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67 Cards in this Set

  • Front
  • Back
What are the musculoskeletal features of neurofibromatosis type 1?
- Skin lesions are the most constant feature with cafe-au-lait spots occurring in 90% of patients.
- Skeletal manifestations of neurofibromatosis are often the result of direct pressure from an adjacent tumor; however, dysplastic changes of bones may also occur.
- Bowing deformity of long bones
- Acute angled scoliosis, particularly when it involves the upper thoracic spine.
- Pseudoarthrosis
- Ribbon-like deformity of the ribs
- Dural ectasia (posterior vertebral body scalloping)
- Multiple NOF
1. What is DDX of numerous sclerotic foci?
2. Where are the lesions in osteopoikilosis found?
3. What are the findings on bone scan in osteopoikilosis?
1. Osteopoikilosis, osteoblastic mets, melorrheostosis, sclerotic form of multiple myeloma, and sarcoidosis.
2. Lesions tend to cluster in a periarticular distribution with a predilection for the epiphysis and metaphysis. They are also commonly seen in the carpus, tarsus, pelvis, and scapula.
3. Bone scan shows absence of increased uptake.
1. What are the 5 D's of neuropathic joints?
2. What are the three presentations of neuropathic arthropathies?
3. What is the imaging appearnce of neuropathic joint?
1. Increased density, joint distention, intra-articular and periarticular debris, joint disorganizatin, dislocation.
2. Hypertrophic, atrophic, and mixed.
3. In atrophic neuroarthropathy, there is resorption of the bone producing a well demarcated transition between lysed and remaining bone. NOTE: other processes that can result in rapid destruction of bone include infection and tumors.
What are the imaging findings of periosteal osteosarcoma?
Radiating osseous spicules that extend from the superficial region of the cortex into the adjacent soft tissue, often in a perpendicular orientation to the cortex.
1. What are some common locations of giant cell tumor?
2. Does the radiographic appearance predict malignant behavior?
3. What is the matrix of GCT?
4. What is characteristic of tumor recurrence in the soft tissues?
5. GCT is associated with what fibro-osseous lesion?
1. About the knee, proximal humerus, distal radius, and pelvis and sacrum.
2. The radiologic appearance does not predict benign or malignant potential.
3. No matrix is seen within the lesion.
4. Tumor recurrence within the soft tissue is often calcified.
5. Associated with paget's disease.
1. What is the etiology of synovial osteochondromatosis?
2. What is the course of synovial osteochondromas in the joint?
3. What are the imaging findings?
4. How do you differentiate from PVNS?
1. Synovial metaplasia of unknown etiology that is characterized by the formation of numerous cartilaginous nodules that project from the synovium into the joint. When the pedicle breaks, these nodules become detached into the joint cavity.
2. Nodules may resorb, enlarge, remain purely cartilaginous, or become calcified or ossified.
3. The disease is monoarticular and affects young and middle-aged adults.
4.
- On radiographs, look for numerous, small, calcified or ossified densities within the joint space.
- MRI usually reveals additional
cartilaginous bodies that are not evident radiographically.
- Intra-articular nodules vary slightly in size but seldom exceed more than 2 to 3 cm in diameter.
- Pressure-erosive changes may develop in the intracapsular cortex
- Mechanical effects of intra-articular bodies promote secondary osteoarthritic changes in the articular cartilage.
4. Synovial choncdromatosis rarely
has an effusion, whereas PVNS commonly has a dense effusion.
1. What are the radiographic findings of rheumatoid arthritis?
2. Is RA always symmetrical?
1. Radiographic features of RA include:
- soft-tissue swelling
- periarticular osteoporosis
- early joint space narrowing
- articular erosions
- marginal erosions
2. Although symmetry is the hallmark of RA, several exceptions are notable. Early in the disease process, involvement may be monoarticular or pauciarticular in 5% to 20% of patients.
What are the imaging findings of melorheostosis?
Begins as linear hyperostosis in the distribution of one sensory nerve (sclerotomal distribution) --> becomes uniform cortical thickening on one side of a bone -->progresses
from one end of the bone to the center.
- Dense linear hyperostosis resembles "flowing candle
wax",
- Hyperostosis may advance to the joint margin or even protrude into the joint.
- Thickening of the cortex and adjacent underlying trabeculae is best demonstrated on CT.
