Tibial cortical lesions: a multimodality pictorial review.

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Review

Tibial cortical lesions: A multimodality pictorial review P.A. Tyler a,∗ , P. Mohaghegh a , J. Foley b , A. Isaac c , A. Zavareh d , C. Thorning e , A. Kirwadi f , I. Pressney a , F. Amary g , G. Rajeswaran h a

Department of Radiology, Royal National Orthopaedic Hospital, Brockley Hill, Stanmore HA7 4LP, UK Department of Radiology, Glasgow Royal Infirmary, 16 Alexandra Parade, Glasgow G31 2ES, UK Department of Radiology, King’s College Hospital, Denmark Hill, London SE5 9RS, UK d Department of Radiology, North Bristol NHS Trust, Frenchay, Bristol BS16 1LE, UK e Department of Radiology, East Surrey Hospital, Canada Avenue, Redhill, Surrey RH1 5RH, UK f Department of Radiology, Manchester Royal Infirmary, Oxford Road, Manchester M13 9WL, UK g Department of Histopathology, Royal National Orthopaedic Hospital, Brockley Hill, Stanmore HA7 4LP, UK h Department of Radiology, Chelsea and Westminster Hospital, 369 Fulham Road, London SW10 9NH, UK b c

a r t i c l e

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Article history: Received 1 April 2014 Received in revised form 1 July 2014 Accepted 9 September 2014 Keywords: Bone Tibia Plain radiographs Magnetic resonance imaging Computer tomography

a b s t r a c t Shin pain is a common complaint, particularly in young and active patients, with a wide range of potential diagnoses and resulting implications. We review the natural history and multimodality imaging findings of the more common causes of cortically-based tibial lesions, as well as the rarer pathologies less frequently encountered in a general radiology department. © 2014 Published by Elsevier Ireland Ltd.

1. Introduction Shin pain is a relatively frequent cause of patient presentation to clinicians and there are a wide variety of cortically based tibial lesions that should be considered in the differential diagnosis. This can cause difficulty for both the clinician and the radiologist when trying to appropriately diagnose and manage the patient. Although an accurate clinical history and examination are extremely important, with the advent of modern techniques, imaging is now essential to either make a definitive diagnosis or to identify those lesions that require biopsy or surgical excision. As a general rule, all patients with a suspected tibial cortical lesion should have a radiograph performed and depending on the findings, cross-sectional imaging can then be used for further evaluation if required. We present a pictorial review of the commonly

∗ Corresponding author. E-mail addresses: [email protected] (P.A. Tyler), [email protected] (P. Mohaghegh), [email protected] (J. Foley), [email protected] (A. Isaac), [email protected] (A. Zavareh), [email protected] (C. Thorning), [email protected] (A. Kirwadi), [email protected] (I. Pressney), [email protected] (F. Amary), [email protected] (G. Rajeswaran).

encountered and important tibial cortical lesions, emphasising the role of CT and MRI and subdividing lesions (for ease of evaluation) into: non-neoplastic and neoplastic.

2. Non-neoplastic tibial cortical lesions 2.1. Tibial stress injuries Tibial stress injuries are the commonest cause of exertional leg pain in athletes, accounting for up to 75% of cases [1]. Stress injuries cause remodelling of bone which progresses as a continuum from osteoclastic bone resorption initially to increased osteoblastic activity as well as periosteal and endosteal proliferation. This results in an imbalance that weakens bone and if untreated can be complicated by fracture. When stress injuries are present, they may be classified as due to fatigue (increased stresses on normal bone) secondary to prolonged repetitive activity or, less commonly, to insufficiency (normal stresses on abnormal bone) secondary to a variety of conditions including osteoporosis, osteomalacia and rheumatoid arthritis [2]. Medial tibial stress syndrome (shin splints) is the term given to stress injuries of the tibia due to fatigue usually in long distance runners. It was first described by Hutchins in 1913 as

http://dx.doi.org/10.1016/j.ejrad.2014.09.006 0720-048X/© 2014 Published by Elsevier Ireland Ltd.

Please cite this article in press as: Tyler PA, et al. Tibial cortical lesions: A multimodality pictorial review. Eur J Radiol (2014), http://dx.doi.org/10.1016/j.ejrad.2014.09.006

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Fig. 1. (a) AP radiograph of the leg demonstrating a periosteal reaction associated with a stress fracture (arrow). (b) Lateral radiograph of the leg, showing diffuse cortical thickening of the anterior tibial diaphysis. (c) Lateral radiograph of the leg demonstrating a subtle linear lucency (arrow).

“spike soreness” in athletes wearing running spikes and is characterised by exercise-induced pain along the posteromedial aspect of the distal 2/3 of the tibia [3]. It results from repetitive mechanical stresses at the insertions of Sharpey’s fibres that connect the medial soleus, the flexor digitorum and their investing fascia to the periosteum of the tibia. In children and short distance runners, fatigue stress injuries occur more proximally in the tibia [4]. Overt fractures may be sclerotic (due to compressive forces) or lucent and transverse, oblique or longitudinal depending on the type and direction of stress [5]. 2.1.1. Plain radiography Radiographs are often used as the first imaging test for a suspected stress injury due to easy availability and relatively low cost. However, they are negative in roughly one third of symptomatic patients and the majority of cortical fractures (up to 94%) go undetected [6,7]. They demonstrate relatively late findings of stress injury including a benign-appearing periosteal callous reaction (Fig. 1a), eccentric thickening and increased sclerosis of the cortex and endosteum (Fig. 1b) and a lucent fracture line (Fig. 1c). The affected cortex may also be osteopaenic and contain small lucent foci, cavitations and striations. 2.1.2. Bone scintigraphy Bone scintigraphy is much more sensitive than radiography and used to be the gold standard imaging test for a stress injury.

