Bone Marrow Edema Patterns in the Ankle and Hindfoot: Distinguishing MRI Features

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1 Musculoskeletal Imaging Pictorial Essay Rios et al. MRI of the Ankle and Hindfoot Musculoskeletal Imaging Pictorial Essay Adriana Martins Rios 1 Zehava Sadka Rosenberg 2 Jenny Teresa Bencardino 2 Silvia Pérez Rodrigo 3 Sara García Theran 4 Rios AM, Rosenberg ZS, Bencardino JT, Rodrigo SP, Theran SG Keywords: ankle, bone marrow edema, foot, MRI DOI: /AJR Received September 26, 2010; accepted after revision February 23, Department of Radiology, Lifecenter Hospital, Ave do Contorno 4747, Serra, Belo Horizonte , 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, Bogotá, Colombia. WEB This is a Web exclusive article. AJR 2011; 197:W720 W X/11/1974 W720 American Roentgen Ray Society Bone Marrow Edema Patterns in the Ankle and Hindfoot: Distinguishing MRI Features 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 single bone. The purpose of this pictorial essay is to provide guidelines based on clinical history and specific MRI patterns and locations to accurately identify the cause of ankle bone marrow edema. We will first 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, fibula, talus, and calcaneus 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 specific MRI patterns and locations to accurately distinguish between the various causes of bone marrow edema in the ankle and hindfoot. T he term bone marrow edema describes nonspecific, ill-defined areas of hypointense and hyperintense signal on T1-weighted and fluid-sensitive sequences, respectively [1, 2]. The cause of bone marrow edema is unclear and may include fluid, hemorrhage, fibrosis, and necrosis. Various diseases with confusingly similar or overlapping MRI features can cause ankle and hindfoot bone marrow edema. This pictorial essay, focusing on fluid-sensitive sequences, provides guidelines based on clinical history, MRI patterns, and specific 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 presented. 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 biomechanics, contusions or fractures, immobilization, complex regional pain syndrome (CRPS), infarcts, osteoarthritis, inflammatory arthritis, neuroarthropathy, and transient osteoporosis. Reliance on the clinical indications for the study and on MRI findings such as fracture lines, osteophytosis, erosions, double line sign, and skin changes 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, reflecting residual red marrow, hyperemia, increased bone remodeling, or altered weight bearing (Fig. 1). Similarly, multiple foci of bone marrow edema may be seen in physically active individuals after strenuous exercise or as a result of altered gait or weight bearing [4]. The cause, again, is unclear and may reflect marrow hyperplasia, microfracture, or bone repair. Initially asymptomatic, the process can evolve, with continuous overuse, to symptomatic 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 pattern is common after ankle inversion injuries and is often noted in the apposing medial malleolus and talus. It can be painful but typically resolves within a few months. Ligament avulsions after inversion injury can also present with edema, but edema is less prominent in those cases [2] (Fig. 2). Bone marrow edema after immobilization can be patchy, subcortical, subchondral, W720 AJR:197, October 2011

