W720 AJR:197, October 2011

can often aid in differentiating these clinical

entities from one another.
Bone marrow edema with several foci of
high signal in multiple ankle and foot bones,
coined high turnover, is commonly seen in
children younger than 15 years [3]. The cause
of this asymptomatic and self-limited process
is likely multifactorial, reecting residual red
marrow, hyperemia, increased bone remodel-
ing, or altered weight bearing (Fig. 1).
Similarly, multiple foci of bone marrow
edema may be seen in physically active in-
dividuals after strenuous exercise or as a re-
sult of altered gait or weight bearing [4]. The
cause, again, is unclear and may reect mar-
row hyperplasia, microfracture, or bone re-
pair. Initially asymptomatic, the process can
evolve, with continuous overuse, to symp-
tomatic stress reaction or stress fracture [3].
Bone marrow edema secondary to bone
impaction or bone contusions is likely the
result of trabecular microfractures, edema,
hemorrhage, or reaction after stress. This pat-
tern is common after ankle inversion injuries
and is often noted in the apposing medial mal-
leolus and talus. It can be painful but typically
resolves within a few months. Ligament avul-
sions after inversion injury can also present
with edema, but edema is less prominent in
those cases [2] (Fig. 2).
Bone marrow edema after immobiliza-
tion can be patchy, subcortical, subchondral,
Bone Marrow Edema Patterns
in the Ankle and Hindfoot:
Distinguishing MRI Features
Adriana Martins Rios
1
Zehava Sadka Rosenberg
2
Jenny Teresa Bencardino
2
Silvia Prez Rodrigo
3
Sara Garca Theran
4
Rios AM, Rosenberg ZS, Bencardino JT,
Rodrigo SP, Theran SG
1
Department of Radiology, Lifecenter Hospital, Ave do
Contorno 4747, Serra,Belo Horizonte 30110-090, Brazil.
Address correspondence to A. M. Rios
(rios.adrianamartins@gmail.com).
2
Department of Radiology, NYU Hospital for Joint
Diseases, New York, NY.
3
Department of Radiology, Hospital Universitario Ramon
y Cajal, Madrid, Spain.
4
Radiology Department, Hospital Universitario Mayor,
Bogot, Colombia.
Muscul oskel et al I magi ng Pi ctori al Essay
WEB
This is a Web exclusive article.
AJR 2011; 197:W720W729
0361803X/11/1974W720
American Roentgen Ray Society
T
he term bone marrow edema de-
scribes nonspecic, ill-dened ar-
eas of hypointense and hyperin-
tense signal on T1-weighted and
uid-sensitive sequences, respectively [1, 2].
The cause of bone marrow edema is unclear
and may include uid, hemorrhage, brosis,
and necrosis. Various diseases with confusingly
similar or overlapping MRI features can cause
ankle and hindfoot bone marrow edema. This
pictorial essay, focusing on uid-sensitive se-
quences, provides guidelines based on clinical
history, MRI patterns, and specic locations for
distinguishing between those causes. Patterns
of bone marrow edema involving multiple
bones simultaneously and involving individual
bones of the ankle and hindfoot will be present-
ed. Obvious fractures, tumors, and infection are
mostly excluded from this discussion.
Multifocal Bone Marrow Edema
Common causes of bone marrow edema in
multiple bones in the ankle and foot include
high turnover in children, stress, altered bio-
mechanics, contusions or fractures, immo-
bilization, complex regional pain syndrome
(CRPS), infarcts, osteoarthritis, inamma-
tory arthritis, neuroarthropathy, and tran-
sient osteoporosis. Reliance on the clinical
indications for the study and on MRI nd-
ings such as fracture lines, osteophytosis,
erosions, double line sign, and skin changes
Keywords: ankle, bone marrow edema, foot, MRI
DOI:10.2214/AJR.10.5880
Received September 26, 2010; accepted after revision
February 23, 2011.