However, magnetic resonance imaging (MRI) in particular is now felt to be more sensitive and specific [6,8]. Bone scintigraphy is used preferentially over MRI in patients who are claustrophobic or have contraindications or in patients with multiple suspected insufficiency fractures. Scintigraphy demonstrates the increased bone metabolic activity associated with a stress injury as an area of increased uptake of Technechium-99m methylene diphosphonate (Fig. 2a and b). 2.1.3. MRI MRI is the most sensitive test for diagnosing the early signs of stress injury, particularly those of the periosteum and cancellous bone (marrow) and it demonstrates adjacent soft tissue abnormalities (Fig. 3a) [7]. The most commonly used classification is by Fredericson et al. [8]: Grade 0: No abnormality. Grade 1: Periosteal oedema with no marrow signal abnormalities. Grade 2: Periosteal oedema and marrow oedema visible only on fluid sensitive sequences (short tau inversion recovery (STIR)/T2weighted). Grade 3: Periosteal oedema and marrow oedema visible on both fluid sensitive and T1-weighted sequences. Grade 4a: Multiple focal areas of intracortical signal abnormality and marrow oedema visible on both T1-weighted (Fig. 3b) and fluid sensitive (Fig. 3c) sequences.



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Fig. 2. Early vascular phase (a), and delayed static phase (b) TC-99 m bone scan, showing increased isotope uptake at the site of the tibial stress fracture (arrows).

Grade 4b: Linear areas of intracortical signal abnormality (suggestive of a stress fracture) and marrow oedema visible on both T1-weighted and fluid sensitive sequences (Fig. 3d). MRI may also demonstrate fascial oedema around the tibial insertion of the soleus muscle. 2.1.4. Computed tomography (CT) CT is not as sensitive as MRI as a single test for stress injury but can demonstrate cortical abnormalities not visible on MRI [9]. It is used as a problem solving tool to complement MRI. CT demonstrates osseous abnormalities in stress injury earlier than plain radiography, including periosteal reaction, cortical thickening (Fig. 4a), cortical striations, lucencies and a discrete stress fracture. The stress fracture is seen earlier on CT than on plain

radiographs, and is well visualised in all imaging planes (Fig. 4b and c). Tibial stress fractures are most commonly transverse or oblique in orientation and these tend to affect the proximal posterior tibial cortex (Fig. 5). Anterior tibial mid-shaft fractures are less common, and have a tendency to result in non-union. Longitudinal stress fractures tend to occur more commonly in non-athletes [10]. 2.2. Melorheostosis Melorheostosis (also known as Leri Disease) is a rare, benign, non-hereditary mesenchymal disorder resulting in a sclerosing bony dysplasia with adjacent soft tissue masses. It most commonly affects one side of a single tubular bone, usually in a lower limb long bone, but may affect multiple bones which may be in a

Fig. 3. (a) Axial proton density fat-suppressed image of the lower leg, with anterior tibial cortical thickening and periosteal reaction (white arrow), and oedema in the pretibial soft tissues (black arrow). Axial T1 (b), and proton density fat-suppressed (c) images showing posteromedial cortical and medullary oedema (arrows) secondary to a tibial stress fracture. (d) Coronal STIR sequence, showing the linear intracortical increased signal intensity of a stress fracture (arrow), associated with marrow oedema.



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Fig. 4. (a) Sagittal reconstruction of the anterior tibia, showing periosteal and cortical thickening and sclerosis (arrow). Axial (b), and oblique coronal (c) CT images showing the linear hypodensity of a stress fracture (arrows).

sclerotome distribution [11]. Involvement of the axial skeleton, skull and thoracic cage is rare. It usually presents with symptoms in late childhood or young adult life but may be detected incidentally at any age and has an equal gender distribution. Clinical presentation is often with pain, stiffness, restricted motion, contractures, soft tissue masses, limb length discrepancy and deformity. Scleroderma-like skin changes may also be seen overlying the areas of bony abnormality [12].

2.2.1. Plain radiography and CT Melorheostosis is characterised by prominent, irregular, longitudinal, cortical and endosteal hyperostosis, with a proximal to distal pattern of extension in long bones, resulting in a classic “dripping candle wax” appearance (Fig. 6a) [13]. Endosteal extension may obliterate the medullary cavity (Fig. 6b). There may be extraosseous involvement resulting in fibrous or vascular soft tissue masses, especially in the periarticular regions, which may calcify or ossify over time (Fig. 6c) [14]. Intra-articular extension into joint spaces may also be seen resulting in joint ankylosis and contractures [15,16]. 2.2.2. MRI The hyperostotic cortical and subcortical changes are low signal intensity on T1- and T2-weighted imaging in keeping with sclerosis (Fig. 7a). The adjacent soft tissue masses have variable signal intensity characteristics depending upon their composition and degree of mineralisation (Fig. 7b). Following administration of intravenous contrast, no enhancement of the cortical hyperostosis is seen, but there is variable enhancement of the soft tissue masses [17]. 2.2.3. 99m Tc-methylene diphosphonate (MDP) bone scan The hyperostotic segments of affected bones often show moderately increased asymmetrical cortical uptake (Fig. 8) which may cross joints to involve contiguous bones, whilst no abnormal uptake is seen in the adjacent uninvolved medullary cavity [18,19]. Melorheostosis often has a chronic progressive clinical course and can lead to significant disability, and surgical management of contractures and limb deformities may be required. Medical therapy with bisphosphonate infusion has been reported to help manage symptoms [20]. 2.3. Venous stasis

Fig. 5. Sagittal STIR sequence demonstrating a posterior proximal tibial stress fracture (arrow), seen as a linear hypointensity with surrounding marrow oedema.

Venous stasis is characterised by periosteal new bone formation due to an increase in mean inserstitial fluid pressure within the bone [21]. It is thought to occur secondary to factors such as tissue hypoxia and venous hypertension [4]. There is no age predilection and the lower extremities are most commonly affected, typically the tibia and fibula. The appearances are usually bilateral and relatively symmetrical but in the context of focal interruption of the




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Fig. 6. (a) AP radiograph of the lower leg in a patient with melorheostosis involving the anterolateral tibial cortex. (b) Axial CT image in a patient with tibial melorheostosis, with extension into the medullary cavity (arrow). (c) Lateral radiograph of the knee in a patient with melorheostosis, demonstrating peri-articular and intra-articular involvement with calcified soft tissue masses (arrows).

osseous blood supply such as with a tibial fracture, the ipsilateral extremity may be affected only.