2 MRI of the Ankle and Hindfoot or subentheseal and may resolve or stabilize within 18 weeks [5] (Fig. 3). A history of immobilization and lack of symptoms can aid in differentiating this process from transient osteoporosis and CRPS. The latter may also have distinguishing skin edema and thickening. Infarcts often involve multiple bones but are typically distinguished by their characteristic serpentine geographic distribution and the double line sign [2]. A wide range of degenerative and inflammatory diseases such as osteoarthritis, rheumatoid arthritis, and seronegative spondyloarthropathies can produce periarticular subchondral bone marrow edema in multiple bones. Radiographic correlation as well as MRI findings such as osteophytes in osteoarthritis, periarticular soft-tissue edema, synovitis, and marginal erosions in rheumatoid arthritis can aid in the diagnosis [6] (Fig. 4A). A periarticular bone marrow edema pattern predominantly in the midfoot may also be noted in diabetic patients with acute early neuroarthropathy; if imaging is performed before bone collapse, a clinical history may be required for distinguishing it from early inflammatory 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 ankle. It is often posttraumatic, related to avulsion fracture or contusion, but other causes such as osteoarthrosis, inflammatory arthritides, and impingement can also produce focal bone marrow edema. Accurate MRI diagnosis is aided by the clinical history and by the exact location of the bone marrow edema relative to adjacent bones, joints, capsule, ligaments, tendons, and fascia. The next section will focus on various causes of focal 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 related to traumatic disorders and their sequelae such as contusions, occult fractures, and avulsions of the flexor retinaculum and syndesmotic and deltoid ligaments and impingements. Reactive bone marrow edema related to posterior tibial tendon (PTT) dysfunction and periarticular bone marrow edema secondary to arthropathies may also be encountered. Patterns of tibial bone marrow edema and their relationship to adjacent osseous and soft-tissue structures are illustrated in Figure 5. Diffuse bone marrow edema in the distal tibia, particularly of the posterior malleolus, may reflect a stress or occult fracture [9]. Osteoarthritis may also produce a diffuse pattern, albeit one that is centered at the tibiotalar articular surface. Anterior and anteromedial tibial bone marrow edema, usually related to bony impingement, may be accompanied by apposing tibial and talar osteophytes, which are easily detected on radiographs (Fig. 6). Anteromedial and anterolateral tibial bone marrow edema may be caused by anterior deltoid or anterior 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 frequently posteromedial, are often associated with opposing medial talar bone marrow edema (Fig. 2). Posterior deltoid ligament avulsion and flexor retinacular injury are other common causes of posteromedial malleolar bone marrow edema [2] (Fig. 8). Mild posterolateral bone marrow edema may reflect 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 distinguished from each other based on the appearance of adjacent osseous and soft-tissue structures such as ligament attachments and the peroneal tendons (Fig. 9). The proximity of the distal fibula to the coil will often produce artifactual increased signal on fat-suppressed fluid-sensitive images. Normal fibular T1 signal and poor suppression of the adjacent subcutaneous fat aid in distinguishing this artifact from true edema (Fig. 10A). Stress and occult fractures often produce diffuse bone marrow edema. Fibular tip bone marrow edema may be caused by an avulsion fracture, calcaneofibular 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 periosteal reaction in the setting of a stress fracture and by the presence of direct contact, sclerosis, and edema of the opposing surfaces of the calcaneus and fibula in the setting of impingement [11] (Fig. 11). Medial distal fibular bone marrow edema is often related to ligamentous avulsion or traction. 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 tibiofibular ligament) or, less commonly, at the level of (posterior talofibular ligament) the retromalleolar fossa (Fig. 12). Osteoarthritis may produce medial fibular and opposing talar bone marrow edema. Lateral and posterolateral fibular bone marrow 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 marrow edema on MRI studies. The cause is frequently 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, early avascular necrosis, transient osteoporosis, and subchondral insufficiency fractures, although more common in the talar body, can all produce diffuse bone marrow edema (Fig. 15). Osteochondral impaction injuries are noted typically in either the medial or the lateral talar trochlea and less commonly at the navicular articulation. Bone marrow edema related to osteochondral injury is frequent in the acute phase but may also occur later as a result of subchondral collapse, cartilage loss, osteoarthritis, or cyst formation [2]. Bone marrow edema as a result of avulsion fracture at the talar attachment of the deep tibiotalar component of the deltoid ligament is an uncommon cause of medial talar edema (Fig. 16). Advanced anterior and anteromedial osseous and, less commonly, soft-tissue impingement can produce opposing tibial and talar neck bone marrow edema, usually with easily depicted osteophytes [13] (Fig. 6). Dorsalis pedis penetrating vessels also occur at the dorsal aspect of the talar neck. Talar head bone AJR:197, October 2011 W721