OBJECTIVE. Many disorders produce similar or overlapping patterns of bone marrow edema
in the ankle. Bone marrow edema may present in a few hindfoot bones simultaneously or in a sin-
gle bone. The purpose of this pictorial essay is to provide guidelines based on clinical history and
specic MRI patterns and locations to accurately identify the cause of ankle bone marrow edema.
We will rst focus on bone marrow edema in general disease categories involving multiple bones,
such as reactive processes, trauma, neuroarthropathy, and arthritides. A discussion of bone marrow
edema in individual bones of the ankle and hindfoot including the tibia, bula, talus, and calcane-
us will follow. Helpful hints for arriving at the correct diagnosis will be provided in each section.
CONCLUSION. After review of this article, radiologists should be able to use their
knowledge of clinical history and specic MRI patterns and locations to accurately distin-
guish between the various causes of bone marrow edema in the ankle and hindfoot.
Rios et al.
MRI of the Ankle and Hindfoot
Musculoskeletal Imaging
Pictorial Essay
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AJR:197, October 2011 W721
MRI of the Ankle and Hindfoot
or subentheseal and may resolve or stabilize
within 18 weeks [5] (Fig. 3). A history of im-
mobilization and lack of symptoms can aid
in differentiating this process from transient
osteoporosis and CRPS. The latter may also
have distinguishing skin edema and thick-
ening. Infarcts often involve multiple bones
but are typically distinguished by their char-
acteristic serpentine geographic distribution
and the double line sign [2].
A wide range of degenerative and inam-
matory diseases such as osteoarthritis, rheu-
matoid arthritis, and seronegative spondy-
loarthropathies can produce periarticular
subchondral bone marrow edema in multiple
bones. Radiographic correlation as well as
MRI ndings such as osteophytes in osteoar-
thritis, periarticular soft-tissue edema, syno-
vitis, and marginal erosions in rheumatoid ar-
thritis can aid in the diagnosis [6] (Fig. 4A).
A periarticular bone marrow edema pattern
predominantly in the midfoot may also be not-
ed in diabetic patients with acute early neuro-
arthropathy; if imaging is performed before
bone collapse, a clinical history may be re-
quired for distinguishing it from early inam-
matory arthritis [7, 8] (Fig. 4B).
Localized Marrow Edema in Specic
Bones of the Ankle
Focal bone marrow edema isolated to a
single bone is a common nding in the an-
kle. It is often posttraumatic, related to avul-
sion fracture or contusion, but other causes
such as osteoarthrosis, inammatory arthri-
tides, and impingement can also produce fo-
cal bone marrow edema. Accurate MRI di-
agnosis is aided by the clinical history and
by the exact location of the bone marrow
edema relative to adjacent bones, joints, cap-
sule, ligaments, tendons, and fascia. The next
section will focus on various causes of fo-
cal bone marrow edema in each of the bones
of the ankle and hindfoot including the tibia,
bula, talus, and calcaneus.
Distal Tibia
The tibia is susceptible to a variety of bone
marrow edema patterns, many of which are re-
lated to traumatic disorders and their sequelae
such as contusions, occult fractures, and avul-
sions of the exor retinaculum and syndesmot-
ic and deltoid ligaments and impingements.
Reactive bone marrow edema related to poste-
rior tibial tendon (PTT) dysfunction and peri-
articular bone marrow edema secondary to ar-
thropathies may also be encountered. Patterns
of tibial bone marrow edema and their relation-
ship to adjacent osseous and soft-tissue struc-
tures are illustrated in Figure 5.
Diffuse bone marrow edema in the distal tib-
ia, particularly of the posterior malleolus, may
reect a stress or occult fracture [9]. Osteoar-
thritis may also produce a diffuse pattern, al-
beit one that is centered at the tibiotalar artic-
ular surface. Anterior and anteromedial tibial
bone marrow edema, usually related to bony
impingement, may be accompanied by appos-
ing tibial and talar osteophytes, which are easily
detected on radiographs (Fig. 6). Anteromedi-
al and anterolateral tibial bone marrow edema
may be caused by anterior deltoid or anteri-
or tibiobular ligament avulsions, respectively
(Figs. 2 and 7). The bone marrow edema may
be mild, as is typical in avulsion injuries [2].
