MSK 2 Flashcards

Question

Answer 1

Ghost sign in clay shovellers fracture. Stable DOI:10.12671/JKFS.2018.31.2.57 Corpus ID: 134649937 Clay-Shoveler's Fracture in an 18-Year-Old Cheerleader: A Case Report Il-Yeong Hwang, S. J. Park, Jae-Ryong Cha Published 2018 Medicine Journal of the Korean Fracture Society Financial support: None. Conflict of interests: None. Clay-Shoveler’s fracture refers to a fracture that is solely developed on the spinous process of the cervical spine or the thoracic vertebrae. This fracture rarely occurs during sporting activities. In this case, an 18-year-old female developed the fracture on the spinous process of the 7th cervical spine and 1st thoracic vertebrae due to the repetitive practice of cheerleading. The patient’s pain was improved by wearing a support device and taking an anti-inflammatory analgesic drug and muscle relaxant. Her case is being followed-up at the outpatient department

Answer 2

Sclerosis and collapse of the second metatarsal head. Case Discussion Freiberg infraction is the name of avascular necrosis of the second metatarsal head.

Answer 3

* Benign * well defined sclerotic border * lack of soft tissue mass * Solid/no periosteal reaction * Geographic bone destruction * Malignant * interrupted periosteal reaction * moth-eaten or permeative destruction * Soft tissue mass * Wide zone of Transition.

Answer 4

* The 'C' in FEGNOMASHIC * AKA a Codman Tumour. * Rare benign cartilaginous neoplasm * Arise in the epiphysis or ephphysis of long bones in young patients. * Pateints \< 20 years old. * Less than 1% of all primary bone tumours. * M\>F * Malignant transformation is possible. * ASSOCIATATIONS: ABCS * HISTOLOGY: Chondroblasts, chondroid matrix, cartilages with occasional giant multinucleated cells) * LOCATION: 70% occur in the humerus, femour and ibia. * 10% inthe hands and feet

Answer 5

Stage 3 Pagets Disease * Paget disease of the bone is a common, chronic bone disorder characterised by excessive abnormal bone remodelling. The classically described radiological appearances are expanded bone with a coarsened trabecular pattern. The pelvis, spine, skull, and proximal long bones are most frequently affected. * Pathology * The aetiology is not entirely known, but it is a disease of osteoclasts. Viral infection (paramyxovirus) 6 in association with genetic susceptibility has been postulated. * There are three classically described stages, which are part of a continuous spectrum 22: * early destructive stage * incipient active * lytic * predominated by osteoclastic activity * intermediate stage * (active, mixed) * osteoblastic as well as osteoclastic activity * late stage * inactive * sclerotic/blastic * These stages correlate well with the imaging findings. * Markers * elevated serum alkaline phosphatase * normal calcium and phosphorus levels * increased urine hydroxyproline

Answer 6

Enchondroma Left hand x-rays demonstrate a fracture through an abnormality of the metaphyseal region of the third proximal phalange characterised by a non-aggressive lytic lesion expanding the local bone. No periosteal reaction. No matrix calcification or ossification. Case Discussion The patient went on to have a resection. Pathology: The specimen consists of multiple tan cartilaginous tissue fragments aggregating to 2.5 x 2.5 x 1 cm. Histology confirmed multiple benign-appearing cartilaginous fragments, in keeping with an enchondroma. Dr Yuranga Weerakkody◉ and Assoc Prof Frank Gaillard◉◈ et al. Enchondromas, also known as chondromas 7, are relatively common intramedullary cartilage neoplasms with benign imaging features. They share histologic features with low-grade chondrosarcoma, and are sometimes classified under the umbrella term low-grade chondral series tumours. Enchondromas account for the 'E' in the popular mnemonic for lytic bone lesions FEGNOMASHIC. Epidemiology most frequently diagnosed in childhood to early adulthood with a peak incidence of 10-30 years most common primary benign bone tumour of hand/wrist account for ~5% (range 3-10%) of all bone tumours, and ~17.5% (range 12-24%) of benign bone tumours 1 Associations Two syndromes are associated with multiple enchondromas: Ollier disease Maffucci syndrome Clinical presentation Enchondromas are most commonly an incidental finding, most significant in that they shouldn't be confused with more aggressive lesions. As a rule, enchondromas should be asymptomatic; however, lesions of the hands/feet may present with pain from pathological fracture or impending fracture 8. Malignant transformation into low-grade chondrosarcoma is rare and may present with pain. Pathology Enchondromas comprise lobules of mature hyaline cartilage which are partially or completely encased by surrounding normal bone 9. The cartilaginous lobules may undergo endochondral ossification, often resulting in the characteristic 'rings and arcs' pattern of mineralisation. They arise from rests of growth plate cartilage/chondrocytes which become isolated within mature bone. Hence, they may be seen in any bone formed from cartilage. By definition, they show no histologic evidence of local invasion (which would suggest low-grade chondrosarcoma). However, it is important to be aware that enchondroma cannot be reliably distinguished from chondrosarcoma by histology, and diagnosis depends on correlation of clinical, imaging, and pathology findings 9. Grossly, lesions are usually \<3 cm, translucent, nodular, and are grossly greyish-blue. Location Enchondromas are typically located in a central or eccentric position within the medullary cavity of tubular bones: small tubular bones of the hands and feet (~50%) 4 proximal phalanx most common 8 large tubular bones e. g. femur, tibia, humerus rare: (consider chondrosarcoma) pelvis ribs scapula Rarely an enchondroma may extend through the cortex and demonstrate an exophytic growth pattern. This is known as an enchondroma protuberans, and may either be seen sporadically or as part of Ollier disease 2. Radiographic features Enchondromas have a somewhat variable appearance by imaging, although characterisation by excluding suspicious features is key. Since most are asymptomatic incidental findings, lesions in a characteristic location and appearance are not usually further investigated. Imaging is generally less helpful in corroborating benignity of lesions in the hands/feet, as well as in enchondromatosis or skeletally immature patients 9. Radiograph and CT Enchondromas have a variable appearance, although typically they are small \<5 cm lytic lesions with non-aggressive features: narrow zone of transition sharply defined margins +/- chondroid calcification (rings and arcs calcification) often no matrix mineralisation (purely lytic) in the hands/feet +/- expansile more commonly in hands/feet may have mild endosteal scalloping should not "grow" through cortex (unless pathologic fracture) pertinent negatives 9: no gross bone destruction no periosteal reaction no soft tissue mass The majority of enchondromas more frequently arise in the metaphyseal region, owing presumably to their origin from the growth plate 1, although they are frequently seen in the diaphysis. They only rarely are seen in the epiphysis, and a cartilaginous lesion in an epiphysis is more likely to be a chondrosarcoma 3. MRI MRI is useful in evaluating soft tissue extension and for confirming the diagnosis. Enchondromas appear as well-circumscribed somewhat lobulated masses replacing marrow 1. T1 intermediate to low-signal internal foci of low signal of “rings and arcs” characteristic of a chondroid matrix T1 C+ (Gd) enhancement is variable and may be seen both peripherally or of translesional septae similar pattern of enhancement may be seen in chondrosarcomas 3,6 T2 sharply defined predominantly high signal internal foci of low signal of “rings and arcs” characteristic of a chondroid matrix no bone marrow or soft tissue oedema Descriptions should include location i.e. central or peripheral presence and amount of endosteal scalloping Differentiation of an enchondroma from low-grade chondrosarcoma is problematic, as they can have similar appearances. See enchondroma vs low-grade chondrosarcoma. Nuclear medicine Increased uptake on the bone scan can be seen with enchondromas. Intense uptake occurs with an underlying pathological fracture or cortical expansion in small bones 5. Treatment and prognosis The majority of enchondromas remain asymptomatic and require no treatment. Pathologic fractures are commonly treated by curettage and bone grafting, with follow-up x-rays to monitor for healing and recurrence. An incisional biopsy is obtained intraoperatively. Recurrence is reported in 2-15% and suggests malignancy 8. If malignant transformation is suspected, which occurs in less than 5% of cases, then treatment is more aggressive 4. Complications pathological fracture malignant transformation into chondrosarcoma Differential diagnosis The differential is significantly affected by the modality in question, and most entities below can be excluded with MRI. The exception is chondrosarcoma. bone infarct chondrosarcoma difficult to distinguish see: enchondroma vs low grade chondrosarcoma intraosseous ganglion other benign lytic bone lesions lytic metastasis to bone granulomatous disease skeletal sarcoidosis skeletal tuberculosis