2.3.1. Plain radiography and CT Venous stasis typically results in a circumferential, smooth, wavy, solid periosteal reaction affecting the mid and distal shaft of the tibia and fibula [4,21]. The periosteal reaction may take up to 3 weeks to develop and may initially be separate from the cortex. As the condition progresses, the periosteal new bone becomes incorporated into the adjacent cortex and the appearance changes to diffuse, mature cortical thickening. Secondary signs of venous stasis are the presence of multiple phleboliths as well as soft tissue swelling due to subcutaneous oedema [21]. Osteopenia may be seen in chronic venous insufficiency, which is often due to disuse.

2.3.2. MRI MRI is used as a problem solving tool, usually to exclude alternative causes for periosteal reaction and cortical thickening such as osteomyelitis. Findings include diffuse subcutaneous oedema,

periosteal reaction and cortical thickening. There may be extension of oedema along fascial planes. The differential diagnosis includes other causes of circumferential periosteal reaction including infection, bone tumours, healing fractures, chronic stress injury and medical conditions such as thyroid acropachy and hypervitaminosis A. The clinical history and examination, diagnostic blood tests and imaging appearance of the adjacent bone often makes the diagnosis relatively straightforward. 3. Neoplastic tibial cortical lesions 3.1. Fibrous cortical defect, non ossifying fibroma and benign fibrous histiocytoma of bone Fibrous cortical defect (FCD), non ossifying fibroma (NOF) and benign fibrous histiocytoma of bone (BFH) are the most common benign fibrous bone tumour and are histologically identical, being composed of benign fibroblasts and histiocytes, scattered with xanthomatic cells (Fig. 9). FCD and NOF are estimated to occur in up to 30% of the asymptomatic population in the 1st and 2nd decade of life, in contrast to BFH, which commonly presents in



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Fig. 7. (a) Coronal T1 weighted image, showing hypointense cortical hyperostosis (arrow). (b) Coronal proton density weighted image of the knee, demonstrating heterogeneous peri-articular soft tissue involvement (black arrow), and tibial cortical hyperostosis (white arrow).

patients over 20 years of age [22,23]. FCD and NOF occur in the metaphysis of the long bones (particularly in the tibia and femur) in the region of intensive bone growth, while BFH typically involves non-metaphyseal locations of long bones and the pelvis, especially the ilium. It has been postulated that these lesions may be due to subperiosteal haemorrhage secondary to injury at a site of muscle attachment [22,24]. Distinction between a FCD and a NOF is made on the basis of age and size, with FCD occurring in young children less than 10 years of age and measuring less than 2 cm in size, in contrast with NOF which occurs in adolescents and measures greater than 2 cm in size [4]. FCD is generally also confined to the cortex whereas NOF can extend into the medullary cavity. They are most commonly an incidental finding although rarely a NOF will present with a pathological fracture. With time they may change in size, become sclerotic or disappear altogether [4]. Multiple NOFs are associated with neurofibromatosis. JaffeCampanacci syndrome is rare and consists of multiple NOFs and extraskeletal congenital abnormalities (such as café-au-lait spots, occular anomalies, cryptorchidism and hypogonadism) [4]. 3.1.1. Plain Radiography and CT Both FCD and NOF are lucent lesions with a narrow zone of transition, typically eccentrically located in the cortical layer of the bone and are usually oval in shape with a long axis parallel to the long axis of the bone [25]. They have a thin sclerotic border that is often scalloped and slightly expansile (Fig. 10). Over time, they heal by gradual intralesional sclerosis (Figs. 11 and 12). BFH has similar imaging appearances of a well-defined radiolucent lesion with up to two-thirds having a sclerotic border. They may be slender and

expand the cortex, with cortical destruction but without periosteal reaction. Location in a non-metaphyseal location is the key to differentiation between BFH and FCD/NOF. The diagnosis can usually be made on radiographs without the need for further imaging or biopsy. 3.1.2. MRI Often seen incidentally on MRI performed for other reasons, FCD, NOF and BFHs are demonstrated as a small intracortical lobulated lesion that is hypointense on T1 (Fig. 13a) and more commonly hypointense than hyperintense on T2. Septae may be visualised and foci of T1 and T2 hypointensity are consistent with haemosiderin and fibrous tissue elements [26]. The contents of the lesion may be solid and/or cystic with the solid component enhancing following intravenous contrast (Fig. 13b and c). 3.2. Osteoid osteoma Osteoid osteoma (OO) is a benign bone tumour accounting for 12% of benign skeletal neoplasms. The majority of the patients are young males with about half of them in the 2nd decade of their life at presentation [27]. The lesion has a central nidus of woven bone and osteoid rimmed with osteoblasts (Fig. 14) which tends to be less than 1.5 cm in size. A reactive zone of thickened bone and fibrovascular tissue is surrounding the lesion. OO is commonly cortical with reactive sclerotic cortical thickening or less commonly it is intramedullary and subperiosteal in an intra- or juxta-articular location. The tumour




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Fig. 8. 99m Tc-methylene diphosphonate (MDP) bone scan, demonstrating increased cortical uptake in a patient with left distal femoral melorheostosis.

may occur in any bone, but most frequently occurs in the metadiaphyseal regions of the long bones, particularly the proximal femur and tibia, and to a lesser extent the spine, hands, feet and craniofacial bones [28]. The typical presenting symptom is a non-radiating dull bone ache at the tumour site which is persistent and can progress to a severe localised pain. The pain is usually worse at night, causing sleep disturbance but remarkable relief is usually achieved by taking non-steroidal anti-inflammatory medication.

Fig. 10. Plain radiograph of a typical intracortical non-ossifying fibroma.