Posteromedial tibial bone marrow edema
is frequently reactive in the setting of PTT
dysfunction [9, 10] (Fig. 8). Contusions and
osteochondral impaction injuries, also fre-
quently posteromedial, are often associat-
ed with opposing medial talar bone marrow
edema (Fig. 2). Posterior deltoid ligament
avulsion and exor retinacular injury are
other common causes of posteromedial mal-
leolar bone marrow edema [2] (Fig. 8). Mild
posterolateral bone marrow edema may re-
ect posterior tibiobular ligament avulsion.
Distal Fibula
Because the bula is a small bone, various
disease processes may cause diffuse edema.
Nevertheless, focal areas of bone marrow
edema can occur and can be distinguished
from each other based on the appearance of
adjacent osseous and soft-tissue structures
such as ligament attachments and the pero-
neal tendons (Fig. 9).
The proximity of the distal bula to the
coil will often produce artifactual increased
signal on fat-suppressed uid-sensitive imag-
es. Normal bular T1 signal and poor sup-
pression of the adjacent subcutaneous fat
aid in distinguishing this artifact from true
edema (Fig. 10A). Stress and occult frac-
tures often produce diffuse bone marrow
edema. Fibular tip bone marrow edema may
be caused by an avulsion fracture, calcaneo-
bular ligament avulsion, or calcaneobular
impingement (Fig. 10B). Because both stress
fracture and calcaneobular impingement
may occur in the setting of hindfoot valgus,
the two entities can be distinguished by the
presence of a fracture line and of perioste-
al reaction in the setting of a stress fracture
and by the presence of direct contact, scle-
rosis, and edema of the opposing surfaces of
the calcaneus and bula in the setting of im-
pingement [11] (Fig. 11).
Medial distal bular bone marrow edema is
often related to ligamentous avulsion or trac-
tion. Based on our experience, the latter will
often manifest as cystlike changes similar to
those seen at the supraspinatus attachment to
the greater tuberosity; these changes typically
appear above (posterior tibiobular ligament)
or, less commonly, at the level of (posterior talo-
bular ligament) the retromalleolar fossa (Fig.
12). Osteoarthritis may produce medial bular
and opposing talar bone marrow edema.
Lateral and posterolateral bular bone mar-
row edema may result from superior peroneal
retinacular injury or friction due to diseased
or dislocated peroneal tendons [12] (Fig. 13).
Talus
The talus is a common site for bone mar-
row edema on MRI studies. The cause is fre-
quently traumatic because of its key location
between the leg and the foot. Other various
disease processes such as impingement and
inammatory arthritides can also produce
talar bone marrow edema (Fig. 14). A large
amount of the talar surface is cartilaginous,
therefore, osteoarthritis with bone marrow
edema can occur at the opposing surfaces
with the tibial plafond, medial malleolus,
bula, calcaneus, and navicular.
Contusions often produce diffuse talar
bone marrow edema but are more common
medially and may be focal in the talar body,
neck, or head [2] (Fig. 2). Fractures, early
avascular necrosis, transient osteoporosis, and
subchondral insufciency fractures, although
more common in the talar body, can all pro-
duce diffuse bone marrow edema (Fig. 15).
Osteochondral impaction injuries are noted
typically in either the medial or the lateral ta-
lar trochlea and less commonly at the navic-
ular articulation. Bone marrow edema relat-
ed to osteochondral injury is frequent in the
acute phase but may also occur later as a result
of subchondral collapse, cartilage loss, osteo-
arthritis, or cyst formation [2]. Bone marrow
edema as a result of avulsion fracture at the
talar attachment of the deep tibiotalar compo-
nent of the deltoid ligament is an uncommon
cause of medial talar edema (Fig. 16).