Answer 7

ligament of wrisberg pseudotear seen at posterior horn/root of lateral meniscus

Answer 8

The carpal boss is a hypertrophied bony protuberance on the dorsal surfaces of the base of the second or third metacarpals, near the capitate and trapezium. It may be bilateral. Pathology The condition may represent one or more of: degenerative osteophyte formation os styloideum (an accessory ossicle of the wrist) bony prominence at the base of the second or third metacarpals (which is often called "styloid process") Pain may be the result of a ganglion, inflamed bursa or extensor tendon slipping over the bony prominence. Radiographic features The radiographic appearance of a carpal boss is characteristic, however optimal visualisation of the boss may be difficult to obtain due to superimposed bony structures. CT may show degenerative disease at a pseudoarthrosis, and MRI may show oedema related to abnormal motion.

Answer 9

AKA: Enostosis Intro: * Cortical bone within cancellous bone * 1-4cm * homogenously dense * well marginated * may be "warm" on bone scan

Answer 10

multicentric osteosarcoma: * synchronous osteoblastic OSA at multiple sites. * has a tendancy to be multi-centric, metaphyseal, and symmetric * occurs exclusively in children ages 5-10 yrs * extremely poor prognosis

Answer 11

MMMSPROOF * METS(osteoblastic) + lyphoma + leukaemia * Myelofibrosis * Mastocytosis * Sickle Cell * Pajets/Piknodisostosis * Renal osteodystrophy * Osteopetrosis * Osteopoikilosis, osteopathica striata * Flurosis

Answer 12

6 Ddx interupted periosteal reaction * Osteosarcoma * Ewings Sarcoma * Osteomyelitis * Chondrosarcoma * LCH * Subperiosteal Haemorrage

Answer 13

Trad use mid third of patella or gracilluys

Answer 14

* HADD of longus coli * abscess

Answer 15

2019 Aug Q98 Robins Osteomyelitis (p. 1195) Osteomyelitis denotes inflammation of bone and marrow, virtually always secondary to infection; bacteria, fungi, viruses, and parasites can all be causes. Osteomyelitis can occur with any systemic infection but is typically a primary solitary focus of disease. Pyogenic Osteomyelitis (p. 1195) Pyogenic osteomyelitis is almost always bacterial; seeding occurs by the following: • Hematogenous spread (common in children, typically involving long bones) • Extension from a contiguous infection (e.g., diabetic foot ulcer) • Open fracture or surgical procedure In half of cases, no organism can be identified. Staphylococcus aureus is responsible for 80% to 90% of the remainder, largely related to receptors that enhance adherence to bone matrix; patients with sickle cell anemia are prone to Salmonella infections. The location of infection is influenced by the osseous circulation, which varies with age. In the neonate, metaphyseal vessels penetrate the growth plate, resulting in infections of the metaphysis, epiphysis, or both; localization of infections in the metaphysis is typical in children. After growth plate closure, the metaphyseal and epiphyseal vessels merge, allowing potential seeding of the epiphyses and subchondral regions.

Answer 16

* poly arthropathy * synovial based process (ddx of synovial based processes RA and Reactive arthritis) * 'symmetric' * periarticular osteoporosis (sign of synovitis) * marginal erosion * intercarpal joints distal RUJ ulnar styloid * MCPS * relative sparing of the PIP and DIP * Synovitis * DIPS usually spared (helps differentiate from OA and Psoriasis) * ECU involvement -\> erodes ulnar styloid * Look for ulnar sided soft tissue swelling. * Synovitis of the DRUJ is another good sign for RA. MRI * look on T1 w image. May be able to see more errosions than apparent on xray * T2 - oedema at DRUJ, carpal bone marrow (osteitis), and around ulnar aspect of wrist. * T1 + C - All the synovium and osteitis enhances. Gout doesn't have enhancement. Psoriasis may enhance a little but to a lesser extent. * If you're ever trying to dx synovitis, you must give contrast.

Answer 17

Medial = tibia has a wine glass shape Lateral = upside down L

Answer 18

ACL cysts/mucoid degeneration * increased sig * drumstick appearance on sag imaging * cystic on coronal * pt complains of fullness in the knee

Answer 19

Rugger jersey spine (hyperparathyroidism) Dr Mostafa El-Feky and Assoc Prof Frank Gaillard◉◈ et al. Rugger jersey spine describes the prominent endplate densities at multiple contiguous vertebral levels to produce an alternating sclerotic-lucent-sclerotic appearance. This mimics the horizontal stripes of a rugby jersey. This term and pattern are distinctive for hyperparathyroidism. Pathology In response to increased bone resorption due to excess parathyroid hormone (PTH) secretion and subsequent loss of bone mass, osteoblasts form an increased amount of osteoid that does not contain hydroxyapatite but does appear opaque on radiographs. The sclerotic bands on the superior and inferior endplates of the vertebral bodies represent accumulations of excess osteoid and appear opaque because of their increased volume when compared to normal bone. Differential diagnosis Paget disease picture frame vertebral body osteopetrosis sandwich vertebrae severe osteoporosis with compression fractures Note: confusingly some authors use the term rugger jersey for osteopetrosis, although most would assume the term refers to hyperparathyroidism. Quiz questions

Answer 20

Fibrous cortical defect Dr Mohamed Saber and Assoc Prof Frank Gaillard◉◈ et al. Fibrous cortical defects (FCD) are benign bony lesions and are a type of fibroxanthoma, histologically identical to the larger non-ossifying fibroma (NOF). Epidemiology Fibrous cortical defects typically occur in children (usually 2-15 years), and indeed are one of the most common benign bony lesions, which combined with non-ossifying fibromas are seen in up to 40% of skeletally immature children/adolescents 3. There is a male predilection by a ratio of 2:1 3. Clinical presentation They are asymptomatic and self-limiting, completely healing by adulthood. Pathology Fibrous cortical defects macroscopically appear as fleshy, fibrous, yellow or tan-brown lesions with variable areas of haemorrhage 3. Microscopic examination reveals the lesions to be highly cellular containing spindle-shaped cells on a background of stromal tissue in a prominent storiform pattern. Foamy histiocytes and multinucleated giant cells are also seen. Mitotic figures and/or cellular dysplasia should not be seen 3. During the healing phase, there is an increase in osteoblastic activity as new bone replaces the defect, gradually being remodelled and completely disappearing 2. Radiographic features FCDs are benign lytic bone lesions, and, along with fibrous dysplasia share the F in the popular mnemonic FEGNOMASHIC. They typically occur in the metaphysis or diametaphyseal junction and appear as small (\<2-3 cm) lucent defects within the cortex that over time become sclerotic as they heal. They are typically located in the distal femur or proximal or distal tibia. They are much less frequently seen in the upper limb 2,3. Importantly, there is no associated soft tissue mass 3. Plain radiograph and CT lucent intracortical defects outlined by a thin rim of sclerosis no involvement of the underlying medullary cavity no periosteal reaction MRI Signal characteristics include: T1: hypointense T2: variable, depending on the phase of healing 3 Nuclear medicine (bone scan) Appearance depends on the phase of the lesion. In general they are negative; however, mild hyperaemia and moderate bone uptake are present during healing. If extensive uptake or hyperaemia is present, then an alternative diagnosis or superimposed fracture should be considered 3. Treatment and prognosis As these lesions are benign, characteristic in appearance and self-limiting, no treatment, biopsy or even follow-up is required in typical cases. If associated with pathological fracture (more common in non-ossifying fibromas) then cast immobilisation until the fracture has healed, followed by biopsy with or without curettage, and bone grafting may be necessary 3. History and etymology Fibrous cortical defect was first described by Dallas Burton Phemister (1882-1951) 5, an American orthopaedic surgeon in 1929 4. Differential diagnosis Possible differential considerations include non-ossifying fibroma (NOF): larger (by definition \>3 cm), bubbly cortical desmoid: posteromedial aspect of the distal femur osteoid osteoma: night pains osteomyelitis stress fracture intracortical osteosarcoma