Some patients may not respond well to long-term analgesia and until recently local surgical excision was considered the only treatment option. In the last two decades, less invasive procedures such as CT-guided drilling with or without ethanol therapy, laser interstitial thermal therapy, cryotherapy, and CT guided radiofrequency ablation (RFA) have been introduced. CT guided RFA in particular is very popular, with reported success rates approaching 90%, hospital stay of less than 24 h and relatively immediate return to normal activity, unlike surgery [29]. 3.2.1. Plain radiography The radiographs show a round or oval radiolucent nidus with surrounding sclerosis (Fig. 15). However, intramedullary and subperiosteal lesions may not have a distinct sclerotic margin or if one is present, it may be distant to the nidus.

Fig. 9. Non-ossifying fibroma: photomicrograph showing a mixture of ‘fibrohistiocytic’ spindle cells (white arrow), foamy macrophages (black arrow) and lymphocytes (white arrow).

3.2.2. Bone scintigraphy Bone scans demonstrate a characteristic pattern of tracer uptake in which the nidus shows increased activity relative to



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Fig. 12. Sagittal CT reformation demonstrating the typical sclerotic margin of a NOF (black arrow), with evidence of healing of the distal aspect of the lesion (white arrow).

Fig. 11. Plain radiograph demonstrating sclerotic in-filling of a NOF, indicating a healing lesion.

its surrounding reactive zone (Fig. 16a and b). This is called the double-density sign and is pathognomonic of osteoid osteoma. Bones scans are particularly helpful in a symptomatic patient in which the radiograph is normal [28].

3.2.3. CT CT is the modality of choice for characterisation and localisation of the lesion. It clearly demonstrates the small well-defined radiolucent nidus within the sclerotic region (Fig. 17a and b). The nidus enhances following intravenous contrast. The pattern of mineralisation in the nidus can vary with punctuate, amorphous, ring-like and dense types [28]. CT can also be used to guide radiofrequency ablation treatment of the lesion (Fig. 17c).

Fig. 13. (a) Axial T1 weighted image of a non-ossifying fibroma located in the lateral tibial metaphyseal cortex (arrow). Sagittal fat suppressed T1 weighted image pregadolinium (b) and post-gadolinium (c), showing predominantly peripheral enhancement of the lobulated non-ossifying fibroma.




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seen almost exclusively in the tibia [30]. It is most often seen in adults in their third or fourth decades of life and exhibits a slight male predominance. Pain and swelling are the most common presenting features, and there is often a history of trauma. Histologically, adamantinoma demonstrates a zonal architecture with a fibrous stroma centrally containing abundant epithelial cells, which decrease in amount towards the periphery of the lesion (Fig. 19) [31].

Fig. 14. Osteoid osteoma: photomicrograph showing a bone forming lesion comprising anastomosing trabeculae of woven bone (white arrows) lined by osteoblasts (black arrow).

3.2.4. MRI On T1-weighted images, the nidus typically reflects a similar signal to that of skeletal muscle (Fig. 18a). The lesion shows variable signal intensity on T2-weighted images (Fig. 18b). There is surrounding bone marrow oedema on both T1- and T2weighted/STIR images (Fig. 18c). The lesion can resemble a stress fracture or osteomyelitis on MRI, particularly when the nidus is hidden by extensive surrounding oedema and in this situation, bone scintigraphy or CT can be used for further evaluation [29]. 3.3. Adamantimoma Adamantinoma is a rare low-grade malignant neoplasm of cortical bone, which predominantly affects long bones, and is

3.3.1. Plain radiography and CT Adamantinoma typically manifests as a multifocal, elongated, eccentric, expansile, lytic lesion in the cortex of the anterior tibial diaphysis with remodelling deformity (Fig. 20a). It frequently exhibits moth-eaten margins, cortical destruction and intramedullary involvement (Fig. 20b) [32]. It may also show a mixed lytic and sclerotic appearance and there can be satellite lesions and extra-osseous extension with adjacent soft tissue masses that are best depicted on CT or MRI.

3.3.2. MRI MRI has a vital role in loco-regional staging and surgical planning of resection margins by demonstrating other foci of disease and any intramedullary or soft tissue extension. Adamantinomas often have a multilocular appearance with a non-specific, heterogeneous high signal intensity pattern on T2-weighted imaging (Fig. 21a), and an intermediate to low signal intensity on T1weighted sequences (Fig. 21b). Foci of low signal intensity on spin-echo sequences are also common due to ossification within the lesion. Marked contrast enhancement may also be observed as some lesions are comprised of vascular components (Fig. 21c) [31,33]. Classic adamantinoma is often locally aggressive and requires radical surgical resection to reduce the risk of subsequent local recurrence and late distant metastases, which are most commonly to the lung.

3.4. Osteofibrous dysplasia Osteofibrous dysplasia (OFD), or ossifying fibroma, is a rare lesion which resembles FD and the stroma of adamantinoma and was first identified as a distinct entity to FD by Campanacci in 1976 [34]. It is a fibro-osseous lesion of undefined neoplastic nature [35] with a strong predilection for the cortex of the tibia and/or fibula, and rarely affects the radius and/or ulna. It is most commonly seen in children less than 10 years old, and is rarely reported in adults. It may present with pain, progressive bowing deformity, pseudo-arthrosis or fracture [36,37]. The distinction between FD, adamantinoma and osteofibrous dysplasia can be made histopathologically as OFD demonstrates osteoblastic rimming and bone zonation which are not seen in the other conditions (Figs. 22 and 23) [4]. OFD has a more favourable prognosis than fibrous dysplasia or adamantinoma, as there is a tendency towards regression of the lesion.

Fig. 15. Lateral plain radiograph showing sclerosis and thickening of the anterior tibial cortex. The nidus is seen as a subtle focus of lucency (arrow).