Advanced anterior and anteromedial osse-
ous and, less commonly, soft-tissue impinge-
ment can produce opposing tibial and talar
neck bone marrow edema, usually with eas-
ily depicted osteophytes [13] (Fig. 6). Dorsa-
lis pedis penetrating vessels also occur at the
dorsal aspect of the talar neck. Talar head bone
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Rios et al.
marrow edema may be caused by contusion,
impaction fracture, and talonavicular osteo-
arthritis, but the possibility of an occult dor-
sal avulsion fracture at the talonavicular joint
should also be considered (Fig. 17).
Posterior talar bone marrow edema is typ-
ically caused by posterior impingement sec-
ondary to a prominent os trigonum or Stieda
process (Fig. 18). Associated ndings may
include capsular thickening, synovitis, soft-
tissue edema, and exor hallucis longus te-
nosynovitis [13]. Cystic changes in the pos-
terior talus may also result from traction or,
less commonly, from avulsion of the poste-
rior talobular ligament.
Talocalcaneal impingement, which is usu-
ally caused by advanced hindfoot valgus and
PTT dysfunction, may show bone marrow
edema, cysts, and sclerosis in the opposing
lateral talus and calcaneus [11] (Fig. 19). Os-
teoarthritis and occult lateral talar process
fractures also produce talar facet and lateral
talar bone marrow edema.
Bone marrow edema at the roof of the si-
nus tarsi is frequently associated with liga-
ment injury and sinus tarsi syndrome but
may also reect erosions due to inammato-
ry arthritis and deposition disease. Based on
our experience, prominent penetrating ves-
sels are also common in this location.
Calcaneus
Calcaneal bone marrow edema is often en-
countered in the setting of trauma and may be
related to stress and occult fractures and liga-
mentous avulsions. Achilles tendon and per-
oneus longus tendon abnormalities can also
produce isolated calcaneal bone marrow ede-
ma. Fasciitis, osteoarthritis, inammatory
arthritides, and impingement are other causes
of calcaneal bone marrow edema (Fig. 20).
Posterior calcaneal tuberosity bone mar-
row edema is usually caused by Achilles in-
sertional tendinosis with or without Haglund
syndrome but may also be caused by inam-
matory arthritis. A Haglund deformity is a
bone prominence on the superior posterior
aspect of the calcaneal tuberosity. A uid-
distended retrocalcaneal bursa can be seen in
both processes. Helpful distinguishing fea-
tures include Haglund deformity in Haglund
syndrome and erosions in inammatory ar-
thritis [14] (Fig. 21). Stress fracture, typi-
cally with a fracture line, is another cause
of posterior calcaneal tuberosity edema (Fig.
22). The fracture line, which is typically ver-
tically oriented, and associated bone marrow
edema are often located along the anterior
aspect of the posterior calcaneal tuberosity.
Bone marrow edema at the most anterosu-
perior aspect of the calcaneal tuberosity is
noted with posterior impingement, often be-
cause of an enlarged lateral talar process.
Plantar fasciitis with calcaneal enthesop-
athy, as a result of either repetitive trauma
or a seronegative spondyloarthropathy, can
produce plantar calcaneal bone marrow ede-
ma. Enthesopathy at the calcaneal origin of
the plantar ligaments can also produce plan-
tar bone marrow edema. Knowledge of the
patients clinical history and recognition of
other sites of enthesopathy and erosions can
aid in the differential diagnosis [15]. Plan-
tar calcaneal bone marrow edema is uncom-
monly caused by occult extraarticular frac-
ture after a direct fall on the heel.
Medial calcaneal marrow edema is not
very common. When present, it may be sec-
ondary to a fracture, subtalar joint arthrop-
athy, subtalar coalition, or an os sustentacu-
lum. A small focal area of lateral calcaneal
bone marrow edema posterior to the poste-
rior subtalar joint is noted with avulsion of
the calcaneobular ligament (Figs. 2 and 23).