Answer 21

haemangeoma

Answer 22

* Purely lytic lesion that lacks the highly aggressive appearance of a conventional OSA (i.e. tumor matrix periosteal reaction) * but is actually much more malignant & has a worse prognosis * Mimicks: ABC! * Rad features: * large lytic lesion * Cystic cavities filled w blood/necrosis

Answer 23

Meniscal root tear Dr Magdalena Chmiel-Nowak◉ and Dr Yuranga Weerakkody◉ et al. Meniscal root tears are a type of meniscal tear in the knee where the tear extends to either the anterior or posterior meniscal root attachment to the central tibial plateau. They often tend to be radial tears extending into the meniscal root. Epidemiology According to one source, they are thought to account for ~10% of all arthroscopic meniscectomies 5. Pathology While they can arise from a number of mechanisms, root tears are generally thought to be chronic 5. Associations ACL tears are associated with posterior horn root tears of the lateral meniscus Radiographic features MRI Best assessed on T2 weighted sequences. When it involves the posterior root, medial root tears are easier to diagnose than lateral root tears. On medial posterior root tears there is often 2: shortening or absence of the root on sagittal images vertical fluid cleft on coronal fluid-sensitive (T2) images On posterior root radial tears of the lateral meniscus, the appearance may be similar to radial tears in other locations. For root tears in general, sagittal imaging may demonstrate a meniscal ghost sign. Other features include: truncation sign on coronal images 4 features meniscal extrusion on coronal plane 4 History and etymology They were first described by M J Pagnani et al. in 1991 6.

Answer 24

* Periarticular * Scleroderma * SLE * Articular * CPPD * Chondrocalcinosis * Joint space-related * neuropathic arthropathy * Synovial osteoenchondromatosis * Osteochondritis dissecans * Osteochondral fracture.

Answer 25

* The achilles tendon is formed by the confluence of the gastrocnemious and the soleus * The critical zone the site of most acute tears is 2-6cm proximal to its calcaneal insertion site * x-ray shows marked soft tissue swelling behind the distal tibial and akle with obliteration of the pre-achilles fat pad * MRI in partial tears shows tendon enlargement and edema, intratendinous areas of increased signal intensity on T2W, and surrounding soft tissue edema * In complete tear: a tendinous gap is present and is filled with high signal blood and edema. * Achilles tendon tear * Achilles tendon tears are the most common ankle tendon injuries, and are most commonly seen secondary to sports-related injury, especially squash and basketball. * Epidemiology * There is strong male over-representation presumably as a result of the predominantly sport related aetiology. Patients are typically aged 30-50 years and have no antecedent history of calf or heel pain. * There are however numerous recognised predisposing factors including: * intratendinous steroid injection * diabetes mellitus * systemic inflammatory illnesses * rheumatoid arthritis * systemic lupus erythematosus * repeated microtrauma * gout * fluoroquinolone antibiotics * ochronosis 4 * hyperparathyroidism * Clinical presentation * Typically patients present with sudden onset of pain and swelling in the Achilles region, often accompanied by an audible snap during forceful dorsiflexion of the foot. A classic example is that of an unfit 'weekend warrior' playing squash. * If complete a defect may be felt and the patient will have only minimal plantar flexion against resistance. * Pathology * The spectrum of tears ranges from microtears to interstitial tears (parallel to the long axis of the Achilles), to partial tears, and eventually to complete tears. * Tears can be acute or chronic, with repeated minor trauma. At the mildest end of the spectrum all that may be present is peritendonitis. * Location * Typically, in a young 'normal' individual, the Achilles tendon ruptures in the 'critical zone', which is a region of relative watershed hypovascularity 2-6 cm proximal to insertion. * Classification * The Achilles tendon tear classification is primarily based on the degree of retraction. * Radiographic features * Plain radiograph * Plain radiographs may show soft tissue swelling and obliteration of pre-Achilles fat pad (Kager's triangle). * Ultrasound * For partial thickness tears * there is often enlargement of the tendon ( \>1 cm) with abnormally hypoechoic or anechoic areas within which correspond to the tear and associated adjacent tendinosis * For full thickness tears * often shows separation of the torn ends with a contour change of the tendon * there is acoustic shadowing at the margins of the tear from sound beam refraction, and adjacent hypoechoic tendinosis * MRI * Appearances can vary: * a full-thickness tear often shows a tendinous gap filled with oedema or blood * complete rupture shows retraction of tendon ends * T2: partial thickness or interstitial tears may show high signal on long TR, and tendon swelling to \>7 mm AP * When a plantaris muscle is present then its tendon is usually spared due to its more anterior insertion on the calcaneum. * Post-operative * post-operative MR imaging may show a tendon gap although this tends to resolve in around 12 weeks 8 * post-operatively, Achilles tendon may appear thicker on MR follow up 9 * Treatment and prognosis * Treatment depends on the extent of the tear. Partial thickness tears can initially be treated conservatively, with surgery reserved for failure of conservative management, on in some cases for high-performance athletes. Full-thickness tears are normally surgically repaired. If the patient is not deemed suitable for surgical repair (frail, ill, etc.) casting of the ankle in the talipes equinus position may be an alternative. * Surgical repair results in a shorter Achilles tendon and better greater calf muscle strength (less soleus atrophy) than non-surgical treatment 10. * History and etymology * A true rupture of the Achilles tendon was first described by Ambroise Pare in 1575 and first reported in the medical literature in 1633 3.

