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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 inflam-

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 findings 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 inflam-

matory arthritis [7, 8] (Fig. 4B).

Localized Marrow Edema in Specific

Bones of the Ankle

Focal bone marrow edema isolated to a

single bone is a common finding in the an-

kle. It is often posttraumatic, related to avul-

sion fracture or contusion, but other causes

such as osteoarthrosis, inflammatory 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,

fibula, 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 flexor 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

reflect 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 tibialbone 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 tibiofibular 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 flexor retinacular injury are

other common causes of posteromedial mal-

leolar bone marrow edema [2] (Fig. 8). Mild

posterolateral bone marrow edema may re-

flect posterior tibiofibular ligament avulsion.

Distal Fibula

Because the fibula is a small bone, various

disease processes may cause diffuse edema.

Nevertheless, focal areas of bone marrow

edema can occur and can be distinguishedfrom 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 fibula to the

coil will often produce artifactual increased

signal on fat-suppressed fluid-sensitive imag-

es. Normal fibular 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-fibular ligament avulsion, or calcaneofibular

impingement (Fig. 10B). Because both stress

fracture and calcaneofibular 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 fibula in the setting of im-

pingement [11] (Fig. 11).

Medial distal fibular 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 typicallyappear above (posterior tibiofibular ligament)

or, less commonly, at the level of (posterior talo-

fibular ligament) the retromalleolar fossa (Fig.

12). Osteoarthritis may produce medial fibular

and opposing talar bone marrow edema.

Lateral and posterolateral fibular 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

inflammatory 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,

fibula, 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, earlyavascular necrosis, transient osteoporosis, and

subchondral insufficiency 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 Stiedaprocess (Fig. 18). Associated findings may

include capsular thickening, synovitis, soft-

tissue edema, and flexor 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 talofibular 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 reflect erosions due to inflammato-

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, inflammatory

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 inflam-

matory arthritis. A Haglund deformity is a

bone prominence on the superior posterior

aspect of the calcaneal tuberosity. A fluid-

distended retrocalcaneal bursa can be seen inboth processes. Helpful distinguishing fea-

tures include Haglund deformity in Haglund

syndrome and erosions in inflammatory 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, canproduce 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 calcaneofibular ligament (Figs. 2 and 23).

More anteriorly, lateral calcaneal bone mar-

row edema may reflect talocalcaneal and cal-

caneofibular 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 fibula are additional helpful signs [11].

Cystic changes and pooling from penetrating

vessels can also produce increased signal atthe 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 finding 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 specific

patterns of bone marrow edema distribution.

References

1. Schmid MR, Hodler J, Vienne P, Binkert CA,

Zanetti M. Bone marrow abnormalities of foot

and ankle: STIR versus T1-weighted contrast en-

hanced fat-suppressed spin-echo MR imaging.

Radiology2002; 224:463469

2. Weishaupt D, Schweitzer ME. MR imaging of the

foot and ankle: patterns of bone marrow signal

abnormalities.Eur Radiol 2002; 12:416426

3. Shabshin N, Schweitzer ME, Morrison WB, et al.

High-signal T2 changes of the bone marrow of the

foot and ankle in children: red marrow or trau-

matic changes. Pediatr Radiol2006; 36:670676

4. Schweitzer ME, White LM. Does altered biome-

chanics cause marrow edema? Radiology 1996;

198:851853

5. Elias I, Zoga AC, Schweitzer ME, Ballehr L,

Morrison WB, Raikin SM. A specific bone mar-

row edema around the foot and ankle following

trauma and immobilization therapy: pattern de-

scription and potential clinical relevance. Foot

Ankle Int2007; 28:463471

6. Weishaupt D, Schweitzer ME, Alam F, Karasick

D, Wapner K. MR imaging of inflammatory joint

diseases of the foot and ankle. Skeletal Radiol

1999; 28:663669

7. Chatha DS, Cunningham PM, Schweitzer ME.

MR imaging of the diabetic foot: diagnostic chal-

lenges.Radiol Clin North Am2005; 43:747759

8. Ahmadi ME, Morrison WB, Carrino JA, et al.

Neuropathic arthropathy of the foot with and

without superimposed osteomyelitis: MR imag-

ing characteristics.Radiology2006; 238:622631

9. Rosenberg ZS, Beltran J, Bencardino JT. From the

RSNA refresher course: Radiological Society ofNorth AmericaMR imaging of the ankle and

foot.RadioGraphics2000; 20:S153S179

10. Morrison WB, Carrino JA, Schweitzer ME, Sand-

ers TG, Raiken DP, Johnson CE. Subtendinous

bone marrow edema patterns on MR images of

the ankle: association with symptoms and tendi-

nopathy.AJR2001; 176:11491154

11. Donovan A, Rosenberg ZS. Extraarticular lateral

hindfoot impingement with posterior tibial tendon

tear: MRI correlation.AJR2009; 193:672678

12. Wang XT, Rosenberg ZS, Mechlin MB, Sch-

weitzer ME. Normal variants and diseases of the

peroneal tendons and superior peroneal retinacu-

lum: MR imaging features.RadioGraphics2005;