More anteriorly, lateral calcaneal bone mar-
row edema may reect talocalcaneal and cal-
caneobular impingements (Figs. 11 and 24).
Hindfoot valgus, sinus tarsi encroachment,
sclerosis, and cysts at the posterior subtalar
joint at the critical angle of Gissane and at the
distal bula are additional helpful signs [11].
Cystic changes and pooling from penetrating
vessels can also produce increased signal at
the critical angle of Gissane (Fig. 25).
More anteriorly and inferiorly, peroneus
longus tendon abnormalities with or without
hypertrophied peroneal tubercle are addition-
al causes of lateral calcaneal bone marrow
edema [9, 12] (Fig. 26). Fractures of the an-
terior process of the calcaneus, often missed
on radiographs, present with lateral calcaneal
bone marrow edema quite far anteriorly.
Summary
Bone marrow edema is a common and
sometimes confusing nding on MRI studies
of the ankle. The most common cause is trau-
ma and may be related to contusions, stress
or occult fractures, or ligamentous avulsions.
Other causes of ankle bone marrow edema in-
clude impingement, arthropathy, and infarcts.
This pictorial essay addresses these various
causes and provides helpful hints for the MRI
diagnosis based on the clinical history, knowl-
edge of anatomy, and familiarity with specic
patterns of bone marrow edema distribution.
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AJR:197, October 2011 W723
MRI of the Ankle and Hindfoot
Fig. 1High turnover in 12-year-old girl. Sagittal
STIR image shows multiple foci of increased bone
marrow signal associated with increased sports-
related activity.
Fig. 2Inversion injury with multiple foci of bone
marrow edema in 36-year-old man. Medial malleolar
and talar contusions (straight white arrows) and
syndesmotic (curved arrow) and calcaneobular
(black arrow) ligament avulsions are seen on coronal
fat-suppressed T2-weighted image. Note deltoid
injury (white arrowhead) and bular coil artifact
(black arrowhead). Medial malleolar edema may also
reect deltoid or exor retinacular avulsions.
A
Fig. 3Immobilization related to multifocal periarticular bone marrow edema seen on sagittal STIR sequences
of 12-year-old girl.
A, Initial MR image shows small talar osteochondral lesion (arrow).
B, Follow-up MR image obtained after 6 weeks of bracing shows talar osteochondral lesion (arrow) as seen in A
but also depicts extensive bone marrow edema in multiple bones related to disuse osteoporosis.
B
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A
Fig. 4Arthritis-related marrow edema in two patients.
A and B, Coronal intermediate fat-suppressed images of 66-year-old woman with inammatory arthritis (A) and
57-year-old man with acute Charcot arthropathy (B). Periarticular bone marrow edema is noted in both cases,
but presence of erosions (arrow, A) can aid in diagnosis of inammatory arthritis. Clinical history, particularly in
early neuroarthropathy, before development of collapse is also useful in B.
B
Anterior
Impingement (asterisks)
Lateral
ATIFL avulsion
PTIFL avulsion
Tibiofibular arthropathy
Fracture
(dark gray area)
ATIFL
PTIFL
Posterior
Contusion or osteochondral injury
Occult posterior malleolar fracture
Impingement
PTT dysfunction (white oval)
(black dots)
Medial and Posteromedial
Contusion or fracture
Deltoid ligament avulsion
Flexor retinacular injury (arrow)
PTT dysfunction (white oval)
(white dots)
Fig. 5Axial drawing illustrates various causes of bone marrow edema in distal tibia. ATIFL = anterior tibiobular ligament, PTIFL = posterior tibiobular ligament, PTT =
posterior tibial tendon.
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MRI of the Ankle and Hindfoot
Fig. 6Syndesmotic ligament injury in 45-year-old
man. Sagittal STIR image depicts anterior tibial
bone marrow edema as a result of impingement with
opposing tibial and talar osteophytes (arrows) and
effusion.