Answer 26

* FEGNOMASHIC * Fibrous dysplasia * Enchondroma * GCT * Non-ossifying fibroma * Oteoblastoma * Met, myeloma * ABC * Simple bone cyst * HPT, heamophila * Infection * Chondromblasma

Answer 27

**_Adamantinoma_** * Adamantinomas are rare, low-grade malignant tumors of unknown etiology that are almost always located in the diaphysis of the mid-tibia. * Clinical * The condition usually presents in patients who are between 20 and 40 years old with regional pain and a palpable mass. * Diagnosis * is made with a biopsy showing nests of epithelial-like cells arranged in palisading or glandular pattern, in a background of fibrous stroma. * Incidence * less than 300 cases have been documented * Demographics * occurs in **young adults** (20 - 40 years of age) * Anatomic location * almost always located in **mid-tibia** * Radiographs * **multiple sharply circumscribed lucent lesions ("soap bubble" appearance) with interspersed sclerotic bone in mid-tibia** * some lesions **may destroy cortex** * may see **bowing of the tibia** * radiographic evolution of lesions is helpful in the diagnosis as lesions may continue to grow and erode thru the cortex * unlike other primary bone tumors, adamantinoma typically shows **no periosteal reaction**

Answer 28

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5934971/#:~:text=Charcot%20spinal%20arthropathy%20(CSA)%2C,of%20deep%20pain%20and%20proprioceptive 2019 Aug Q96 Abstract Charcot spinal arthropathy (CSA) is a rare progressive disorder of vertebral joint degeneration that occurs in the setting of any condition characterized by **decreased afferent innervation with loss of deep pain and proprioceptive sensation in the vertebral column.** While surgical circumferential arthrodesis remains the most effective treatment modality, it is associated with multiple complications, including hardware construct failure. This manuscript represents an up-to-date narrative review of the treatment of CSA, its associated complications, and complication prevention. Keywords: Bone morphogenetic protein, Charcot spinal arthropathy, circumferential arthrodesis, spinal cord injury Go to: INTRODUCTION Charcot spinal arthropathy (CSA), also commonly known as spinal neuroarthropathy or neuropathic spinal arthropathy, is a rare progressive disorder of vertebral joint degeneration that occurs in the setting of any condition characterized by decreased afferent innervation, involving loss of deep pain and proprioceptive sensation in the vertebral column. Neuropathic arthropathy was first described by Jean-Martin Charcot in 1868.[1] The first case of CSA was reported in 1884 by Kronig in a patient with tabes dorsalis secondary to tertiary syphilis.[2] Historically, CSA was most commonly reported in the setting of tertiary syphilis. Nowadays, as a consequence of low incidence of syphilis due to improved antibiotic therapy, CSA presents almost exclusively in patients who have suffered traumatic spinal cord injury (SCI).[3,4,5,6,7] CSA secondary to traumatic SCI occurs 17 years after injury on average.[8] Less commonly, CSA may present secondary to syringomyelia, meningocele, myelomeningocele, diabetes mellitus, peripheral neuropathies, anesthetic leprosy, congenital analgesia, Parkinson's disease, arachnoiditis, transverse myelitis, and others.[8,9,10,11,12] In cases of CSA involving gross spinal instability and absence of medical comorbidities that would otherwise cause contraindication, surgery has become the preferred treatment modality. While posterior-only reconstruction has been indicated in mild cases with minimal bony involvement, the majority of CSA today is treated by circumferential arthrodesis. In addition to improvements in surgical technique, the application of a multimodal treatment model, including the use of bone morphogenetic protein (BMP), has reduced the rates of treatment failure.[13] We present a comprehensive narrative review describing the treatments for CSA, associated complications, and their prevention, with an emphasis on circumferential arthrodesis involving both an anterior and posterior-column construct. Go to: PATHOPHYSIOLOGY/DIAGNOSTICS While the etiology of CSA remains disputed, two theories have gained prominence. The neurotraumatic theory hypothesizes that abnormal motion and spinal instability secondary to loss of deep pain and proprioceptive sensation in the posttraumatic SCI vertebral column results in repetitive microtrauma that leads to inflammation of the subchondral bone and articular cartilage.[9,14] Ultimately, the chronic inflammation results in facet joint destruction, intervertebral disc degeneration, progressive deformity, and spinal instability [Figure 1].[13] Conversely, the neurovascular theory describes the onset of hypervascular regions in the subchondral bone due to underlying systemic pathologies such as diabetic neuroarthropathy or autonomic dysfunction. This leads to increased osteoclastic resorption, causing microfractures that ultimately result in facet joint destruction and gross instability.[8]

Answer 29

Case courtesy of Dr Chris O'Donnell, Radiopaedia.org, rID: 58172 E is false. Hemochromatosis (skeletal manifestations) Dr Dai Roberts◉ and Assoc Prof Frank Gaillard◉◈ et al. Hemochromatosis is a systemic disease which affects many organs systems, including the joints, characterized by hemosiderin and calcium pyrophosphate deposition. For a general discussion, and for links to other system specific manifestations, please refer to the article on hemochromatosis. Radiographic features chondrocalcinosis: particularly knees and triangular fibrocartilage arthropathy symmetrical loss of joint space, subchondral cysts close association with CPPD which is often seen concurrently most commonly hands (MCP, carpal, PIP) with the characteristic hook like/ beak-like osteophytes projecting from radial ends of 2nd and 3rd metacarpals more extensive involvement from the second to the fifth MCP and radial hook-like/drooping osteophytes are more characteristic than in CPPD 3 can also affect the knee, hip, and elbow generalized osteoporosis (~25%) or osteopaenia (~40%) 4 Differential diagnosis On imaging consider: calcium pyrophosphate deposition disease (CPPD) osteoarthritis distal hand joints rather than MCP joints psoriatic arthritis

Answer 30

15 Ddx non-interupted periosteal reaction 1. Caffy disease 2. Thyroid acropachy/Gauchers/Treated scurvy/pachydermoperiostosis etc 3. Chondrosarcoma 4. osteoid osteoma 5. osteoblastoma 6. ABC 7. Chondromyxoid fibroma 8. periosteal chondroma 9. chondroblastoma 10. OM 11. LCH 12. Healing fracture 13. juxtacortical myositis ossificans 14. Hypertrophic Osteoarthropathy 15. Haemophila https://www.youtube.com/watch?v=otDM3-fHnzc

Answer 31

prepatella bursitis

Answer 32

**_Melorheostosis_** * Dr Robert Foley and Dr Hani Makky ALSALAM et al. * Melorheostosis, also known as Leri disease, is an uncommon mesenchymal dysplasia manifesting as regions of sclerosing bone with a characteristic dripping wax appearance (a.k.a. flowing candle wax appearance). * Epidemiology * Although changes occur in early childhood, age at presentation is often later, and the condition often remains occult until late adolescence or early adulthood. In only approximately half of the cases is the diagnosis made before the age of 20 2. * There is no recognised familial predisposition 3. * Clinical presentation * The condition, especially in childhood, is usually asymptomatic, being diagnosed as an incidental finding on radiographs obtained for another purpose 1,3. When melorheostosis does manifest clinically, the most common presentation is of joint contracture or pain, which are more common in adults 3. * Pathology * Distribution * Melorheostosis can be either monostotic or polyostotic and tends to be monomelic. It has a predilection for long bones of the limbs, although it can be seen almost anywhere. Hands and feet are not infrequently involved whereas involvement of the axial skeleton is rare 1,2. The condition has a tendency to give a sclerotome distribution. Uncommonly, it can present with a mineralised peri-articular mass. * Associations * sclerodermic skin changes: thickening and fibrosis of overlying skin * hyperpigmentation of overlying skin 4 * muscle atrophy * vascular tumours and malformations * other tumours, e.g. osteosarcoma, malignant fibrous histiocytoma 4 * Buschke-Ollendorff syndrome * Radiographic features * Plain radiograph * Radiographs are considered sufficient for establishing the diagnosis. * Five patterns have been described 1: * classic * periosteal cortical thickening is characteristic, but endosteal thickening is also seen in many cases, especially when the age of onset is in adolescence, where it may be purely endosteal 5 * thick undulating ridges of bone, reminiscent of molten wax (dripping wax appearance or flowing candle wax appearance) * confined to sclerotomes, and can be seen apparently flowing across joints to the next bone * osteoma-like * myositis ossificans-like * osteopathia striata-like * mixed * Not infrequently features of melorheostosis, osteopathia striata and osteopoikilosis may co-exist in a so-called overlap syndrome, termed mixed sclerosing bone dysplasia. These conditions may share an underlying aetiology (loss of function mutations in the LEMD3 gene) 1. * MRI * Usually, the lesions show low signal on all imaging sequences, with no enhancement. * Nuclear medicine * An increase in radiotracer uptake is usually present on late phase bone scans 2. * Treatment and prognosis * The disease is of variable severity, but in general follows a chronic progressive course in adults and a faster course in children, occasionally resulting in substantial disability from contractures or deformity. * Conservative management is often unrewarding, and in severe cases, surgical intervention may be required, including tendon release, osteotomies and even amputation 1-3. * History and etymology * The condition was first written up in the literature by the French neurologist Andre Leri (1875-1930) 7 and J Joanny in 1922 6. * The name is derived from the Ancient Greek words for limb (melos) and flow (rhe), due to its characteristic appearance of flowing hyperostosis 1,3.