1. Where are the calcium pyrophosphate crystals deposited?
1.
- Hyaline cartilage: calcifications appear thin and parallel the contour of the bony articular surface.
- Fibrocartilage (menisci of the knee, the triangular fibrocartilage of the wrist, the labrum of the hip, and the annular ligaments of the spine): calcifications tend to appear thick, shaggy, and irregular.
- Entheses (insertion of tendons and ligaments on bone)
- Synovium: Synovial calcifications are often cloudlike.
- Capsule: capsular calcifications tend to be either linear or irregular.
2.
1. What is the ddx of diaphyseal cortical thickening in a child?
2. What is the ddx of diaphyseal cortical thickening in an adult?
1. For children:
- Engelmann's disease
- Osteopetrosis
- Infantile cortical hyperistosis
- vitamin A poisoning.
2. For adults
- Van Buchem's syndrome
- Hyperphosphatasemia
- Melorheostosis
- Erdheim-Chester disease
- Ribbing's disease: adult equivalent of Engelmann's disease.
- Chronic infection
1. What are the radiographic findings in acromegaly?
2. What disease can mimic the radiographic and clinical findings of acromegaly?
1.
- Tall
- FACE: coarsening of facial features with macrognathia, frontal bossing from enlarged frontal sinuses, increased separation of teeth
HANDS: expansion of the distal tuft of the phalanx, increased separation of fingers giving a spade-like appearance.
SPINE: DISH like ossification, posterior vertebral body scalloping, enlargement of the vertebral body.
SKULL: enlargement of the sella with erosion of the posterior wall.
2. Pachydermoperiostitis.
Wha is ddx of diffuse periosteal reaction?
1. Secondary hypertrophic osteoarthropathy:
- painful
- affects long tubular bones of the upper and lower extremities. Initially, the diaphysis are affected followed by metaphysis.
- synovitis and soft tissue swelling may also be seen
2. Pachydermoperiostosis (primary hypertrophic osteoarthropathy)
3. Venous stasis: tends to affect the lower extremities
4. Thyroid acropachy:
- periostitis is asymptomatic and occurs in the small bones of the hadns and feet
- look for exaphthalmos and pretibial myxedema.
5. Hypervitaminosis A
What are the radiographic manifestations of sickle cell disease?
- Coarsening of the osseous trabeculation
- Diminished bone density
- Vertebral bodies demonstrate characteristic biconcave contours ("fish vertebrae") or central depressions that are the result of diminished bone growth induced by sludging of red blood cells.
- Bone-in-bone appearances in the long bones are created by infarctions.
- Hip and shoulder pain may indicate the presence of avascular necrosis.
1. What is the etiology of gout?
2. What is the difference between primary (idiopathic) and secondary form?
3. What are the common places for gout?
4. What are the radiographic and MRI appearance of gout?
5. What causes bone marrow edema?
6. What is Lesch-Nyhan syndrome?
1. Deposition of sodium urate monohydrate crystals in soft tissues.
2.
- Primary (idiopathic): over-production of uric acid and abnormal renal excretion of urate caused by an enzymatic deficiency.
Secondary: increased production of uric acid caused by excessive breakdown of nucleoproteins (polycythemia vera, myelofibrosis, leukemia, multiple myeloma, anemias, psoriasis, and glycogen storage diseases) and renal failure.
3. 1st MTP and 5th MCP joints.
4.
Radiographs: lumpy bumpy soft tissue swelling; erosions with overhanging edges; sclerosis around the erosions; normal joint space.
MRI: Juxta-articular masses may enhance, however, they are typically dark on BOTH T1 and T2WI. Increased marrow signal intensity and periosteal reaction can mimic malignant process.
5. Intraosseous migration of monosodium urate crystals and synovitis.
6. X-linked recessive disorder characterized by mental retardation, self-mutilation, choreoathetosis, hyperurecemia, and uric acid nephrolithiasis.
What are the radiographic findings of hyperparathyroidism?
1.
HANDS: Acroosteolysis; subperiosteal resorption most pronounded on the radial aspect of the middle phalanx; TFCC calcification.
SKULL: Salt and pepper skull
PELVIS: SI joint erosions and widening
CLAVICLE: subchondral erosion the AC joint.
KNEE: subperiosteal resorption along the proximal medial tibia.
Brown tumor (focal collection of fibrous tissue, giant cells, and osteoclasts).