3.4.1. Plain radiography and CT OFD typically manifests as a long, lytic lesion in the anterior cortex of the tibial diaphysis with a well-defined geographic border and an adjacent sclerotic band (Fig. 24a and b). It may be multifocal, and may show ground-glass matrix mineralisation, intramedullary involvement and very rarely soft tissue extension [32]. Bowing deformity and pathological fracture may also be seen. CT is useful in assessing the extent of the lesion, identifying satellite lesions, and for pre-operative planning.



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Fig. 16. Early vascular phase (a), and delayed static phase (b) of a Tc-99m isotope bone scan, showing increased isiotope uptake in an osteoid osteoma. Note the intense uptake in the nidus, on a background of surrounding moderately increased uptake on the delayed phase.

Fig. 17. Sagittal oblique reformat (a), and axial image (b) of a tibial osteoma demonstrating a hypodense central nidus (arrows) with a mildly calcified matrix and surrounding cortical sclerosis. (c) Axial image during radiofrequency ablation, showing a radiofrequency needle in the nidus of the osteoid osteoma.

Fig. 18. (a) Coronal T1 weighted image of the isointense nidus (arrow), within an area of hypointense cortical thickening. (b) Axial proton density image of the nidus of the osteoid osteoma (white arrow). The marrow in the tibial medulla returns an intermediate to high signal intensity (black arrow). (c) Sagittal STIR image of the osteoid osteoma (thick white arrow), with surrounding marrow oedema (black arrow), and a thin, regular periosteal respone (thin white arrow).




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Fig. 19. Adamantinoma: photomicrograph showing cleft-like spaces (black arrows) lined by epithelial cells (grey arrows), set in a fibrous stroma (white arrows).

3.4.2. MRI OFD often exhibits homogeneous intermediate signal intensity on T1-weighted sequences (Fig. 25a) a variable cystic to solid appearance on T2-weighted imaging (Fig. 25b) and a variable contrast enhancement pattern (Fig. 25c). 3.5. Osteofibrous dysplasia-like adamantimoma Osteofibrous dysplasia-like adamantinoma (OFD-LA), also called differentiated, regressing or juvenile adamantinoma, is another pathological entity with similarities to both OFD and adamantinoma [36]. OFD and OFD-LA are differentiated at histology by the number of epithelial cells present and their staining characteristics (Figs. 26 and 27) [32,36]. OFD, OFD-LA and adamantinoma have been shown to share similar cytogenetic abnormalities and are considered to be related conditions along the same pathogenic spectrum with overlapping clinical and imaging features [32,36,38,39]. Longer lesions with moth-eaten margins, cortical destruction and complete intramedullary extension are more frequently seen with classical adamantinoma than with OFD or OFD-LA [32]. OFD may spontaneously regress with skeletal maturity and has traditionally been treated conservatively with clinical and imaging observation, and bracing for deformity. However, some cases may progress to debilitating bony deformity without surgical intervention. Furthermore, some lesions showing OFD or OFD-LA at needle biopsy have been upgraded to classic adamantinoma following surgical resection, highlighting the possibility of unrepresentative

Fig. 20. (a) Plain radiograph showing an expansile mixed lucent and sclerotic tibial cortical adamantinoma, with secondary tibial bowing (arrow). (b) Axial CT image showing an anterior tibial adamantinoma (arrow), with extension into the medullary canal.

sampling with needle biopsies and the importance of imaging correlation to identify aggressive features [32,40]. Curettage and localised subperiosteal excision of OFD lesions have been shown to carry a risk of recurrence, whereas no recurrences have been shown with extraperiosteal excision of OFD [41]. Therefore, some specialist bone tumour surgical units suggest more radical surgery for OFD [41]. 3.5.1. Plain radiography, CT and MRI OFD-LA imaging features are similar to OFD and lesions can only be distinguished histiologically. However, there is reported medullary cavity involvement in 56% of OFD-LA compared with 40% in OFD.

Fig. 21. Axial T2 (a), T1 (b) and T1 post gadolinium (c) images showing the heterogeneous anterior tibial adamantinoma (arrows), demonstrating intra-medullary extension and post contrast enhancement.



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Fig. 22. Osteofibrous dysplasia: photomicrograph showing a fibro-osseous lesion composed of bland spindle cells (black arrow) and trabeculae of woven bone (white arrows).

Fig. 23. Osteofibrous dysplasia: cytokeratin highlights scattered stromal cells (black arrow).

Fig. 24. Lateral radiograph (a), and axial CT image (b), of a well-defined expansile intracortical osteofibrous dysplasia lesion, showing minor intra-medullary extension (arrow).

Fig. 25. Coronal T1 (a), sagittal T2 (b), and axial T1 fat-suppressed post contrast (c) of the anterior tibial osteofibrous dysplasia lesion (arrows), demonstrating diffuse post contrast enhancement.

Fig. 26. Osteofibrous dysplasia-like adamantinoma: photomicrograph showing a fibro-osseous lesion composed of bland spindle cells (black arrow) and trabeculae of woven bone (white arrow).




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4. Tibial Intra-medullary lesions with typical cortical involvement 4.1. Brodie’s abscess

Fig. 27. Osteofibrous dysplasia-like adamantinoma: immunohistochemistry shows nests of cytokeratin positive cells (black arrows).

A Brodie’s abscess is a chronic infective lesion originating in the medullary cavity, but which typically progresses to involve the cortex and, for this reason, has been included in the review. In 1832, Sir Benjamin Collins Brodie described three young male patients with gradually worsening tibial pain over many years, whose symptoms were ultimately sufficiently severe to require surgery [42]. Following macroscopic examination of the amputated limbs, he described intra-osseous pus-containing cavities lined by highly vascular and exquisitely sensitive granulation tissue surrounded by sclerotic bone. Although these patients had a chronic form of osteomyelitis, the term “Brodie’s abscess” is considered in contemporary literature to occur in the subacute form of the disease [43–45]. Brodie’s original description of the surgical findings helps to explain the radiological appearances. Brodie’s abscess is most common in the lower limb metaphysis of young male patients and is characterised by an insidious onset of symptoms and normal laboratory markers [43,45,46]. The tibia is the most commonly affected bone and Staphylococcus aureus the most common pathogen although cultures are sterile in 20–43% of cases [45–47]. 4.1.1. Plain radiography Radiographically, a Brodie’s abscess typically appears as a well-defined round or ovoid radiolucent lesion within the metaphysis measuring 0.5–9 cm with thick surrounding sclerosis and a periosteal reaction (Fig. 28) [47,48]. If the lesion becomes tethered

Fig. 28. Plain radiograph of a Brodie’s abscess involving the distal tibia, seen as a metaphyseal lucency with a mildly sclerotic superior margin, extending across the growth plate (arrow).