Answer 33

* Permeative (ie moth eaten) describes multiple small endosteal lesion sor holes often with poorly defined margins with sparing of the cortex. Ie it is a bone marrow process. * Round cell tumors * Eosinophilic Granuloma * Lymphoma * Infection * OSA https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5686981/

Answer 34

Flowing ossifications Dr Praveen Jha and Dr René Pfleger◉ et al. Flowing ossifications are seen in diffuse idiopathic skeletal hyperostosis (DISH). They are defined as heterotopic ossifications involving the anterior longitudinal ligament, paraspinal connective tissues and annulus fibrosus of at least four contiguous vertebral bodies and are originally described on lateral radiographs of the spine. Typically there are radiolucencies between the anterior aspect of the vertebral bodies and the flowing ossifications of the anterior longitudinal ligament. The radiolucencies again classically end at the level of the vertebral endplates. See also syndesmophytes parasyndesmophytes Although often used synonymously, they actually have their own definition. As always in those cases, one has to decide for oneself, if one wants to be a "lumper" or a "splitter". Parasyndesmophytes Dr Henry Knipe◉◈ and Dr René Pfleger◉ et al. Parasyndesmophytes or floating syndesmophytes are, as the name suggests, paravertebral dystrophic soft tissue calcifications or heterotopic ossifications. Pathology They are known to be seen in psoriatic arthritis and reactive arthritis 4. Radiographic features Initially they begin at a distance from the vertebral body and intervertebral space. In early disease they are best described as thick and fluffy or thin and curvilinear densities on one side of the spine, parallelling lateral surface of vertebrae and disci. Eventually they will grow to form large and bulky masses, merging with the underlying bone and disc. Differential diagnosis Late stages can render differentiation from the related counterparts syndesmophytes and flowing ossifications somewhat difficult. Syndesmophyte Mrs. Syeda Salma Talib and Dr Prashant Mudgal et al. Syndesmophytes are calcifications or heterotopic ossifications inside a spinal ligament or of the annulus fibrosus. They are seen in only a limited number of conditions including: ankylosing spondylitis ochronosis fluorosis reactive arthritis psoriatic arthritis They can be classified as marginal (along the margins of the vertebral bodies) or non marginal (larger and bulky away from the vertebral bodies). Ankylosing spondylitis classically displays symmetrical marginal syndesmophytes. Radiographic features Appearance on plain radiographs comprises vertical and symmetrical calcification of the lateral margins of the intervertebral disc space. Differential diagnosis syndesmophyte: paravertebral ossifications that run parallel with the spine c.f. osteophytes which typically protrude perpendicular to the spine enthesophyte: located at an attachment of a ligament or tendon, not associated with a joint

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* Septic arthritis

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* Solid periosteal reaction * osteoid osteoma * Stress fracture

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tend to get tibial avulsion rather then ACL tear

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look for a tear near by

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**_PVC exposure Transverse Acro-osteolysis case:_** https://journals.sagepub.com/doi/pdf/10.1177/003591577606900419 **_Acro-osteolysis_** Dr Daniel J Bell◉ and Dr Yuranga Weerakkody◉ et al. Acro-osteolysis (plural: acro-osteolyses) refers to resorption of the distal phalanx. The terminal tuft is most commonly affected. It is associated with a heterogeneous group of pathological entities and, some of which can be remembered by using the mnemonic PINCH FO. When there is linear bone resorption of the midshaft of the distal phalanx with a relatively spared terminal tuft, the condition is also referred to as band acro-osteolysis and carries a more limited differential diagnosis. Pathology Multiple digits Terminal tuft resorption scleroderma 4 Raynaud disease psoriatic arthritis thermal injury extreme cold: frostbite extreme heat: burns, electricity trauma hyperparathyroidism epidermolysis bullosa porphyria drugs phenytoin (occurs in infants of epileptic mothers treated with phenytoin) 7 ergot poisoning/abuse insensitivity to pain, e.g. leprosy, congenital insensitivity to pain juvenile chronic arthritis dermatomyositis vascular occlusion 5 reactive arthritis 6 pityriasis rubra pilaris (very rare skin condition) 8 pachydermoperiostosis 9 sarcoidosis 16 Midshaft resorption (band acro-osteolysis) polyvinyl chloride (PVC) exposure 10 primary acro-osteolysis: Hajdu-Cheney syndrome hyperparathyroidism (also causes terminal tuft resorption) scleroderma 11 (also causes terminal tuft resorption) idiopathic non-familial acro-osteolysis 15 pyknodysostosis 13, 14 (also causes terminal tuft hypoplasia) biomechanical in guitar players 11 Single digit epidermal inclusion cyst 3 glomus tumour of digit 3

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Osteochondral defect Dr Yahya Baba◉ and Assoc Prof Frank Gaillard◉◈ et al. Osteochondral defects (OCD) or lesions (OCL) are focal areas of damage with articular cartilage damage and injury of the adjacent subchondral bone plate and subchondral cancellous bone. Terminology Osteochondral defect is a broad term that describes the morphological change of a localised gap in the articular cartilage and subchondral bone 5. It is often used synonymously with osteochondral injury/defect and in the paediatric population. Isolated lesions of cartilage or subchondral bone are not considered an OCD 6. Please note that OCD is a commonly used abbreviation for both osteochondral defect and osteochondritis dissecans, two closely related conditions. Pathology Aetiology osteochondritis dissecans: thought to be due to repeated microtrauma articular collapse secondary to avascular necrosis or subchondral insufficiency fracture osteochondral impaction fracture postsurgical (e.g. following anterior cruciate ligament repair) Location The recognised sites of osteochondral defects are: femoral condyle (most common in the lateral aspect of the medial femoral condyle) humeral head talus capitellum of the humerus Staging Osteochondral injuries are graded according to the stability and location of the fragment and presence of secondary degenerative changes (see: osteochondral injury staging). Radiographic features Plain radiograph and CT Both x-rays and CT are able to detect displaced defects with ease. However, they are insensitive to grading lower stage lesions and are inadequate in predicting stability. MRI MRI is the modality of choice, with high sensitivity and specificity for the detection of separation of the osteochondral fragment (see: osteochondral injury staging and osteochondritis dissecans surgical staging). This is essential in determining management. T1 the signal is variable with intermediate to low signal adjacent to fragment and variable fragment signal T2 high signal line (rim sign) demarcating fragment from bone usually indicates an unstable lesion, however, false positives can result from oedema low signal loose bodies, outlined by high signal fluid donor defect filled with high signal fluid high signal subchondral cysts Treatment and prognosis Treatment depends on the location and size of the defect as well as the presence of secondary degenerative changes. When the latter is present, then joint replacement is often the only feasible treatment. At earlier stages (stage 1 to 4), a number of options exist including: osteochondral autograft (same patient) osteochondral allograft (cadaveric donor) subchondral bone drilling chondral shaving and abrasion Osteochondral injury staging Dr Mostafa El-Feky◉ and Assoc Prof Frank Gaillard◉◈ et al. Osteochondral injury staging system for MRI attempts to grade the stability and severity of osteochondral injury and is used to plan management. stage I injury limited to articular cartilage MRI findings: subchondral oedema x-ray findings: none stage II cartilage injury with associated subchondral fracture but without detachment thin sclerotic margin x-ray findings: usually none; may see fracture as sclerotic or osteopenic area two subtypes 2,3 type A: cystic on CT and/or oedema on MRI type B: non-displaced and incompletely undercut by fluid (MR) or lucency (CT), with an open connection to the articular cartilage (essentially 2a without oedema on MRI) stage III detached, non-displaced fragment MRI findings: high signal around osteochondral fracture (rim sign) but not displaced x-ray findings: slight lucency between osteochondral fragment and remainder of the bone stage IV osteochondral fragment displaced usually joint effusion present, surrounding fragment and filling donor site x-ray findings: increased lucency between osteochondral fragment and remainder of the bone, or loose body with donor site irregularity stage V subchondral cyst formation secondary degenerative change x-ray findings: secondary osteoarthritis

