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#2 BOARDS > Radiology 2 > Flashcards

Radiology 2 Flashcards

1
Q

Osteopenia

A
  • Means “poverty of bone” and is used to refer to the nonspecific radiographic findings of decreased bone density
  • When 30-50% of bone mass is lost, radiographs reveal osteopenia
  • The bone mass loss in osteopenia leads to defective bone quality and strength, causing a marked risk for osteoporosis
  • More resorption than formation of bone
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2
Q

Osteoporosis

A
  • Reserved for the clinical entity or diagnosis
  • A metabolic disease that accompanies many other disease processes, including endocrine/nutritional disorders
  • The amount of bone present per unit of volume is reduced, but bone composition is normal ***
  • Characterized by progressive loss of bone mass due to increased resorption as well as decreased bone production
  • Bone becomes fragile and susceptible to fracture because there is not only bone mass reduction, but also deterioration of the microarchitecture of the bone tissue
  • 6 different types – we focus on primary type 1 seen in post-menopausal women and primarily affects trabecular bone, whereas type 2 affects trabecular and cortex
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3
Q

Osteomalacia

A
  • Characterized histologically as a disorder with excessive amounts of uncalcified osteoid
  • Unlike osteoporosis, osteomalacia is a qualitative change in the bone (there isn’t just less of it, it is different) due to the inadequate or delayed mineralization of osteoid
  • Since osteoid formation exceeds matrix mineralization, total osteoid tissue is increased and growth rate is decreased
  • Many metabolic disorders interfere with bone matrix deposition and mineralization and cause osteomalacia
  • Etiologies include: vitamin D deficiency (dietary) and malabsorption (GI disease), hypophosphatemia (oncogenic osteomalacia) and mineralization inhibitors (aluminum)
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4
Q

Difference between osteomalacia and Rickets

A
  • Decreased bone mineralization in the adult skeleton = Osteomalacia
  • Decreased bone mineralization in the infant/child skeleton = Rickets
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5
Q

Radiographic features of chronic osteopenia

A

o Highly subjective because processing influences appearance (lucency) of bones
o **Cortical and **cancellous bone resorption is best identified using DP foot films (AP) with attention focused on the 2nd, 3rd and 4th metatarsals – don’t use MO views to assess
o **Cortical bone: endosteal resorption, intracortical tunneling (resorption along surface of Haversian canals), and/or subperiosteal resorption
o **Cancellous bone: prominent trabeculations
o KNOW that osteopenia includes both cortical and cancellous bone changes

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6
Q

Radiographic features of acute osteopenia

A 
o	Spotty (mottled or moth-eaten) loss of bone density, particularly in periarticular regions
o	Associated with causes of regional osteoporosis, such as immobilization or disuse
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7
Q

Radiographic features of generalized osteoporosis

A

The radiographic feature of generalized osteoporosis is chronic osteopenia, which includes one or more of the following:
o **Prominent primary trabeculations
o **Thinning of the cortices
o ***Intracortical striations (tunneling)

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8
Q

Radiographic features of regional osteoporosis

A

The radiographic findings of regional osteoporosis (affects one extremity – focal disorder) can be seen acutely or chronically and are associated with disuse, CRPS, denervation, fracture, inflammation, etc.
o Spotty (moth-eaten, mottled, patchy) osteopenia in cancellous bone, especially periarticular regions, appearing as small, oval or round, lucencies within the affected bone
o **KNOW SPOTTY for REGIONAL OSTEOPOROSIS*
o **Ill-defined broad (4-8 mm) transverse bands of decreased density at subchondral or metaphyseal locations
o **Sub-periosteal bone resorption (in severe cases, especially CRPS)

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9
Q

Radiographic features of osteomalacia

A
  • Uncalcified osteoid
  • Radiographic features of osteomalacia are nonspecific, consisting primarily of osteopenia
  • Bowing of long tubular bones may occur
  • Pseudofracture (“Looser zone” or “milkman fracture”): transversely oriented, incomplete radiolucency of tubular bones is a classic radiographic sign
  • The lucent line may be bordered by sclerosis and are usually located along the compressive side of the bone
  • This tends to be bilateral and symmetrical, and a common location for the Looser zone is the femur
  • NOTE the Looser zone of osteomalacia is found on the inner border of a long bone, which distinguishes it from hypophosphatasia where the looser line is on the outer cortex of the bone
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10
Q