25:587602 [Errata in RadioGraphics 2005;

25:1436 andRadioGraphics2006; 26:640]

13. Hopper MA, Robinson P. Ankle impingement syn-

dromes.Radiol Clin North Am2008; 46:957971

14. Schweitzer ME, Karasick D. MR imaging of disor-

ders of the Achilles tendon.AJR2000; 175:613625

15. Narvez JA, Narvez J, Or tega R, et al. Painful

heel: MR imaging findings.RadioGraphics2000;

20:333352


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Fig. 1High turnover in 12-year-old girl. SagittalSTIR image shows multiple foci of increased bonemarrow signal associated with increased sports-

related activity.

Fig. 2Inversion injury with multiple foci of bonemarrow edema in 36-year-old man. Medial malleolarand talar contusions (straight white arrows) and

syndesmotic (curved arrow) and calcaneofibular(black arrow) ligament avulsions are seen on coronalfat-suppressed T2-weighted image. Note deltoidinjury (white arrowhead) and fibular coil artifact(black arrowhead). Medial malleolar edema may alsoreflect deltoid or flexor retinacular avulsions.

A

Fig. 3Immobilization related to multifocal periarticular bone marrow edema seen on sagittal STIR sequencesof 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 Abut 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.Aand B,Coronal intermediate fat-suppressed images of 66-year-old woman with inflammatory arthritis ( A) and57-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 inflammatory arthritis. Clinical history, particularly inearly neuroarthropathy, before development of collapse is also useful in B.

B

AnteriorImpingement (asterisks)

LateralATIFL avulsionPTIFL avulsionTibiofibular arthropathy

Fracture(dark gray area)

ATIFL

PTIFL

PosteriorContusion or osteochondral injuryOccult posterior malleolar fracture

ImpingementPTT dysfunction (white oval)

(black dots)

Medial and PosteromedialContusion or fractureDeltoid ligament avulsionFlexor retinacular injury (arrow)PTT dysfunction (white oval)

(white dots)

Fig. 5Axial drawing illustrates various causes of bone marrow edema in distal tibia. ATIFL = anterior tibiofibular ligament, PTIFL = posterior tibiofibular ligament, PTT =posterior tibial tendon.


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Fig. 6Syndesmotic ligament injury in 45-year-oldman. Sagittal STIR image depicts anterior tibialbone marrow edema as a result of impingement wi thopposing tibial and talar osteophytes (arrows) and

effusion.

Fig. 7Syndesmotic ligament injury in 37-year-oldwoman. Minimal bone marrow edema, typical ofavulsion injury, is noted on axial proton density fat-suppressed image at avulsion site of anteroinferior

tibiofibular ligament (long arrow) from tibia. Notealso minimal edema (short arrow) in medial tibia as aresult of flexor retinaculum injury.

Fig. 8Axial fat-suppressed proton density imageof 47-year-old woman. Partial tear of posterior tibial

tendon (thinarrow) may cause spurring and reactivebone marrow edema in posteromedial tibia and

medial malleolus (thickarrow).

Lateral and TipCoil artifact (dark gray area)Fibular tip fracture

CFL avulsion

Calcaneofibular impingement

(white stars)

MedialATIFL traction or avulsion (black star)

PTIFL traction or avulsion (black asterisk)

Talofibular arthropathy (white shaded area)

AnteriorATIFL traction or avulsion

(black star)

DiffuseStress fracturePTIFL

ATIFL

PTIFL

PTFL

CFL

PosteriorPeroneal tendon dysfunctionSuperior peroneal retinacular injury

PTIFL avulsion (black asterisk)

(white asterisks)

Fig. 9Frontal (top) and axial (bottom)drawings illustrate various causes ofbone marrow edema in distal fibula.Bone marrow edema pattern in fibulais often nonspecific because of smallsize of fibula. Nevertheless, in manyinstances, exact location of bonemarrow edema can aid in accuratediagnosis.PTIFL = posterior tibiofibular ligament,PTFL = posterior talofibular ligament,CFL = calcaneofibular ligament,ATIFL = anterior tibiofibular ligament.


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Fig. 10Distal fibular tip bone marrow edema.Aand B, Coronal fat-suppressed proton densityimages of 37-year-old man (A) and 25-year-oldwoman (B) show increased signal in distal fibular

tips related to coil artifact (A) and distal fibular tipfracture (B). Proximity of distal fibula to coil canproduce artifactual increased signal (star, A) on fluid-sensitive images (A) that may be difficult to discernfrom 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 Bconfirm diagnosis of fracture.