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* Tumour * GCT (closed physis) * EG * Chondroblastoma * clear cell chondrosarcoma * Mets * Infection * Osteomyelitis * TB * Subchondral cyst * arthropathy * CPPD * OA * RA Haemophilia * Interosseous ganglion

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Meniscal flounce Dr Andrew Dixon◉ and Assoc Prof Frank Gaillard◉◈ et al. Meniscal flounces refer to the "ruffled" appearance of the inner margin of knee menisci. They were initially thought to be only an arthroscopic finding, as a result of joint distension and anaesthetic muscle relaxants but they are occasionally seen on MRI. Epidemiology Meniscal flounces are uncommon with initial studies suggesting a frequency of around 0.2% on MRI scans, however more recently a frequency of up to 5% in relation to the medial meniscus has been reported.1,4 It is far more common to be seen with the medial meniscus than the lateral meniscus. Pathology They are not associated with an increased incidence of meniscal tears, but can be mistaken for one. They reflect a degree of redundancy in the medial meniscus and are typically seen in the flexed knee. Radiographic features MRI In the sagittal plane the flounce is seen as a wave or kink in the inner margin of the meniscus. In the coronal plane, they may make the inner margin of the meniscus appear truncated or blurred and simulate a small radial tear. Whenever a flounce is identified it is important to check that there are no ligamentous or capsular injuries that may be resulting in the laxity. This is particularly important if a lateral meniscal flounce is seen, as these are rare and may be a sign of popliteomeniscal fascicle injury/deficiency with hypermobile meniscus. History and etymology Out of interest, a flounce is a ruffle placed around a garment (often undergarment) as a decoration. Differential diagnosis radial-type meniscal tear

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**_Unilateral facet dislocation_** The vertebral body of C6 is anteriorly displaced relative to C7. The C6/7 facet joints are abnormally aligned, with one dislocated anteriorly (locked), and the other almost perched. Case Discussion A radiograph was performed at a rural centre before the patient was transferred to a tertiary trauma, where a CT confirmed the diagnosis (scan not available). Classically as one of the facets is still normally aligned, the amount of anterolisthesis is limited to less that 25 - 50%. Both facets would need to be dislocated to achieve greater anterolisthesis.

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* AKA: Skier's Thumb * Results from disruption of the _UCL_ * Associations: # base of proximal phalanx * Xray: stress views required if no # is identified

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* Alcohol/Amyloid * Sickle Cell * Exogenous Steroids * Perthes/pancreatitis * Trauma * Infection * Caisson disease * Lupus * Exrays (radiation), ESRF * Gaucher disease Also rheumatoid

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* Symmetric bilateral swelling * RA (most common) * any infllmatory arthritis * Asymmetric swelling of one digit * Sausage digit * Psoriasis * reiter syndrome * Lumpy bumpy soft tissue swelling. * Gout * amyloidosis * Multicentric Reticulohistiocytosis * Sarcoid

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* Onion skin Periosteal reaction * Ewings Sarcoma * LCH * Osteosarcoma * Osteomyelitis

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dashboard injury ## Footnote anterior force to tibia in a flexed knee (e.g. knees against dashboard in motor vehicle collision, or fall onto flexed knee) contusion pattern: anterior tibia +/- posterior patella associated with posterior cruciate ligament (PCL) tear

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Cyclops lesion (knee) Dr Mohamed Saber and Assoc Prof Frank Gaillard◉◈ et al. The cyclops lesion, also known as localised anterior arthrofibrosis, is a painful anterior knee mass that arises as a complication of anterior cruciate ligament (ACL) reconstruction, although has rarely been reported in patients with ACL injuries that have not been reconstructed. Epidemiology Cyclops lesions occur with an estimated frequency of ~5% (range 1-9.8%) of patients following ACL reconstruction. They are rarely encountered in patients who have not had ACL reconstruction but have nonetheless sustained ACL injuries 3. Clinical presentation Patients present with pain during extension of the affected knee, with an eventual audible and palpable “clunk”, occurring typically 8 to 32 weeks (16 weeks on average) after ACL repair 3. The term cyclops syndrome is used in patients with a post ACL reconstruction decrease in knee extension 4. Pathology The exact aetiology is uncertain and may be related to gradual fraying and bunching up of remnant ACL or graft fibres, excessive fibrosis, or alternatively due to the uplifting of fibrocartilaginous tissue during drilling of the tibia for anterior cruciate ligament reconstruction, which serves as a nidus for fibrous tissue deposition. Impingement of the graft in knee extension is also postulated 4. The end result, regardless of cause, is a rounded fibrous mass sitting in the anterior intercondylar notch. Pathologically, the lesion consists of central granulation tissue lined by synovium and surrounded by dense fibrous tissue. Radiographic features MRI As with other internal derangements of the knee, MRI is the modality of choice for assessing the postoperative knee. On MRI, a soft-tissue mass is seen anteriorly or anterolaterally in the intercondylar notch near the tibial insertion of the reconstructed anterior cruciate ligament. Because of its fibrous content, a cyclops lesion typically has intermediate to low signal intensity with all pulse sequences. Lesion signal is usually heterogeneous and there is variable contrast enhancement. There are no differentiating features on MRI between symptomatic and asymptomatic lesions. Treatment and prognosis Treatment is arthroscopic excision. History and etymology The lesion was so named because of its bulbous appearance and characteristic focal areas of reddish-blue discolouration (from venous channels) that resemble an eye at arthroscopy. Differential diagnosis nodular synovitis localised intraarticular giant cell tumour of the tendon sheath See also arthrofibrosis

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An olecranon spur is an extra-articular enthesophyte seen at the posterior portion of the proximal ulna's olecranon within the superficial aspect of the central triceps tendon insertion point. Epidemiology Olecranon spurs are commonly seen in patients with conditions such as tendinitis of the triceps, bursitis and gout. It is also believed to be more prevalent in patients who have a history of elbow trauma, or those who partake in repetitive forceful elbow extension activities 1. They can be an incidental finding. Clinical presentation They can be found in asymptomatic individuals or in patients who present with posterior midline elbow pain. Radiographic features The spur often curves upwards and possesses a faint radiolucent line at the base, which is thought to be due to the spur's formational developmental process as the calcified fibrocartilage thickens and forms small osseous nodules that overtime will fuse 1,2. Careful inspection of the base is therefore warranted to ensure it is not fractured 3. In the case of an incidental finding, one should look for secondary signs of inflammation such as swelling, or clarifying if the patient has midline posterior elbow pain, as the patient may be asymptomatic.