Fig. 29. Axial images through the distal tibial metaphysis (a), epiphysis (b) and sagittal CT reformation (c) showing extension of a metaphyseal Brodies abscess through the distal tibial anterior epiphyseal cortex, seen as an elongated lucency with surrounding sclerosis.



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to the growth plate, the cavity can elongate during growth and extend into the diaphysis in a snake like manner, described by Letts as the “serpentine sign” [49]. Progression leads to osseous tunnelling and cortical penetration with the formation of a cloaca and soft tissue inflammation, although fistula formation is rare. The presence of a sequestrum, an irregular sclerotic focus of dead bone located eccentrically within the cavity, is highly specific for a Brodie’s abscess [45,48]. 4.1.2. CT CT demonstrates the radiographic findings with greater sensitivity (Fig. 29a–c) and is superior to MRI in detecting a sequestrum [50,51].

CT can also be used to guide percutaneous diagnostic aspiration/biopsy for microbiological and histological analysis to confirm the pathology and guide antimicrobial treatment [52]. Percutaneous CT guided aspiration and irrigation of the cavity can also be performed for therapeutic purposes [53]. 4.1.3. MRI MRI is the most sensitive and specific imaging technique to evaluate a Brodie’s abscess. The central necrotic abscess fluid is hyperintense on T2/STIR, hypointense on T1 and does not enhance following contrast. A thin rim of highly vascular granulation tissue lines the abscess cavity, demonstrating signal hyperintensity on T2 and STIR sequences, which may be more hyperintense than

Fig. 30. (a) Axial T2 weighted image through a distal tibial Brodie’s abscess, showing the double line of granulation tissue (black arrow), located between the hypointense sclerotic rim (thick white arrow), and the hyperintense abscess cavity (black arrow). (b) Sagittal T1 weighted image of the ankle demonstrating the penumbra sign of intermediate signal intensity granulation tissue between the hypointense sclerotic rim and the central fluid-filled abscess cavity (arrows). Axial pre-gadolinium (c), and post-gadolinium (d) T1 weighted images of the tibial diaphysis, showing a peripherally enhancing subcortical abscess extending through the anteromedial tibial cortex, into the overlying soft tissues (arrows).




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Fig. 31. Chondromyxoid fibroma: photomicrograph showing myxoid nodules (white arrow) crossed by cellular osteoclast-rich septa.

the central abscess fluid. This results in a “double line” sign [54]. On T1 it is also hyperintense and it enhances avidly with contrast. The granulation tissue lines the sclerotic wall of the cavity which is hypointense on T1, T2 and STIR (Fig. 30a). On T1 images, this results in the “penumbra sign”, with the hyperintense granulation tissue appearing as a thin penumbra between the hypointense central abscess fluid and the peripheral hypointense sclerotic wall (Fig. 30b) [54]. This occurs in 27–75% of cases and is said to be more sensitive than the double line sign, which is seen in only 22% of cases [54,55]. It is also more specific (96–99%) than the double line sign, which is also seen in avascular necrosis [54,55]. Nevertheless, it is not pathognomonic and is also seen in eosinophilic granuloma, chondrosarcoma, intraosseous ganglia and in benign cystic bone

Fig. 32. Plain AP (a) and lateral (b) radiographs of a 40 year old man show a welldefined, eccentric, lucent lesion (arrows) in the proximal tibial metaphysis involving the anterior cortex.

lesions following curettage [56]. The adjacent bone marrow is usually oedematous and hyperintense on T2/STIR and hypointense on T1. The intra-medullary abscess may extend through the cortex and form a soft tissue abscess (Fig. 30c and d). 4.1.4. 18 FDG PET/CT Although not used routinely (due to cost and lack of availability) when the MRI appearances are equivocal and clinical suspicion is high, 18 FDG PET/CT can serve as a useful adjunct. The metabolically

Fig. 33. Axial T1W (a), axial T2W (b) and sagittal STIR (c) images (same lesion as the plain radiographs) show the lesion with intermediate signal intensity on T1W image (a), heterogeneous hyperintense signal on T2W image (b) and uniformly hyperintense on STIR sequence image (c).



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active granulation tissue utilises 18 FDG resulting in increased uptake at this site. Anatomical correlation with the CT component of the study can provide confirmation of the source [57]. 4.2. Chondromyxoid fibroma Chondromyxoid fibroma (CMF) was first described by Jaffe and Lichtenstein in 1948 [34]. It is the least common neoplasm derived from cartilage with an incidence of less than 1% of all tumour and tumour-like conditions of the bone [58–60]. It is a rare benign cartilage tumour containing variable amounts of chondroid, fibrous and myxoid tissue (Fig. 31) [59,61]. Most of the cases are seen in second and third decades of life with no sex predilection [59,60]. CMF most commonly arises in the metaphysis of long tubular bones, with a predilection for the knee joint, particularly the proximal tibia [62,63]. Clinically CMFs present with slow onset pain and swelling or also may be asymptomatic and found incidentally on radiography or MRI. Imaging is used to help characterise lesions and differentiate from other bone tumours or alternative cause for symptoms, but definitive diagnosis is made on histopathological analysis. The differential diagnoses for CMF include aneurysmal bone cysts, giant cell tumour of the bone, enchondroma, nonossifying fibroma, fibrous dysplasia and chondrosarcoma [61]. Treatment options include curettage and packing with allogenic bone, en bloc resection, wide excision and amputation.