3 Rios et al. marrow edema may be caused by contusion, impaction fracture, and talonavicular osteoarthritis, but the possibility of an occult dorsal avulsion fracture at the talonavicular joint should also be considered (Fig. 17). Posterior talar bone marrow edema is typically caused by posterior impingement secondary to a prominent os trigonum or Stieda process (Fig. 18). Associated findings may include capsular thickening, synovitis, softtissue edema, and flexor hallucis longus tenosynovitis [13]. Cystic changes in the posterior talus may also result from traction or, less commonly, from avulsion of the posterior talofibular ligament. Talocalcaneal impingement, which is usually 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). Osteoarthritis and occult lateral talar process fractures also produce talar facet and lateral talar bone marrow edema. Bone marrow edema at the roof of the sinus tarsi is frequently associated with ligament injury and sinus tarsi syndrome but may also reflect erosions due to inflammatory arthritis and deposition disease. Based on our experience, prominent penetrating vessels are also common in this location. Calcaneus Calcaneal bone marrow edema is often encountered in the setting of trauma and may be related to stress and occult fractures and ligamentous avulsions. Achilles tendon and peroneus longus tendon abnormalities can also produce isolated calcaneal bone marrow edema. Fasciitis, osteoarthritis, inflammatory arthritides, and impingement are other causes of calcaneal bone marrow edema (Fig. 20). Posterior calcaneal tuberosity bone marrow edema is usually caused by Achilles insertional tendinosis with or without Haglund syndrome but may also be caused by inflammatory arthritis. A Haglund deformity is a bone prominence on the superior posterior aspect of the calcaneal tuberosity. A fluiddistended retrocalcaneal bursa can be seen in both processes. Helpful distinguishing features include Haglund deformity in Haglund syndrome and erosions in inflammatory arthritis [14] (Fig. 21). Stress fracture, typically with a fracture line, is another cause of posterior calcaneal tuberosity edema (Fig. 22). The fracture line, which is typically vertically oriented, and associated bone marrow edema are often located along the anterior aspect of the posterior calcaneal tuberosity. Bone marrow edema at the most anterosuperior aspect of the calcaneal tuberosity is noted with posterior impingement, often because of an enlarged lateral talar process. Plantar fasciitis with calcaneal enthesopathy, as a result of either repetitive trauma or a seronegative spondyloarthropathy, can produce plantar calcaneal bone marrow edema. Enthesopathy at the calcaneal origin of the plantar ligaments can also produce plantar bone marrow edema. Knowledge of the patient s clinical history and recognition of other sites of enthesopathy and erosions can aid in the differential diagnosis [15]. Plantar calcaneal bone marrow edema is uncommonly caused by occult extraarticular fracture after a direct fall on the heel. Medial calcaneal marrow edema is not very common. When present, it may be secondary to a fracture, subtalar joint arthropathy, subtalar coalition, or an os sustentaculum. A small focal area of lateral calcaneal bone marrow edema posterior to the posterior subtalar joint is noted with avulsion of the calcaneofibular ligament (Figs. 2 and 23). More anteriorly, lateral calcaneal bone marrow edema may reflect talocalcaneal and calcaneofibular 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 at the critical angle of Gissane (Fig. 25). More anteriorly and inferiorly, peroneus longus tendon abnormalities with or without hypertrophied peroneal tubercle are additional causes of lateral calcaneal bone marrow edema [9, 12] (Fig. 26). Fractures of the anterior 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 trauma and may be related to contusions, stress or occult fractures, or ligamentous avulsions. Other causes of ankle bone marrow edema include impingement, arthropathy, and infarcts. This pictorial essay addresses these various causes and provides helpful hints for the MRI diagnosis based on the clinical history, knowledge 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 enhanced fat-suppressed spin-echo MR imaging. Radiology 2002; 224: Weishaupt D, Schweitzer ME. MR imaging of the foot and ankle: patterns of bone marrow signal abnormalities. Eur Radiol 2002; 12: 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 traumatic changes. Pediatr Radiol 2006; 36: Schweitzer ME, White LM. Does altered biomechanics cause marrow edema? Radiology 1996; 198: Elias I, Zoga AC, Schweitzer ME, Ballehr L, Morrison WB, Raikin SM. A specific bone marrow edema around the foot and ankle following trauma and immobilization therapy: pattern description and potential clinical relevance. Foot Ankle Int 2007; 28: 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: Chatha DS, Cunningham PM, Schweitzer ME. MR imaging of the diabetic foot: diagnostic challenges. Radiol Clin North Am 2005; 43: Ahmadi ME, Morrison WB, Carrino JA, et al. Neuropathic arthropathy of the foot with and without superimposed osteomyelitis: MR imaging characteristics. Radiology 2006; 238: Rosenberg ZS, Beltran J, Bencardino JT. From the RSNA refresher course: Radiological Society of North America MR imaging of the ankle and foot. RadioGraphics 2000; 20:S153 S Morrison WB, Carrino JA, Schweitzer ME, Sanders TG, Raiken DP, Johnson CE. Subtendinous bone marrow edema patterns on MR images of the ankle: association with symptoms and tendinopathy. AJR 2001; 176: Donovan A, Rosenberg ZS. Extraarticular lateral hindfoot impingement with posterior tibial tendon tear: MRI correlation. AJR 2009; 193: Wang XT, Rosenberg ZS, Mechlin MB, Schweitzer ME. Normal variants and diseases of the peroneal tendons and superior peroneal retinaculum: MR imaging features. RadioGraphics 2005; 25: [Errata in RadioGraphics 2005; 25:1436 and RadioGraphics 2006; 26:640] 13. Hopper MA, Robinson P. Ankle impingement syndromes. Radiol Clin North Am 2008; 46: Schweitzer ME, Karasick D. MR imaging of disorders of the Achilles tendon. AJR 2000; 175: Narváez JA, Narváez J, Ortega R, et al. Painful heel: MR imaging findings. RadioGraphics 2000; 20: W722 AJR:197, October 2011