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Mimic of NOF This is OM

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lies just deep to the MCL

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Jumper's knee Dr Mostafa El-Feky◉ and Assoc Prof Frank Gaillard◉◈ et al. Jumper's knee is a chronic insertional injury of the posterior and proximal fibres of the patellar tendon at the site of its origin at the inferior pole of the patella. Many authors consider jumper's knee to be the adult form of Sinding-Larsen-Johansson disease 1 . Some suggest instead that jumper's knee is a mid-substance patellar tendinopathy.

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Chondrosarcoma * Low grade chondrosarcoma. * Case Discussion * Differential diagnosis is bone infarct (on plain film) and enchondroma. Dr Bahman Rasuli◉ and R Bronson et al. Chondrosarcomas are malignant cartilaginous tumours that account for ~25% of all primary malignant bone tumours. They are most commonly found in older patients within the long bones and can arise de novo or secondary from an existing benign cartilaginous neoplasm. On imaging, these tumours have ring-and-arc chondroid matrix mineralisation with aggressive features such as lytic pattern, deep endosteal scalloping and soft-tissue extension. Epidemiology The typical presentation is in the 4th and 5th decades and there is a slight male predominance of 1.5-2:1. Clinical presentation Patients usually present with pain, pathological fracture, a palpable lump or local mass effect. Hyperglycaemia can occur as a paraneoplastic syndrome. Pathology The histology of chondrosarcomas can differ according to their subtype (see below). In general, these tumours are multilobulated (due to hyaline cartilage nodules) with central high water content and peripheral endochondral ossification. This accounts not only for the high T2 MRI signal (see below) but also for rings and arcs calcification or popcorn calcification. Grading Chondrosarcomas are divided into three (sometimes four) grades based primarily on cellularity (see: chondrosarcoma grading). Subtypes Chondrosarcomas are either primary, arising de novo, or secondary and arise from a pre-existent cartilaginous mass (see: secondary chondrosarcoma). Primary conventional intramedullary chondrosarcoma (or central chondrosarcoma): low, intermediate or high grade (see: chondrosarcoma grading) juxtacortical chondrosarcoma: low, intermediate or high grade clear cell chondrosarcoma myxoid chondrosarcoma: usually intermediate grade mesenchymal chondrosarcoma: usually high grade extraskeletal chondrosarcoma dedifferentiated chondrosarcoma Secondary Arising from pre-existing cartilaginous lesions: osteochondroma solitary osteochondroma hereditary multiple exostoses enchondroma solitary enchondroma Ollier disease Maffucci syndrome Distribution long bones: 45% (the reason is that the cartilage is more abundant in the long, tubular bones) femur: 20-35% tibia: 5% upper limb (especially proximal humerus): 10-20% pelvis: 25% especially around the triradiate cartilage ribs: 8% patients often younger than at other sites anterior ribs/costochondral junction spine: 7% greater male predominance 2-4:1 thoracic most common location posterior elements and vertebral body 45% posterior elements only 40% vertebral body only 15% scapula: 5% sternum: 2% head and neck (including cervical spine): 6-7% craniofacial: 2% (see chondrosarcoma of the skull base) hands and feet: rare cf. enchondromas Radiographic features Imaging findings vary somewhat with different subtypes but do have some general features. Below are typical imaging appearances which are best demonstrated by conventional chondrosarcomas. In general chondrosarcomas are large masses at the time of diagnosis, usually \>4 cm in diameter and \>10 cm in 50% of cases. Plain radiograph lytic (50%) intralesional calcifications: ~70% (rings and arcs calcification or popcorn calcification) endosteal scalloping: affecting more than two-thirds of the cortical thickness (c.f. less than two-thirds in enchondromas) moth-eaten appearance or permeative appearance in higher grade tumours (see chondrosarcoma grading), e.g. myxoid, dedifferentiated and mesenchymal chondrosarcomas cortical remodelling, thickening and periosteal reaction are also useful in distinguishing between an enchondroma and low-grade chondrosarcoma (see enchondroma vs. low-grade chondrosarcoma) CT The features seen on CT are the same as on plain film, but are simply better seen: 94% of cases demonstrate matrix calcification, c.f. 60-78% on plain film endosteal scalloping cortical breach, seen in ~90% of long bone chondrosarcoma, c.f. only ~10% of enchondromas soft tissue mass: tumour cellularity, and therefore density, increases with increased grade of the tumour heterogenous contrast enhancement MRI T1: low to intermediate signal iso- to slightly hyperintense cf. muscle iso- to slightly hypointense cf. grey matter (see chondrosarcoma of the base of skull) T2: very high intensity in non-mineralised/calcified portions gradient echo/SWI: blooming of mineralised/calcified portions T1 C+ (Gd) most demonstrate heterogeneous moderate to intense contrast enhancement. enhancement can be septal and peripheral rim-like corresponding to fibrovascular septation between lobules of hyaline cartilage Nuclear medicine Typically chondrosarcomas demonstrate increased uptake on bone scan, seen in over 80% of cases, and usually the uptake is quite intense. This is useful in helping to distinguish low-grade chondrosarcoma from an enchondroma as the latter has increased uptake in ~20% of cases, and usually to a lesser degree (see: enchondroma vs low grade chondrosarcoma). Treatment and prognosis Prognosis varies with both grade and location. In general: grade grade 1: 90% 5-year survival grade 3: 29% 5-year survival location long bones have a better prognosis than axial skeleton Quiz questions