Hypophosphatasia

A
  • Hypophosphatasia is a condition characterized by reduced levels of alkaline phosphatase (ALP)*** in serum, bone and other tissues
  • Caused by a variety of mutations in ALP gene
  • Rare, but increased frequency in Canadian Mennonites
  • Severity depends on age of presentation, but no curative treatment exists
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11
Q

Hypophosphatasia x-ray findings

A
  • ***Bowing and shortening of long tubular bones
  • ***Osteochondral spurring
  • May be rickets-like findings at the zone of provisional calcification
  • May be chondrocalcinosis articularis and Looser zone present (NOTE: Looser zone in hypophosphatasia is on the outer cortex, whereas Looser zone in osteomalacia is on the inner cortex)
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12
Q

Hyperparathyroidism

A
  • Increased levels of parathyroid hormone (PTH), which indirectly leads to increased osteoclastic activity and ultimately leads to the removal of calcium from bone, which then enters the blood
  • Excessive PTH secretion has 3 forms (primary, secondary, tertiary)
  • ***Primary: parathyroid abnormality (i.e. tumor of parathyroid) leads to hypercalcemia
  • ***Secondary: low calcium levels (I.e. from vitamin D deficiency)
  • ***Tertiary: hyperplasia of parathyroid gland and loss of response to serum calcium levels, most often seen in patients with chronic renal failure
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13
Q

Hyperparathyroidism x-ray findings

A
  • ***Subperiosteal bone resorption (other sites of bone resorption include: periarticular, intracortical, endosteal, subchondral, entheseal)
  • ***Oseitis fibrosis cytica: or “Von Recklinghausen disease of bone, where fibrous tissue replaces bone that is removed
  • ***Brown tumors: or osteoclastomas, which are circular radiolucent (lytic) lesions that correspond to “hot spots” on bone scan and when seen in the lower extremity are most commonly seen in the calcaneus – they resemble metastatic lesions
  • ***Soft tissue calcifications: these can also be seen, especially with secondary hyperparathyroidism
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14
Q

Renal osteodystrophy

A
  • A form of tertiary hyperparathyroidism
  • Patients with CRF demonstrate bony abnormalities known as renal osteodystrophy or renal bone disease
  • Not usually seen in patients until they are on hemodialysis
  • Biopsy can show either increased or decreased bone turnover
  • Chronic kidney disease causes hyperphosphatemia, which causes an increase in PTH and stimulates osteoclastic activity
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15
Q

Renal osteodystrophy x-ray findings

A
  • Radiographic findings parallel those of hyperparathyroidism, osteoporosis and osteomalacia/rickets
  • ***Calcification of soft tissue and vessels is frequent, especially in high serum calcium and phosphorus concentrations
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16
Q

Rickets

A
  • Epiphyseal region abnormality
  • Disease of growing bone that is unique to children/adolescent
  • Caused by failure of osteoid to calcify, which involves impaired mineralization at the physis, resulting in deformity and impaired linear growth of long bones
  • Etiologies include vitamin D deficiency, abnormal metabolism of vitamin D, dietary calcium deficiency, chronic hypophosphatemia
  • GI disorders associated with low vitamin D, calcium and phosphorus absorption can cause this
  • Acquired or inherited renal tubular abnormalities causing resorptive defects can also cause it
  • Histologically, we see an increased number of disorganized cells and therefore increased width and thickness at the growth plate or more specifically, the zone of provisional calcification
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17
Q

X-ray findings in Rickets

A

Non-specific
o General retardation of body growth, osteopenia and bowing of long tubular bones

Characteristic (most pronounced at knee and ankle)
o ***Widening of the physis (due to excessive cartilage build-up)
o Decreased density at the zone of provisional calcification (due to decreasing mineralization)
o Irregularity of the physeal margin of the zone of provisional calcification – “fraying” or “paint-brush” appearance due to variable calcifications of the enlarged cartilage mass
o Widening and cupping of the metaphysis (as the disorganized mass of cartilage expands
o In fast growing long bones (tibia) there can be transverse metaphyseal lines of increased density may be seen, representing the growth arrest and recovery lines of Harris or Park
o Genu varum or genu valgum may be seen in crawling toddlers

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18
Q

Scurvy (hypovitaminosis C)