Fig. 34. Fibrous dysplasia: photomicrograph showing a fibro-osseous lesion composed of bland spindle cells (grey arrow) and ‘C’ shaped trabeculae of woven bone (white arrows).

4.2.1. Plain radiography and CT On conventional plain radiographs, CMF appears as a welldefined, lobulated, expansile, lucent, medullary lesion with a sclerotic rim in the metaphysis of a long tubular bone with an average size of 3–10 cm (Fig. 32a and b). It is normally round or oval and the long axis of the lesion lies parallel to that of the bone [59]. In the long bones, it is normally eccentric, whereas in thin bones such as the ribs, fibula and small tubular bones, it may be more centrally placed [60]. It can extend into the diaphysis but rarely into the epiphysis [64]. In a review of 38 cases, Wilson et al. reported that cortical expansion was one of the most consistent plain radiograph findings, present in 89% of the cases [62]. Like all chondroid lesions, CMF does demonstrate matrix calcification although less so than most chondral lesions. Plain radiographs uncommonly demonstrate this calcification [59]. Compared with plain radiographs, CT can better demonstrate the well-defined margins, cortical changes and intra-lesional calcification seen in CMF. However, whilst CT can increase the confidence that a lesion is cartilaginous, it rarely adds much more to the diagnosis [64]. 4.2.2. MRI The main role of MRI in the management of CMF is in preoperative evaluation to accurately determine the extent of the tumour and aid a complete surgical excision to reduce the chance of recurrence [64]. MRI features of CMF can be nonspecific. In a series of 19 cases, Kim et al. reported that on T1-weighted images, CMF showed hypointense to intermediate signal intensity and hyperintense foci in approximately 40% of cases [61]. On T2-weighted images, all lesions were hyperintense. In 60% of cases there was a peripheral intermediate signal band with central hyperintense signal, while in the remaining 40% there was a diffusely hyperintense heterogeneous pattern (Fig. 33a–c) [61]. On contrast enhanced T1-weighted images, peripheral nodular enhancement was noted in approximately 70% of the cases with diffuse enhancement in the rest. Overall, the most helpful MRI findings in CMF are a peripheral intermediate signal band and central hyperintense signal on T2-weighted images, which correspond to the peripheral nodular enhancement and central non-enhancing portion on contrast

Fig. 35. AP radiograph of the right lower leg, showing a pathological fracture through a diaphyseal fibrous dysplasia lesion (arrow). Note the ground glass matrix and mild expansion and cortical thinning, best appreciated at the lateral margin of the lesion.




enhanced images respectively [61]. Periosteal reaction, adjacent abnormal bone marrow or soft-tissue signal and cortical abnormality can also be seen on MRI. 4.2.3. Bone scintigraphy and angiography Tc-99 bone scintigraphy demonstrates markedly increased uptake in the periphery, while there is little uptake on Ga-67citrate scintigraphy. On Thallium-201 scintigraphy, there will be strong accumulation of the entire lesion in early and late scans and as such, it may be clinically useful to help distinguish CMF from chondrosarcoma [62]. On angiography, CMF may demonstrate slight neovascularisation and it is therefore of limited value in diagnosis [62,64]. 4.3. Fibrous dysplasia Fibrous dysplasia (FD) is defined as a tumour of undefined neoplastic nature [34] representing a developmental dysplasia of bone with an incidence of 7% in which abnormal differentiation of osteoblasts leads to replacement of normal marrow and

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cancellous bone by immature bone and fibrous stroma [65,66]. FD is a medullary lesion that displays classical radiological features including secondary cortical changes. Histologically, FD demonstrates scattered spindles of woven bone within a fibrocellular matrix although the proportions of each can vary (Fig. 34). Occasionally there can be foci of cartilage which should not be mistaken for chondrosarcoma. FD can undergo secondary aneurysmal bone cyst formation due to haemorrhage and can be complicated by pathogical fracture and rarely, malignant change which occurs in 0.5% of cases. FD may be monoostotic or polyostotic. 75% cases occur before the age of 30 and the male to female ratio is 1:1. Monostotic FD is more common accounting for 70–85% of cases. In polyostotic FD, patients present earlier in life, 67% by the age of 10 years. 30–50% patients with polyostotic FD have café-aulait spots and endocrine disorders. McCune–Albright syndrome presents with polyostotic FD, ipsilateral café-au-lait spots and endocrine disturbance, usually precocious puberty in girls. In Mazabraud’s syndrome, FD is usually polyostotic and patients present with multiple soft tissue myxomas, typically in large muscle groups [65,66]. 4.3.1. Plain radiography The radiographic appearances are widely variable depending on the degree of fibrous, osseous or cystic change. Typically an FD lesion is intramedullary, expansile and radiolucent with a homogenous, ground glass appearance which is similar to cancellous bone density but without a visible trabecular pattern (Fig. 35) [30]. It usually has a thin rim of reactive bone that is more sharply defined on the inner border. As the lesion grows, its diameter increases resulting in mild expansion but the thin rim of bone remains, although this may be too thin to detect radiographically. Slow endosteal

Fig. 36. Coronal reformat showing the ground glass matrix (thick arrow), and endosteal scalloping (thin arrow) of fibrous dysplasia.

Fig. 37. Coronal T1 weighted (a), and STIR (b) of tibial fibrous dysplasia, returning a low signal intensity on T1, and an intermediate signal intensity on the STIR sequence (white arrows). Note the surrounding soft tissue oedema, secondary to the pathological fracture through the cranial aspect of the lesion (black arrow).



