0 (preclinical and
AVN can be suggested
only if it has already been
diagnosed in the
Stage 1 (preradiologic)
Stage 1 represents the early resorptive
stage. Late in this stage, plain
radiographs may show minimal
osteoporosis and/or blurring and poor
definition of the bony trabeculae.
Osteoporosis appears when one third
of the mineral content of bone has
Demineralization is evident. It may be
generalized or patchy or appear in the form
of small cysts within the femoral head.
Demineralization is the first manifestation of
the stage and it represents resorption of
dead bone. Patchy sclerosis appears , usually
in the superolateral aspect of the femoral
head . Patchy sclerosis appears as increased
density on radiographs and may be diffuse,
focal, or in a linear arc, which is concave
superiorly. Patchy sclerosis usually coexists
with demineralization, appearing as
alternating regions of increased density and
Stage 3 (early collapse of the femoral
A linear subcortical lucency, representing a
fracture line, is present immediately
beneath the articular cortex. It may extend
into the articular cartilage at the
superolateral aspect of the femoral head.
This is termed the crescent sign and is best
demonstrated on a frogleg view . The
subarticular cortex may remain attached to
the cartilage and is separated from the
underlying femur by soft tissue, termed the
eggshell sign. The femoral head initially
preserves its round appearance, but later, it
demonstrates collapse. This may be
indicated by joint-space widening.
Stage 4 Further flattening of the
femoral head occurs with loss of its
smooth convex contour . Fragments
of bone and cartilage may separate
from the underlying femur, roam freely
within the hip joint, and become loose
Severe collapse and destruction of
the femoral head leads to progressive
DJD with joint space narrowing,
marginal osteophyte formation, and
subchondral cyst formation.
Stage 0 is both preclinical and preradiologic. Most
patients with stage 0 disease are identified when
imaging is performed to evaluate AVN in the
contralateral hip or to exclude other diseases.
Stage 1 demonstrates normal radiograph findings or
shows minimal demineralization or blurred trabeculae.
Pain in the anterior groin or thigh is common. Limited
ROM in the hip may be present.
Stage 2 shows diffuse or localized areas of sclerosis,
lucencies, or both within the femoral head. Clinical
signs persist or worsen.
Stage 3 is characterized by the crescent sign
Stage 4 demonstrates marked collapse and fracture
involving the articular surface. Segmental flattening of
the femoral head demonstrates an out-of-round
Stage 5 is characterized by the development of DJD.
Early CT signs of AVN
Osteoporosis is the first sign visible. Later, the central
bony asterisk is distorted, appearing as clumping
and fusion of the peripheral asterisk rays. Clumping
appears as spots or as hyperdense "roads" of
various width .
Fatty marrow is present in the femoral capital epiphysis and
the greater trochanter .This has high signal on T1-weighted
images (T1WIs) and T2-weighted images . Hematopoietic
marrow, when present, is found in the femoral neck,
intertrochanteric region, and acetabulum. It has low signal
on T1WIs and high signal on T2WIs
The medullary cavity contains prominent vertically orientated
linear striations of low signal on all imaging sequences
extending from the inferolateral aspect to the superomedial
aspect of the femoral head. These represent the
weightbearing trabeculae and are analogous to the asterisk
sign seen on CT scans . The medullary cavity is surrounded by
a sharply marginated low-intensity line representing the
cortex of the bone. Cortex and trabeculae have weak MRI
signals because of a low concentration and decreased
mobility of hydrogen ions
A thin high-signal line, representing the articular cartilage,
surrounds the outer margin of the femoral head. A curvilinear
low-signal line, representing the physis, crosses the marrow of
the femoral neck laterally to medially
T1-weighted images: A peripheral band of low
signal is present in the superior portion of the
femoral head outlining a central area of bone
marrow. This is considered to represent the
reactive interface between the necrotic and
reparative zones and extends to the subchondral
bone plate .
T2-weighted images: The inner border of the
peripheral band demonstrates high signal. This
may represent chemical shift artifact because
the position of the signal changes when the
phase and frequency directions are changed.
This is termed the double-line sign and is
pathognomonic for AVN . The outer low-signal
ring represents the interface of repair tissue with
the necrotic zone.
Single-photon emission computed tomography
A cold spot (photon-deficient region) within the femoral
head is highly specific for AVN and is the earliest
scintigraphic evidence of AVN. This usually is seen 7-10 days
after the ischemic event.
Over a period of weeks to months, increased uptake
representing revascularization and repair surrounds and
eventually replaces the region of photopenia. The central
region of photopenia with surrounding zone of increased
uptake is termed the doughnut sign.
Perfusion and static planar radionuclide imaging
Initially, uptake is decreased in the perfusion and static
phases, which represents the early ischemic event. Later,
uptake is decreased within the femoral head in the perfusion
phase and increased around the cold region in the static
phase. The latter represents the reactive zone around the
infarcted segment. The increased uptake from the reparative
zone eventually replaces the photopenic region.