A
  • Caused by insufficient dietary intake of vitamin C, which is needed for collagen synthesis and is an important part of bone
  • There are two types: pediatric scurvy (Barlow disease) and adult scurvy
  • Still common today due to lack of fresh fruit and vegetables in diet
  • Risk factors: bottle-fed infants with no vitamin C supplementation, elderly, males living alone, chronic alcoholism, high cigarette use
  • Clinical manifestations are due to fragile vessel walls leading to bleeding, and damage to synovial blood vessels and microfractures leading to bleeding in joints
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19
Q

Scurvy x-ray findings

A

Metaphyseal region features (pediatric)
o Transverse line of increased density bordering the growth plate, due to the thickened zone of provisional calcification (“white line of scurvy/Frankel”)
o Transverse line of decreased density adjacent to the line of increased density on its metaphyseal side that consists of detritus (referred to as the “scurvy line,” scorbutic zone and Trummerfeldzone)
o Small, beak-like outgrowths or extension of the zone of provisional calcification along its margins (“Pelkan spur/beak”)
o Subepiphyseal infarctions in an area of brittle and decreased trabeculae (“corner/angle sign”)

Periostitis (pediatric)
o Extensive periostitis along the entire length of bone secondary to subperiosteal hemorrhage stimulating the periosteum

Adult
o Radiographic findings are limited in the adult, despite extremity pain and swelling
o May be some osteoporosis and rarely, bone resorption at the joints due to hemarthrosis

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20
Q

Acromegaly

A
  • A disorder in adults with increased growth hormone output, commonly due to a pituitary adenoma, which results in severe disfigurement, serious complicating conditions and premature death if left unchecked
  • Gigantism is the result of increased growth hormone in a child with open growth plates
  • Acromegaly causes increased bone turnover and appendicular cortical bone mass
  • Low rate of fracture is seen in acromegaly despite high prevalence of osteoporosis due to the anabolic effect of GH on trabecular and cortical bone, which persists after acromegaly remission
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21
Q

Acromegaly x-ray findings

A
  • Abnormalities of soft tissue, joint spaces and bone are seen in acromegaly
  • Increased soft tissue volume seen in heel pad greater than 25 mm (male) or 23 mm (female)***
  • Joint space widening due to cartilage thickening
  • Prominent bones with enlarged met heads and distal phalanx ungula tuberosities, thickened metatarsal shafts and spars found at enthuses
  • Proximal phalangeal shafts appear narrow in girth
  • Acromegalic arthropathy (resembles OA) can occur, consisting of osteophytes, eburnation, subchondral geode formation, joint space narrowing and calcification of a ligament and joint capsule entheses
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22
Q

Osteogenesis imperfecta

A
  • Hereditary disorder characterized by an involvement of bones and extra-skeletal tissues (skin, teeth, sclerae, ligaments), resulting in abnormal metaphyseal and periosteal ossification caused by deficient osteoid production
  • Sometimes called “brittle bone disease” due to the increased tendency to fracture
  • Abnormal maturation of collagen occurs in both mineralized and non-mineralized tissues
  • Type 1: most common, mild form with fractures but no dwarfing or bone deformity
  • Type 2: neonatal and lethal
  • Type 3: rare, demonstrates dwarfing and extreme fragility of bones (fractures common)
  • Type 4: variable findings ranging from short stature and bone deformity to normal height
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23
Q

Osteogenesis imperfeca x-ray findings

A
  • Diffuse **osteopenia, presenting occasionally with coarse trabeculae, **diminished bone girth and ***flared metaphyses
  • An obvious complication of osteogenesis imperfecta is fracture, which can show excessive bone callus formation
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24
Q

Hypoparathyroidism radiographic findings

A
  • ***Brachy-metatarsalgia: Condensed, shorter, wider metatarsals
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25
Q

Paget’s disease

A
  • Second most common aging bone disorder following osteoporosis (excluding fracture)
  • Chronic disorder of excessive abnormal bone remodeling, resulting in enlarged, deformed bones
  • 3-4% of those older than 40 are affected, more frequently in men, and 1-% of those older than 70 are affected
  • Etiology is unknown with controversial evidence for both genetic and environmental as well as viral factors proposed
  • Alkaline phosphatase and hydroxyproline will be ELEVATED
  • Can affect any bone in the body, but predominates in axial skeleton with the most common bones being the femur and tibia, seldom the calcaneus (and asymptomatic in the foot)
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26
Q