What are the imaging findings of radiation osteitis?
- Transient growth arrest (children)
- Periostitis
- Osteopenia and cortical lysis with coarsening of the trabeculae.
- Uncommonly, cortical thickening and osteosclerois mimicking Paget's disease
- Pathologic fractures which frequently undergo resorption or non-union.
- Osteonecrosis
- Narrow zone of transition with the adjacent normal bone
What tumors arise from or adjacent to the cortex?
- Myositis ossificans
- Parosteal osteosarcoma
- Juxtacortical chondroma
- Juxtacortical chondrosarcoma
- Osteochondroma
1. What is the most common location for Parosteal osteosarcoma?
2. What are the features of parosteal osteosarcoma?
3. How are MRI and CT helpful in the characterization?
4. What is the DDX of a juxtacortical mass?
1. 70% of parosteal osteosarcomas arise around the posterior aspect of the knee.
2. Slow-growing malignant tumor of bone arising from the periosseous tissues adjacent to the cortex.
- osteoblastic, exophytic, broad-based mass arising from the surface of the bone.
- As it enlarges, the tumor has a tendency to encircle the bone, resulting in a thin radiolucent zone that separates the tumor from the underlying bone.
- The cortex and medullary cavity usually do not become invaded until late in the course of the disease.
3. MRI is useful for assessment of the bone marrow and surrounding soft tissues, whereas CT is optimal for assessment of cortical integrity.
4.
- myositis ossificans: more dense peripherally rather than centrally
- cortical desmoid tumor
- osteochondroma: normal appearing marrow and cortical bone.
What processes lead to tendon rupture/tear?
- Repeated microtrauma (tendinosis)
- Renal disease
- Crystal diseases such as gout and
calcium pyrophosphate deposition
- Diabetes mellitus
- Rheumatoid arthritis
- Systemic lupus erythematosus
- Hyperparathyroidism
1. What are the causes of periarticular calcifications?
2. What are the causes of metastatic calcification?
3. What is idiopathic tumoral calcinosis?
1.
- Idiopathic tumoral calcinosis
- Metastatic calcification
- Collagen vascular diseases such as dermatomyositis and scleroderma.
2.
- Hyperparathyroidism
- Hypoparathyroidism
- Renal osteodystrophy
- Hypervitaminosis D
- Milk-alkali syndrome
- Sarcoidosis
- Processes associated with
massive bony destruction such as metastasis.
3.
- Rare condition characterized by masslike deposits of calcium salts around joints
- Calcific masses are painless
- Typically involves the shoulders, hips, and elbows
- Usually affects young pts presenting between the ages of 6 and 25 years
- Strong affinity for black people
- Fluid-fluid level may be evident in
the region of dense calcifications
1. What are complications of Paget's disease?
2. How does sarcomatous degeneration present?
3. What is the MRI appearance of Paget's disease?
1. Fracture, increased propensity for mets, arteriovenous fistula leading to vascular steal, sarcomatous degeneration.
2.
- osteolysis causing focal destruction of the bone.
- soft tissue mass
- disruption of the cortex
- bony spiculation
- lack of a healing response in a persistent fracture
- abrupt increase in alkaline phosphatase.
3. MRI appearance of Paget's disease depends on the phase of the disease (lytic, sclerotic, mixed).
- During the lytic phase: there is extensive bone marrow edema which can be confused for a neoplastic process.
- During the sclerotic phase: regions of diminished signal intensity within the medullary cavity reflect bone repair. Coarsened trabeculae and thickened cortex may be seen. Although thickened, the cortex appears irregular and laminated with intermediate SI.
1. What is the etiology of osteomalacia?
2. What are the imaging findings in osteomalacia?
3. What is the etiology of osteoporosis?
1. Accumulation of uncalcified osteoid due to vitamin D deficiency (rickets in kids). It can be due to dietary deficiency of calcium or vitamin D, deficient absorption of calcium or phosphorus, renal failure, liver disease.
2.
- Loss of bone density
- Mottled radiolucency and diminished trabeculations with coarsening of the remaining trabeculae
- Ill defined cortices (especially endosteum).
- Softening of bone (bowing)
- Pseudofracture (Looser's zone)
- SPINE: sharp cortical margins with prominent vertical trabeculations (owing to loss of horizontal trabeculae) mimicking renal osteodystrophy or osteopetrosis, however, the underlying bone density is decreased in osteomalacia. Also look for associated anterior wedging and compression fxs.