A B

Fig. 11Calcaneofibular impingement associatedwith flatfoot in 57-year-old man. Coronal fat-suppressed proton density image shows directcontact and bone marrow edema at opposingsurfaces of calcaneus and fibula (stars). Increased

tibiocalcaneal angle (lines) indicates hindfoot valgus.

Fig. 12Axial fat-suppressed proton density imageof 35-year-old woman depicts cystlike bone marrowedema (arrow) as a result of posterior tibiofibularligament traction on fibula.

Fig. 13Superior peroneal retinaculum injury in37-year-old man. Axial T2-weighted image showsbone marrow edema in lateral distal fibula ( longarrow) secondary to old superior peroneal retinacularavulsion. Note thickened superior peronealretinaculum (short arrow). Peroneal tendons are innormal position but were clinically dislocatable.


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Articular Surface and DomeTibiotalar arthropathy

Contusion

Subchondral fracture

Osteochondral talar lesion

(black dots)

Lateral

Talocalcaneal impingementTalobibular arthropathy

Lateral process fracture (jagged black line)

Osteochondral injury (black dots)

(white shaded area)

MedialContusion

Osteochondral injury

Tibiotalar arthropathy (white asterisks)

Deltoid avulsion (dotted line)

Neck and Sinus TarsiVascular 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)

AnteriorTalar 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 talofibular ligament.

Fig. 15Subchondral talar insufficiency fracture.Sagittal ST IR image of 76-year-old woman showsdiffuse talar bone marrow edema associated withfocal flattening and lo w signal of talar articularsurface (arrow). Bone marrow edema resolved 2months later.

Fig. 16Deltoid ligament avulsion. Axial fat-suppressed image of 37-year-old man shows medial

talar edema due to avulsion fr acture (arrow) attalar at tachmen t of deep tib iotal ar band of del toidligament.

Fig. 17Sagittal STIR image shows dorsal talaravulsion fracture (arrow) in 49-year-old man. Thisfracture is often missed on radiographs and on MRimages.


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Fig. 18Posterior talar impingement. Sagittal STIRimage of 37-year-old man shows bone marrow edemain posterior talus as a result of enlarged Stieda

process (star) impinging against calcaneus. Bonemarrow edema in opposing posterior calcanealpseudofacetlike prominence (curved arrow) is alsoappreciated. There is also synovitis and soft-tissueedema (straight arrows).

Fig. 19Talocalcaneal impingement as a result offlatfoot deformity and hindfoot valgus. Sagittal STIRimage of 63-year-old woman shows bone marrow

edema and cystic changes in opposing lateral talusand calcaneus (arrows).

Sinus TarsiVascular grooves

Traction cysts

Osteoid osteoma

(white asterisk)

AnteriorAvulsion injury (black star)

Subchondral impaction (white dots)

MedialSubtalar coalition

FractureOs sustentaculum

(black dots)

LateralCalcaneofibular 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 inferiorAchilles tendinosis

Erosions

Haglund syndrome (white stars)

Stress fracture (jagged black line)

Subtalar arthropathy (white shaded area)Plantar fasciitis (black asterisk)

Fig. 20Drawingsdepict various causesof bone marrow edemain calcaneus. Lateral(top) and frontal (bottom)views are shown. CFL =calcaneofibular ligament.


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Fig. 21Haglund syndrome in 55-year-old man.

Bone marrow edema in Haglund deformity (star),seen on this sagittal STIR image, is associated withretrocalcaneal bursitis (long arrow) and insertionalAchilles tendinosis (short arrows).

Fig. 22Stress fracture of posterosuperior

calcaneus in 43-year-old woman. Vertical fractureline (arrows) is outlined by bone marrow edema onthis sagi ttal STIR image.

Fig. 23Ligament avulsions. Sagittal STIR image

of 38-year-old man shows two foci of minimal bonemarrow edema as a result of avulsions of bifurcate(long arrow) and calcaneofibular (short arrow)ligaments.

Fig. 24Hindfoot valgus and calcaneofibularimpingement in 69-year-old woman. Sagittal STIRimage shows that there is abnormal contact betweendistal fibula and lateral calcaneus and reveals markedbone marrow edema and cystic changes of opposing

bony surfaces (arrows).

Fig. 26Peroneus longus tendinosis with calcanealfriction in 34-year-old man. Axial T2-weightedimage depicts reactive bone marrow edema (whitearrow) as a result of peroneus longus ten dondysfunction (black arrow).

Fig. 25Calcaneal vascular grooves (arrow), seenon this sagittal STIR image of 25-year-old woman, atcritical angle of Gissane are common and maybe quite extensive.

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