Stages of Paget’s disease

A
  • Stage 1: incipient and active lytic phase with giant multinucleated osteoclasts that resorb bone
  • Stage 2: active mixed phase with osteoblasts and osteoclasts present, but excessive osteoblast activity is disordered and causes architecturally abnormal bone to be laid down at affected sites
  • Stage 3: late, inactive blastic phase or silent stage where osteoblastic activity declines
27
Q

X-ray findings in stage 1 of Paget’s disease

A

Stage 1: Osteolytic
o Affects the skull (osteoporosis circumscripta) and long bones
o Short lived and causes resorption starting in the subchondral area and spreading to the metaphysis then diaphysis giving a “blade of grass” or “flame” appearance

28
Q

X-ray findings in stage 2 of Paget’s disease

A

Stage 2: Osteolysis and osteosclerosis

o Diaphysis appears lucent, where epiphyseal and metaphyseal regens appear sclerotic

29
Q

X-ray findings in stage 3 of Paget’s disease

A

Stage 3: Osteosclerosis
o Involves mainly proximal long bones
o Cortical thickening, bone enlargement and coarsened trabeculae
o If tibia is affected, may involve anterior bowing or “sabre-shin deformity” and Pseudofracture (similar to that of osteomalacia) along the anterior surface

30
Q

Sickle cell anemia

A
  • Caused by production of abnormal hemoglobin, which binds with other abnormal hemoglobin molecules within RBCs causing rigid deformation of the RBC (sickle shape)
  • The sickle shaped RBCs cause sludging and congestion of vascular beds, followed by ischemia and tissue infarction
31
Q

Complications of sickle cell anemia

A
  • Dactylitis: an acute vaso-occlusive crisis commonly seen in black children (6 mo-6yr) with sickle cell that includes painful swelling of feet, toes, hands, fingers and has an associated fever
  • Osteomyelitis: a serious complication of sickle cell, most commonly seen in the diaphyseal region of long bones (femur, tibia) and involves (1) salmonella, (2) staph aureus, (3) gram negative enteric bacilli
32
Q

Sickle cell anemia x-ray findings

A
  • Dactylitis appears radiographically normal initially, but periostitis occurs within 10 days of onset of symptoms, causing the metatarsals or phalanges to appear rectangular in shape
  • Following periostitis, we see cortical thinning, attenuation of the medullary canal and irregular densities within the medullary canal
  • Acute crises may be radiographically normal due to ischemia preceding infarction manifestation
  • NOTE: bone infarcts look SCLEROTIC, not LUCENT
  • Osteonecrosis may be an incidental finding due to silent infarction in sick cell patients
33
Q

Thalassemia

A
  • AKA “Cooley anemia”
  • Characterized by abnormal hemoglobin synthesis with three forms: major, minor, intermedia
  • Thalassemia major is the most severe and demonstrates the most common radiologic features
34
Q

Thalassemia x-ray findings

A
  • Widening of the marrow cavity (mirroring the degree of marrow hyperplasia seen)
  • Cortex thinning
  • Coarse trabeculations with “honeycomb” appearance
  • Widening of the metaphysis and epiphysis of long tubular bone, resembling “Erlenmeyer flask”
35
Q

Osteopetrosis

A
  • AKA “stone bone” or “marble bone disease” due to defective osteoclast function and a defect in bone resorption resulting in increased bone density and reduction in bone marrow space
  • Radiographically we see an inability to differentiate between cortex and medullary cavity in tubular bone due to excessive bone formation
  • Results in denser and more brittle bone
  • ***Mahoney: can also see “Erlenmeyer flask” and “bone inside of bone” and thick bands of sclerosis
36
Q

Types of osteopetrosis

A
  • Two types: autosomal recessive (ARO, malignant, contenita) and autosomal dominant (ADO, benign, tarda)
  • ARO: occurs in infancy, death by 10 years of age
  • ADO type I: benign form with low fracture rate due to increased bone strength, extremity involvement is uncommon, but can see diffuse sclerosis and cortical thickening of tubular bones
  • ADO type II: diffuse bone sclerosis with “bone within a bone” appearance with sclerotic transverse bands in femoral and tibial metaphyses
37
Q