4 MRI of the Ankle and Hindfoot Fig. 1 High turnover in 12-year-old girl. Sagittal STIR image shows multiple foci of increased bone marrow signal associated with increased sportsrelated activity. A Fig. 2 Inversion 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 calcaneofibular (black arrow) ligament avulsions are seen on coronal fat-suppressed T2-weighted image. Note deltoid injury (white arrowhead) and fibular coil artifact (black arrowhead). Medial malleolar edema may also reflect deltoid or flexor retinacular avulsions. Fig. 3 Immobilization 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 AJR:197, October 2011 W723

5 Rios et al. Medial and Posteromedial Contusion or fracture Deltoid ligament avulsion Flexor retinacular injury (arrow) PTT dysfunction (white oval) A Fig. 4 Arthritis-related marrow edema in two patients. A and B, Coronal intermediate fat-suppressed images of 66-year-old woman with inflammatory 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 inflammatory arthritis. Clinical history, particularly in early neuroarthropathy, before development of collapse is also useful in B. (white dots) Anterior Impingement (asterisks) Posterior Contusion or osteochondral injury Occult posterior malleolar fracture Impingement PTT dysfunction (white oval) ATIFL PTIFL (black dots) B Lateral ATIFL avulsion PTIFL avulsion Tibiofibular arthropathy Fracture (dark gray area) Fig. 5 Axial drawing illustrates various causes of bone marrow edema in distal tibia. ATIFL = anterior tibiofibular ligament, PTIFL = posterior tibiofibular ligament, PTT = posterior tibial tendon. W724 AJR:197, October 2011

6 MRI of the Ankle and Hindfoot Fig. 6 Syndesmotic 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. Medial ATIFL traction or avulsion (black star) PTIFL traction or avulsion (black asterisk) Talofibular arthropathy (white shaded area) PTIFL PTFL Fig. 7 Syndesmotic ligament injury in 37-year-old woman. Minimal bone marrow edema, typical of avulsion injury, is noted on axial proton density fatsuppressed image at avulsion site of anteroinferior tibiofibular ligament (long arrow) from tibia. Note also minimal edema (short arrow) in medial tibia as a result of flexor retinaculum injury. ATIFL PTIFL Posterior Peroneal tendon dysfunction Superior peroneal retinacular injury PTIFL avulsion (black asterisk) CFL Diffuse Stress fracture Lateral and Tip Coil artifact (dark gray area) Fibular tip fracture CFL avulsion Calcaneofibular impingement (white asterisks) Fig. 8 Axial 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). (white stars) Anterior ATIFL traction or avulsion (black star) Fig. 9 Frontal (top) and axial (bottom) drawings illustrate various causes of bone marrow edema in distal fibula. Bone marrow edema pattern in fibula is often nonspecific because of small size of fibula. Nevertheless, in many instances, exact location of bone marrow edema can aid in accurate diagnosis. PTIFL = posterior tibiofibular ligament, PTFL = posterior talofibular ligament, CFL = calcaneofibular ligament, ATIFL = anterior tibiofibular ligament. AJR:197, October 2011 W725