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resorption results in endosteal scalloping but there should not be a periosteal reaction unless there is a pathological fracture [30]. In monostotic FD, the commonest sites are: ribs (28%), proximal femur (23%) and craniofacial bones (20%). In polyostotic FD, two or more bones are involved in more than 75% of the skeleton. The femur, tibia and pelvis are most commonly affected. The Harrison groove (horizontal depressions of the 6th and 7th costal cartilages at the site of attachment of the anterior portion of the diaphragm), coxa vara, protrusion acetabuli, the Sheperd’s crook deformity of the femur and bowing of the tibia can all be seen as secondary deformities, particularly in larger lesions [67]. 4.3.2. CT CT is useful when radiography is equivocal and it is the best test to demonstrate the cortical rim of reactive bone around the lesion which is known as the “rind sign” [4]. It is also the best way to assess for a ground glass appearance which is typical of FD (Fig. 36). 4.3.3. MRI MRI is a useful adjunct to CT and is the best way to assess the content of the lesion. The signal intensity is determined by the predominant tissue type: fibrous – low to intermediate on all sequences (Fig. 37a and b); cystic degeneration – low on T1 and hyperintense on T2/STIR; subacute haemorrhage – hyperintense on T1 and T2 with fluid–fluid levels. Following intravenous contrast, solid areas show uniform enhancement and cystic areas show rim enhancement. 5. Conclusion There are a variety of pathological entities that should be considered in the differential diagnosis of a tibial cortical lesion. We have described those that are common or important, emphasising the typical imaging features that aid in making the diagnosis. Cross sectional imaging is usually helpful when a plain radiograph is equivocal and CT guided biopsy is typically performed in cases without an unequivocally benign appearance on multi-modality imaging. Conflict of interest The authors declare that they have no conflict of interest. References [1] Anderson MW, Greenspan A. Stress fractures. Radiology 1996;199(1):1–12. [2] Pentecost RL, Murray RA, Brindley HH. Fatigue insufficiency, and pathologic fractures. J Am Med Assoc 1964;187:1001–4. [3] Hutchins CP. Explanation of spike soreness in runners. Am Phys Ed Rev 1912;18(1):31–5. [4] Levine SM, Lambiase RE, Petchprapa CN. Cortical lesions of the tibia: characteristic appearances at conventional radiography. Radiogr: Rev Publ Radiol Soc North Am Inc 2003;23(1):157–77. [5] Devas M. Stress fractures. Churchill Livingstone: Edinburgh; 1975. [6] Ishibashi Y, Okamura Y, Otsuka H, Nishizawa K, Sasaki T, Toh S. Comparison of scintigraphy and magnetic resonance imaging for stress injuries of bone. Clin J Sport Med: Off J Can Acad Sport Med 2002;12(2):79–84. [7] Gaeta M, Minutoli F, Scribano E, Ascenti G, Vinci S, Bruschetta D, et al. CT and MR imaging findings in athletes with early tibial stress injuries: comparison with bone scintigraphy findings and emphasis on cortical abnormalities. Radiology 2005;235(2):553–61. [8] Fredericson M, Bergman AG, Hoffman KL, Dillingham MS. Tibial stress reaction in runners. Correlation of clinical symptoms and scintigraphy with a new magnetic resonance imaging grading system. Am J Sports Med 1995;23(4):472–81. [9] Gaeta M, Minutoli F, Vinci S, Salamone I, D’Andrea L, Bitto L, et al. Highresolution CT grading of tibial stress reactions in distance runners. Am J Roentgenol 2006;187(3):789–93. [10] Saifuddin A. Musculoskeletal MRI. London: Hodder Arnold; 2008. [11] Rhys R, Davies AM, Mangham DC, Grimer RJ. Sclerotome distribution of melorheostosis and multicentric fibromatosis. Skelet Radiol 1998;27(11): 633–6.

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[57] Fathinul F, Nordin A. F-FDG PET/CT as a potential valuable adjunct to MRI in characterising the Brodie’s abscess. Biomed Imag Intervent J 2010;6(3):e26. [58] Lersundi A, Mankin HJ, Mourikis A, Hornicek FJ. Chondromyxoid fibroma: a rarely encountered and puzzling tumor. Clin Orthopaed Relat Res 2005;439:171–5. [59] Rahimi A, Beabout JW, Ivins JC, Dahlin DC. Chondromyxoid fibroma: a clinicopathologic study of 76 cases. Cancer 1972;30(3):726–36. [60] Budny AM, Ismail A, Osher L. Chondromyxoid fibroma. J Foot Ankle Surg: Off Publ Am Coll Foot Ankle Surgeons 2008;47(2):153–9. [61] Kim HS, Jee WH, Ryu KN, Cho KH, Suh JS, Cho JH, et al. MRI of chondromyxoid fibroma. Acta Radiol 2011;52(8):875–80. [62] Wilson AJ, Kyriakos M, Ackerman LV. Chondromyxoid fibroma: radiographic appearance in 38 cases and in a review of the literature. Radiology 1991;179(2):513–8. [63] Wu CT, Inwards CY, O‘Laughlin S, Rock MG, Beabout JW, Unni KK. Chondromyxoid fibroma of bone: a clinicopathologic review of 278 cases. Hum Pathol 1998;29(5):438–46. [64] Stacy GS. Chondromyxoid fibroma imaging. E-Medicine 2013. Available from: http://emedicine.medscape.com/article/388738-overview-showall [65] Fitzpatrick KA, Taljanovic MS, Speer DP, Graham AR, Jacobson JA, Barnes GR, et al. Imaging findings of fibrous dysplasia with histopathologic and intraoperative correlation. Am J Roentgenol 2004;182(6):1389–98. [66] Stoker DJ, Saifuddin A. Bone tumours (1): general characteristics and benign lesions. In: Adam A, Dixon AK, Grainger RGDr, Allison DJ, editors. Grainger and Allison’s diagnostic radiology: a textbook of medical imaging. 5th ed. Churchill Livingstone; 2008. Andy Adam, Adrian K. Dixon; consulting editors, Ronald G. Grainger, David J. Allison. ed. [Edinburgh] [Chapter 47]. [67] Harris WH, Dudley Jr HR, Barry RJ. The natural history of fibrous dysplasia. An orthopaedic, pathological, and roentgenographic study. J Bone Joint Surg Am Vol 1962;44-A:207–33.


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