Melorheostosis

A
  • “Leri disease” is a rare dysplasia characterized by a “flowing” hyperostosis along the cortex of tubular bones
  • Usually asymptomatic, but can cause limb stiffness and pain, skin changes (sclerodermatous skin lesions), hemangiomas, circulation problems (lymphedema), joint contractures, muscle atrophy and functional limitations
  • Chronic progressive disease with age of onset determining severity of symptoms
38
Q

Radiographic findings in melorheostosis

A
  • Radiographically, hyperostosis along one site of bone’s periphery, extending along its entire length which appears like wax flowing down the side of a candle (“wavy, sclerotic bony contour”) which can partially or fully obliterate the medullary canal
39
Q

Osteopoikilosis

A
  • Inherited, autosomal dominant skeletal dysplasia that is NOT associated with symptomology
  • Etiology is unknown, but thought to be associated with a loss-of-function gene mutation
40
Q

Radiographic features of osteopoikilosis

A
  • Radiographically we see unequal distribution of numerous small, well-defined, homogenous circular foci of increased density (hyperostotic areas) mimicking multiple bone islands
  • These hyperostotic areas are found at the ends of long bones and in tarsal bones
41
Q

Osteopathia striata

A
  • Typically asymptomatic, most likely inherited, possibly due to mesodermal mosaic dysfunction
  • Radiographically, linear and regular, fine bands of increased and decreased density extend from the metaphysis to the diaphysis, running parallel to the shaft of long bones
  • This is of no medical/clinical significance and is not clear if the striations reflect increased or decreased bone density or increased risk for osteoporosis or spontaneous fracture
42
Q

Pyknodysostosis

A
  • Autosomal recessive disorder caused by a chromosome mutation leading to diffuse sclerosis of bone and associated with recurrent fractures and dwarfism
  • Radiographically, generalized increased bone density (osteosclerosis) and narrowing of the medullary canals
  • Characteristic features: hypoplasia/acro-osteolysis of distal phalanges and bone fragility
43
Q

Fluorosis

A
  • Chronic fluorine intoxication causes clinical manifestations of joint pain, limited ROM and palpable thickening of the tibia
  • All fluorine that is not excreted by the kidneys (50%) is retained by calcified tissues
  • Radiographically, osteopenia (prone to fractures), ligament calcification, enthesopathy and thickening of periosteal surfaces of bones
  • Classic skeletal fluorosis: advanced manifestations with abnormal fracturing and distinctive increased bone density
44
Q

Hypervitaminosis D

A
  • Overdose of vitamin D can be acute or chronic and causes hypercalcemia, hyperphosphatemia and normal to low PTH level
  • Causes sever clinical pain due to periarticular calcinosis, severe disruption of endochondral bone formation with excessive calcification of the proliferating cartilage cells causing widening of the zone of provisional calcification
  • Radiographically, causes generalized increase in bone density, increased calcification of the soft tissues (blood vessels and around joints)
45
Q

Venous stasis

A
  • Chronic inflammation with venous insufficiency is associated with periosteal new bone formation, which increases in severity with severity of venous insufficiency
  • Periostitis is seen in 10-60% of patients with severe venous stasis, commonly in the tibia
  • The periostitis is often an incidental finding and may be caused by periosteal hyperemia
  • Soft tissue calcification is commonly associated
  • Linear white line along the course of the bone where the vein sits on the bone it causes periostitis
46
Q

Hypertrophic osteoarthropathy osteoarthropathy

A
  • Clinical syndrome consisting of digital clubbing, extremity enlargement and swollen joints with no signs of acute inflammation and enlargement of bones seen in later stages
  • X-rays can diagnose hypertrophic osteoarthropathy
47
Q

Primary hypertrophic osteoarthropathy

A
  • Primary (hereditary or idiopathic): insidious onset, mostly common in black adolescent males, predominant finding is periostitis which causes a thickened and sometimes shaggy appearing cortex that extends to the epiphysis
48
Q

Secondary hypertrophic osteoarthropathy

A
  • Secondary (pulmonary hypertrophic osteoarthropathy): results from cardiopulmonary disease, hepatic disease, GI disease or malignancies (i.e. bronchogenic carcinoma) and demonstrates periostitis that is distinct from the underlying cortex, meaning that it is more linear than it is shaggy or irregular, mostly occurring in the tibia and fibula and along the diaphysis of metatarsals and phalanges, causes a dull ache with synovitis
49
Q

What else can you see with hypertrophic osteoarthropathy?