Fig. 7Syndesmotic ligament injury in 37-year-old
woman. Minimal bone marrow edema, typical of
avulsion injury, is noted on axial proton density fat-
suppressed image at avulsion site of anteroinferior
tibiobular ligament (long arrow) from tibia. Note
also minimal edema (short arrow) in medial tibia as a
result of exor retinaculum injury.
Fig. 8Axial fat-suppressed proton density image
of 47-year-old woman. Partial tear of posterior tibial
tendon (thin arrow) may cause spurring and reactive
bone marrow edema in posteromedial tibia and
medial malleolus (thick arrow).
Lateral and Tip
Coil artifact (dark gray area)
Fibular tip fracture
CFL avulsion
Calcaneofibular impingement
(white stars)
Medial
ATIFL traction or avulsion (black star)
PTIFL traction or avulsion (black asterisk)
Talofibular arthropathy (white shaded area)
Anterior
ATIFL traction or avulsion
(black star)
Diffuse
Stress fracture
PTIFL
ATIFL
PTIFL
PTFL
CFL
Posterior
Peroneal tendon dysfunction
Superior peroneal retinacular injury
PTIFL avulsion (black asterisk)
(white asterisks)
Fig. 9Frontal (top) and axial (bottom)
drawings illustrate various causes of
bone marrow edema in distal bula.
Bone marrow edema pattern in bula
is often nonspecic because of small
size of bula. Nevertheless, in many
instances, exact location of bone
marrow edema can aid in accurate
diagnosis.
PTIFL = posterior tibiobular ligament,
PTFL = posterior talobular ligament,
CFL = calcaneobular ligament,
ATIFL = anterior tibiobular ligament.
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Fig. 10Distal bular tip bone marrow edema.
A and B, Coronal fat-suppressed proton density
images of 37-year-old man (A) and 25-year-old
woman (B) show increased signal in distal bular
tips related to coil artifact (A) and distal bular tip
fracture (B). Proximity of distal bula to coil can
produce artifactual increased signal (star, A) on uid-
sensitive images (A) that may be difcult to discern
from true abnormalities. Normal T1 images of this
area (not shown) supported diagnosis of coil artifact.
Presence of cortical discontinuity (arrow, B) and soft-
tissue edema in B conrm diagnosis of fracture.
A B
Fig. 11Calcaneobular impingement associated
with atfoot in 57-year-old man. Coronal fat-
suppressed proton density image shows direct
contact and bone marrow edema at opposing
surfaces of calcaneus and bula (stars). Increased
tibiocalcaneal angle (lines) indicates hindfoot valgus.
Fig. 12Axial fat-suppressed proton density image
of 35-year-old woman depicts cystlike bone marrow
edema (arrow) as a result of posterior tibiobular
ligament traction on bula.
Fig. 13Superior peroneal retinaculum injury in
37-year-old man. Axial T2-weighted image shows
bone marrow edema in lateral distal bula (long
arrow) secondary to old superior peroneal retinacular
avulsion. Note thickened superior peroneal
retinaculum (short arrow). Peroneal tendons are in
normal position but were clinically dislocatable.
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AJR:197, October 2011 W727
MRI of the Ankle and Hindfoot
Articular Surface and Dome
Tibiotalar arthropathy
Contusion
Subchondral fracture
Osteochondral talar lesion
(black dots)
Lateral
Talocalcaneal impingement
Talobibular arthropathy
Lateral process fracture (jagged black line)
Osteochondral injury (black dots)
(white shaded area)
Medial
Contusion
Osteochondral injury
Tibiotalar arthropathy (white asterisks)
Deltoid avulsion (dotted line)
Neck and Sinus Tarsi
Vascular grooves (dotted line)
Fracture
Anterior impingement (arrow)
Traction sinus tarsi ligaments (white oval)
Erosions (white oval)
(black dots)
Posterior
Posterior impingement (white star)
PTFL traction (black star)
Subtalar arthropathy or coalition (white shaded area)
Talocalcaneal impingement (black asterisk)
Anterior
Talar head impaction or fracture (white dots)
Dorsal talar avulsion fracture (black oval)
Fig. 14Drawings depict various causes of bone marrow edema in talus. Lateral (top) and frontal (bottom) views are shown. PTFL =
posterior talobular ligament.