7 Rios et al. Fig. 11 Calcaneofibular impingement associated with flatfoot in 57-year-old man. Coronal fatsuppressed proton density image shows direct contact and bone marrow edema at opposing surfaces of calcaneus and fibula (stars). Increased tibiocalcaneal angle (lines) indicates hindfoot valgus. A Fig. 12 Axial fat-suppressed proton density image of 35-year-old woman depicts cystlike bone marrow edema (arrow) as a result of posterior tibiofibular ligament traction on fibula. B Fig. 10 Distal fibular 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 fibular tips related to coil artifact (A) and distal fibular tip fracture (B). Proximity of distal fibula to coil can produce artifactual increased signal (star, A) on fluidsensitive images (A) that may be difficult 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 softtissue edema in B confirm diagnosis of fracture. Fig. 13 Superior peroneal retinaculum injury in 37-year-old man. Axial T2-weighted image shows bone marrow edema in lateral distal fibula (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. W726 AJR:197, October 2011

8 MRI of the Ankle and Hindfoot Neck and Sinus Tarsi Vascular grooves (dotted line) Fracture Anterior impingement (arrow) Traction sinus tarsi ligaments (white oval) Erosions (white oval) Articular Surface and Dome Tibiotalar arthropathy Contusion Subchondral fracture Osteochondral talar lesion (black dots) Anterior Talar head impaction or fracture (white dots) Dorsal talar avulsion fracture (black oval) Medial Contusion (black dots) Osteochondral injury Tibiotalar arthropathy (white asterisks) Deltoid avulsion (dotted line) Posterior Posterior impingement (white star) PTFL traction (black star) Subtalar arthropathy or coalition (white shaded area) Talocalcaneal impingement (black asterisk) Lateral Talocalcaneal impingement (white shaded area) Talobibular arthropathy Lateral process fracture (jagged black line) Osteochondral injury (black dots) Fig. 14 Drawings depict various causes of bone marrow edema in talus. Lateral (top) and frontal (bottom) views are shown. PTFL = posterior talofibular ligament. Fig. 15 Subchondral talar insufficiency fracture. Sagittal STIR image of 76-year-old woman shows diffuse talar bone marrow edema associated with focal flattening and low signal of talar articular surface (arrow). Bone marrow edema resolved 2 months later. Fig. 16 Deltoid ligament avulsion. Axial fatsuppressed 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. 17 Sagittal STIR image shows dorsal talar avulsion fracture (arrow) in 49-year-old man. This fracture is often missed on radiographs and on MR images. AJR:197, October 2011 W727

9 Rios et al. Anterior Avulsion injury (black star) Subchondral impaction (white dots) Sinus Tarsi Vascular grooves Traction cysts Osteoid osteoma Medial Subtalar coalition Fracture Os sustentaculum Fig. 18 Posterior 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). (white asterisk) (black dots) Fig. 19 Talocalcaneal impingement as a result of flatfoot 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). Lateral Calcaneofibular impingement (dark gray area) Peroneal tendon dysfunction (white oval) CFL avulsion (black oval) Subtalar arthropathy (white shaded area) Talocalcaneal impingement Peroneal tendons Posterior and inferior Achilles tendinosis (arrow) Erosions Haglund syndrome (white stars) Stress fracture (jagged black line) Subtalar arthropathy (white shaded area) Plantar fasciitis (black asterisk) Fig. 20 Drawings depict various causes of bone marrow edema in calcaneus. Lateral (top) and frontal (bottom) views are shown. CFL = calcaneofibular ligament. W728 AJR:197, October 2011

10 MRI of the Ankle and Hindfoot Fig. 21 Haglund 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. 24 Hindfoot valgus and calcaneofibular impingement in 69-year-old woman. Sagittal STIR image shows that there is abnormal contact between distal fibula and lateral calcaneus and reveals marked bone marrow edema and cystic changes of opposing bony surfaces (arrows). Fig. 22 Stress 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. 25 Calcaneal 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. Fig. 23 Ligament 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 calcaneofibular (short arrow) ligaments. Fig. 26 Peroneus 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). AJR:197, October 2011 W729