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Segond Fracture

Answer 56

CPPD at dens

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Osteochondroma Dr Mohammad Taghi Niknejad and Assoc Prof Frank Gaillard◉◈ et al. Osteochondromas are a relatively common imaging finding, accounting for 10-15% of all bone tumours and approximately 35% of all benign bone tumours. Although usually thought of as a benign bone tumour, they may be thought of as a developmental anomaly. They are frequently asymptomatic and have very low malignant potential if sporadic and solitary. Epidemiology Osteochondromas develop during childhood (period of most rapid skeletal growth), but once formed remain for the rest of the individual's life. They can present at any age and are most frequently found incidentally. They are usually sporadic, but can be part of: hereditary multiple exostoses (HME): also known as diaphyseal aclasis Trevor disease: also known as dysplasia epiphysealis hemimelica Malignant transformation occurs in the cartilage cap, and is uncommon in sporadic solitary osteochondromas (~1%), whereas in the setting of hereditary multiple exostoses the rate is much higher (5-25%) 5. Clinical presentation Symptomatic presentation is either due to mechanical effects of the lesion, fracture, or malignant transformation. Mechanical symptoms include: impingement upon nearby structures: nerve compression vascular compression reactive myositis palpable lump bursal formation and bursitis Fractures occur typically through the neck of pedunculated lesions. Ongoing growth and or pain after skeletal maturity has been reached is suspicious for malignant degeneration. Pathology Osteochondromas are considered a chondroid neoplasm and are primarily a part of the growth plate which separates and continues growing independently, without an associated epiphysis, usually away from the nearby joint. The medullary cavity is continuous with the parent bone, and hyaline cartilage caps them. Osteochondromas can be congenital or occur as a result of previous trauma to the growth plate, including previous irradiation 3,4. Location They most commonly arise from the appendicular skeleton, especially around the knee 3: lower limb: 50% of all cases 3 femur (especially distal): most common: 30% tibia (especially proximal): 15-20% less common locations: feet, pelvis upper limb humerus: 10-20% less common locations: hands, scapula spine: the posterior elements of the spine are an uncommon but not rare site for these tumours Radiographic features Plain radiograph An osteochondroma can be either sessile or pedunculated and is seen in the metaphyseal region typically projecting away from the epiphysis. There is often associated broadening of the metaphysis from which it arises. The cartilage cap is variable in appearance. It may be thin and difficult to identify, or thick with rings and arcs calcification and irregular subchondral bone. New cortical irregularity or continued growth after skeletal maturity has been reached, as well as frankly aggressive features (e.g. bony destruction, large soft tissue component, metastases) are all worrying for malignant transformation. CT CT demonstrates the same findings as on radiograph but is better able to demonstrate medullary continuity and the cartilage cap. Ultrasound Ultrasound is able to demonstrate the cartilage cap very accurately as a hypoechoic region bounded by bone on its deep surface and muscle/fat superficially. MRI MRI is the best imaging modality to assess cartilage thickness (and thus assessing for malignant transformation), the presence of oedema in bone or adjacent soft tissues, and visualising neurovascular structures in the vicinity. The cartilage cap of osteochondromas appears the same as cartilage elsewhere, with intermediate to low signal on T1 and high signal on T2 weighted images. A cartilage cap of over 1.5 cm in thickness is suspicious for malignant degeneration 3. With intravenous gadolinium administration, enhancement of benign lesions is normally seen in the tissue that covers the cartilaginous cap which is fibrovascular in nature, however, the cartilaginous cap itself should not enhance. Nuclear medicine During growth, osteochondromas demonstrate increased uptake on bone scans, but with time they become no more active than normal bone. Presence of increased activity in adulthood should raise the possibility of a complication (e.g. fracture, malignancy). Treatment and prognosis As they represent normal growth of a growth plate in an abnormal direction, they often stop growing with the rest of the skeleton 3. In most instances, no treatment is required. The osteochondroma can be locally resected for cosmetic or mechanical reasons. If malignant transformation occurs (~1% in solitary osteochondromas and ~5-25% with hereditary multiple exostoses) then the resultant chondrosarcoma is usually of low grade (67-85% of cases), and surgery is usually curative (70-90%) 3,5. Limb-sparing wide local excision usually suffices. The features associated with sarcomatous transformation can be remembered by the mnemonic GLAD PAST 1: growth after skeletal maturity lucency (new) additional scintigraphic activity destruction (cortical) pain after puberty and soft tissue mass thickened cartilage cap greater than 1.5cm Local recurrence is seen in both benign and malignant lesions, due to spillage of cartilage cells into the resection bed. Rates are estimated at 2% and up to 15% respectively 3. Differential diagnosis Imaging differential considerations include: hands: bizarre parosteal osteochondromatous proliferation (BPOP): arises from the bone cortex and lacks medullary continuity humerus: supracondylar spur: projects towards the elbow joint malunited fracture

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* Syncronous osteoblastic OSA at multiple sites * Usually metaphyseal and symmetric * Exclusively in children 5-10yrs * Poor Prognosis

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Cortical desmoid tumour mimic

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Ewing sarcoma Dr Tee Yu Jin◉ and Assoc Prof Frank Gaillard◉◈ et al. Ewing sarcomas are the second most common malignant primary bone tumors of childhood after osteosarcoma, typically arising from medullary cavity with invasion of the Haversian system. They usually present as moth-eaten destructive permeative lucent lesions in the shaft of long bones with large soft tissue component without osteoid matrix and typical onion skin periostitis. It may also involve flat bones and appears sclerotic in up to 30% of cases. Epidemiology Ewing sarcoma typically occurs in children and adolescents between 10 and 20 years of age (95% between 4 and 25 years of age), and has a slight male predilection (M:F 1.5:1) 1,2. The Ewing sarcoma family of tumors primarily occurs in white patients. In the United States, the incidence in Asians/Pacific Islanders is about one-half that in Caucasians, while the incidence among African Americans is one-ninth that in Caucasians 12. Clinical presentation Presentation is non-specific with local pain being by far the most common symptom. Occasionally a soft tissue mass may be palpable. Pathological fractures also occur. Systemic symptoms including fever may be present. ESR is also elevated. Pathology Ewing sarcoma is a small round blue cell tumor with regular sized primitive appearing cells. It is closely related to the soft tissue tumors pPNET, Askin tumor and neuroepithelioma, which collectively are referred to as Ewing sarcoma family of tumors (ESFT) 1. They share not only microscopic appearances but also demonstrate a non-random t(11;22)(q24;q12) chromosome rearrangement. Location lower limb: 45% femur most common pelvis: 20% upper limb: 13% spine and ribs: 13% (see thoracic Ewings sarcoma) sacrococcygeal region most common 4 skull/face: 2% Alternatively 3: long bones: 50-60% femur: 25% tibia: 11% humerus: 10% flat bones: 40% pelvis: 14% scapula ribs: 6% (thoracic Ewing sarcoma) As far as location within long bones, the tumor is almost always metadiaphyseal or diaphyseal 2-3: mid-diaphysis: 33% metadiaphysis: 44% metaphysis: 15% epiphysis: 1-2% Radiographic features Ewing sarcomas tend to be large with poorly marginated tumors, with over 80% demonstrating extension into adjacent soft tissues. It should be noted that pPNET often extend into bone, making the distinction difficult. Plain radiograph and CT The appearance of these tumors is very variable, but they usually have clearly aggressive appearance. Common findings include 2: permeative: 76% laminated (onion skin) periosteal reaction: 57% sclerosis: 40% They occasionally demonstrate other appearances, including Codman triangles, spiculated (sunburst) or thick periosteal reaction and even bone expansion or cystic components. Soft tissue calcification is uncommon, seen in less than 10% of cases 2. MRI T1: low to intermediate signal T1 C+ (Gd): heterogeneous but prominent enhancement T2: heterogeneously high signal, may see hair on end low signal striations Nuclear medicine Ewing sarcomas demonstrate increased uptake on both Gallium67-citrate and all three phases of the Technetium99m methylene diphosphonate bone scans 6. Treatment and prognosis Systemic chemotherapy is the mainstay of treatment with surgery and/or radiotherapy playing a role depending on the location and size of the tumor. What was once a uniformly fatal tumor now has respectable survival rates, although these vary with location. Spinal tumors for example have up to 86% long term survival compared to 25% of sacrococcygeal tumors 4. The overall 5 year survival is in the order of 50-75% of patients with local disease only at the time of presentation 5. Prognosis is significantly impacted by the presence of distant metastases at the time of diagnosis, which is far more common for the pelvis (25-30%) compared to extremities (\<10%) 5. Metastases most frequently go to bone or lungs. History and etymology It is named after James Stephen Ewing (1866-1943), an American pathologist, who first described his eponymous tumor in 1920 8,11. Differential diagnosis other Ewing sarcoma family of tumors pPNET: large soft tissue component with extension into bone Askin tumor: chest wall osteosarcoma: more often has amorphous calcified matrix classically perimetaphyseal, Ewing sarcoma also occurs in other locations more prevalent around the knee and in the proximal humerus, in other locations Ewing sarcoma is the more frequent of the two osteomyelitis metastatic disease hematological malignancy eosinophilic granuloma 9 neuroblastoma (

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1. Rheumatoid 2. post-traumatic distal slavicular osteolysis 3. Myeloma 4. Mets 5. Osteomyelitis X-ray Interpretation: Shoulder Injuries | Radiopaedia.org Key Points post-traumatic osteolysis of the distal end of the clavicle may be seen in patients following AC joint injuries these injuries can be unilateral or bilateral as the result of a single traumatic event or repetitive strain history of trauma or repetitive strain is important, otherwise, differential diagnoses may be considered a useful mnemonic to remember the differentials is SHIRT Pocket: S: scleroderma H: hyperparathyroidism I: infection (osteomyelitis) R: rheumatoid arthritis T: trauma P: progeria

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