Fig. 15Subchondral talar insufciency fracture.
Sagittal STIR image of 76-year-old woman shows
diffuse talar bone marrow edema associated with
focal attening and low signal of talar articular
surface (arrow). Bone marrow edema resolved 2
months later.
Fig. 16Deltoid ligament avulsion. Axial fat-
suppressed image of 37-year-old man shows medial
talar edema due to avulsion fracture (arrow) at
talar attachment of deep tibiotalar band of deltoid
ligament.
Fig. 17Sagittal STIR image shows dorsal talar
avulsion fracture (arrow) in 49-year-old man. This
fracture is often missed on radiographs and on MR
images.
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Fig. 18Posterior talar impingement. Sagittal STIR
image of 37-year-old man shows bone marrow edema
in posterior talus as a result of enlarged Stieda
process (star) impinging against calcaneus. Bone
marrow edema in opposing posterior calcaneal
pseudofacetlike prominence (curved arrow) is also
appreciated. There is also synovitis and soft-tissue
edema (straight arrows).
Fig. 19Talocalcaneal impingement as a result of
atfoot deformity and hindfoot valgus. Sagittal STIR
image of 63-year-old woman shows bone marrow
edema and cystic changes in opposing lateral talus
and calcaneus (arrows).
Sinus Tarsi
Vascular grooves
Traction cysts
Osteoid osteoma
(white asterisk)
Anterior
Avulsion injury (black star)
Subchondral impaction (white dots)
Medial
Subtalar coalition
Fracture
Os sustentaculum
(black dots)
Lateral
Calcaneofibular impingement (dark gray area)
Peroneal tendon dysfunction (white oval)
CFL avulsion (black oval)
Subtalar arthropathy
Talocalcaneal impingement
(white shaded area)
Peroneal tendons
(arrow)
Posterior and inferior
Achilles tendinosis
Erosions
Haglund syndrome (white stars)
Stress fracture (jagged black line)
Subtalar arthropathy (white shaded area)
Plantar fasciitis (black asterisk)
Fig. 20Drawings
depict various causes
of bone marrow edema
in calcaneus. Lateral
(top) and frontal (bottom)
views are shown. CFL =
calcaneobular ligament.
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AJR:197, October 2011 W729
MRI of the Ankle and Hindfoot
Fig. 21Haglund syndrome in 55-year-old man.
Bone marrow edema in Haglund deformity (star),
seen on this sagittal STIR image, is associated with
retrocalcaneal bursitis (long arrow) and insertional
Achilles tendinosis (short arrows).
Fig. 22Stress fracture of posterosuperior
calcaneus in 43-year-old woman. Vertical fracture
line (arrows) is outlined by bone marrow edema on
this sagittal STIR image.
Fig. 23Ligament avulsions. Sagittal STIR image
of 38-year-old man shows two foci of minimal bone
marrow edema as a result of avulsions of bifurcate
(long arrow) and calcaneobular (short arrow)
ligaments.
Fig. 24Hindfoot valgus and calcaneobular
impingement in 69-year-old woman. Sagittal STIR
image shows that there is abnormal contact between
distal bula and lateral calcaneus and reveals marked
bone marrow edema and cystic changes of opposing
bony surfaces (arrows).
Fig. 26Peroneus longus tendinosis with calcaneal
friction in 34-year-old man. Axial T2-weighted
image depicts reactive bone marrow edema (white
arrow) as a result of peroneus longus tendon
dysfunction (black arrow).
Fig. 25Calcaneal vascular grooves (arrow), seen
on this sagittal STIR image of 25-year-old woman, at
critical angle of Gissane are common and may
be quite extensive.
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