A
  • Mahoney: Clubbing of the digits, toes are enlarged/swollen and joints are painful
50
Q

Hypervitaminosis A

A
  • Increased levels of vitamin A due to treatment or consumption will stimulate periosteal new bone formation, which will cause cortical thickening, most notably at the metaphysis
  • Radiographic features are limited to children and soft tissue nodules will be found adjacent to cortical abnormalities
51
Q

Thyroid acropachy

A
  • Rare manifestation of Grave’s disease (autoimmune hypothyroid) or less commonly Hashimoto’s and associated with tobacco use
  • Clinical manifestations include clubbing and skin tightness of digits, soft tissue swelling and pain in distal small joints
  • Radiographically, solid periosteal reaction is present that may appear thick or thin, feathery, lacy, frothy or shaggy, and can appear speculated and perpendicular to the shaft
  • The periosteal reaction tends to be bilateral and involves the tubular bones of the foot, mid-diaphyseal and symmetrical
52
Q

Tuberous sclerosis

A
  • An autosomal dominant disease with the classic triad of mental retardation, epilepsy and harmatomas
  • Radiographically produces a wavy periostitis of metatarsal and phalanges as well as patchy increased densities that are island-like as well as lucent areas in diaphyses
  • Mahoney: Causes fibromas around the nails
53
Q

Different types of soft tissue calcifications - KNOW FOR BOARDS

A
  • Metastatic calcifications
  • Generalized calcinosis
  • Dystrophic calcification
54
Q

Metastatic calcifications

A

o Occurs in normal tissue and results from a disturbance in calcium or phosphorus metabolism (i.e. hyperparathyroidism, hypoparathyroidism, renal osteodystrophy)

55
Q

Generalized calcinosis

A

o Presents as calcium deposition in the skin and subcutaneous tissue in the presence of normal calcium metabolism
o Three types: calcinosis circumscripta (collagen vascular disease), calcinosis interstitialis universalis (effects the young), tumoral calcinosis (large mass on extensor joint surface)

56
Q

Dystrophic calcification

A

o Calcium is deposited in damaged or devitalized tissue in absence of a generalized metabolic derangement
o Most common form seen in foot and ankle following neoplasm, inflammation, trauma

57
Q

Differential diagnosis for dystrophic calcification

A

VINDAT

  • V = Vascular (i.e. phlebolith***)
  • I = Infection
  • N = Neoplasm (i.e. osteosarcoma)
  • D = Drugs (i.e. vitamin D)
  • A = Autoimmune (i.e. dermatomyositis, scleroderma)
  • T = Trauma
58
Q

Describe what is meant by heterotopic ossification

A
  • Heterotopic ossification describes bone formation at an abnormal anatomical site (soft tissue) which is associated with genetic disorders, musculoskeletal trauma, neurologic injury and venous insufficiency
59
Q

Forms of myositis ossifications

A
  • Myosistis ossificans progressive
  • Myosistis ossificans circumscripta
  • Myosistis ossificans assocaited with neurologic disease
  • Heterotropic ossificans
  • Pseudomalignant myositis ossificans
60
Q

Myosistis ossificans progressive

A

o Rare genetic dysplasia with (a) recurrent, painful soft tissue swelling that leads to heterotopic ossification and (b) congenital malformation of the great toe
o Soft tissue ossification is widespread and progressive with no treatment

61
Q

Myosistis ossificans circumscripta

A

Myositis ossificans circumscripta = ALL YOU NEED TO KNOW FOR THE TEST***
o Most common form, caused by localized trauma (single blow, muscle tear, repeated minor trauma), where pain increases and a mass develops with cartilaginous consistency within 4-7 weeks
o Need to biopsy the bone to differentiate it from osteogenic malignancy

Histologically

  • Myositis ossificans = osteoid at the periphery of the lesion
  • Osteosarcoma = osteoid at the center of the lesion
62
Q

Myosistis ossificans assocaited with neurologic disease

A

o May be due to a variety of neurologic causes

63
Q

Heterotropic ossificans

A

o Has been reported in venous insufficiency (postmenopausal females primarily) and does not fit any other categories (no history of trauma or congenital malformation)

64
Q

Pseudomalignant myositis ossificans

A

o Similar to circumscripta, but without a history of trauma

o Can radiographically mimic a soft tissue sarcoma

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