3. In osteoporosis, there is decreased osteoid production but normal mineralization.
What is an involucrum?
Involucrum is a layer of new bone growth outside existing bone seen in pyogenic osteomyelitis. It results from the stripping off of the periosteum by the accumulation of pus within the bone, and new bone growing from the periosteum.
1. What is heterotopic ossification (HO)?
2. What are the three forms of HO?
3. What is the progression of MO?
1. Formation of an mature, lamellar bone in the soft tissues
2.
TRAUMATIC HO:
- occurs after fractures or dislocations or after procedures (total hip replacement and internal fixation of fxs)
NEUROGENIC HO:
- occurs after traumatic brain injuires, spinal cord trauma, strokes, infxn, or tumor of CNS.
MYOSITIS PROGRESSIVA:
- rare hereditary disease characterized by progressive deposition of heterotopic bone throughout the skeleton.

3.
- Initially, soft tissue mass and swelling
- 3 weeks = floccular calcifications in the periphery of the lesion
- 6-8 weeks = lamellar bone with a well defined cortex surrounding a central radiolucent area. There is a radiolucent zone separating the lesion from the underlying cortex.
What are the radiographic findings of leukemia?
- Skeletal involvement is present in nearly every case, although detectable osseous changes are conspicuous in only 75% of patients.
- Note that leukemia is an infiltrative marrow disease characterized by neoplastic proliferation of one of the blood forming cells. The leukemic cells replace normal bone marrow and lead to diffuse OSTEOPENIA.
- Discrete osteolytic lesions may mimic multiple myeloma.
- Radiolucent metaphyseal bands may be seen.
What is the DDX of diffuse and band-like acroosteolysis?
DIFFUSE PATTERN:
- Hyperparathyroidism
- Collagen vascular disease (scleroderma) and vasculitis (Raynaud's phenomenon)
- Psoriasis
- Thermal injury
- Neuropathic joint
- Pyknodysostosis
- Leprosy (Hansen's disease)

BAND-LIKE:
- Polyvinyl chloride exposure (associated with angiosarcoma of the liver)
- Hadju Cheney (osteoporosis and compression fxs in the spine).
What are the imaging findings of osteoid osteoma?
- Central lucent nidus which may calcify
- Reactive sclerosis: degree of reactive bone formation is influenced by the location of the nidus. For example, an intracapsular location of an OO elicits less reactive sclerosis. Also if the affected bone is small, sclerosis may be minimal or absent.
- Periostitis
- If OO is the spine, look for scoliotic curvature of the spine (spine is concave on the side of the lesion).
1. What are the findings of reflex sympathetic dystrophy?
2. How do you differentiate RSD from inflammatory arthritis?
1. Soft-tissue swelling and regional osteoporosis (periarticular) secondary to resorption of cancellous or trabecular bone in the metaphyseal region.
2. RSD does not lead to jont space narrowing. Inflammatory arthritis to both joint space narrowing and periarticular osteopenia.



leads
1. What is an osteoma?
2. How does an osteoma differ from a bone island?
3. What are common locations for an osteoma?
4. What kinds of symptoms does it produce?
1. Masslike protrusion of extremely dense mature bone arising from the periosteum.
2. Bone island occurs in the medullary cavity, whereas, an osteoma arises from the periosteum.
3. Skull, facial bones, and tubular bones. There is high frequency of osteoma in the frontal sinus. When it affects the calvarium, it can arise from either skull table; although the outer table is much more commonly affected.
4. Symptoms are usually related to encroachment of the protruding mass into a space, such as the sinuses, orbits, cranial vault, or mouth.
1. What is the classic radiographic appearance of bone infarct?
2. How can you differentiate from an enchondroma?
3. What processes cam alter the appearance of a bone infarct?
4. What are the radiographic changes associated with cystic degeneration?
5. What are the radiographic changes associated with malignant degeneration?
1. Intramedullary lesion with serpentine rim of dense sclerosis surrounding a variably calcified central area.
2. Enchondromas lack peripheral rim of sclerosis.
3. Infarcts can undergo two processes that may alter their appearance -- Cyst formation and malignant degeneration.
4. Cysts may erode the endosteal cortex resulting in cortical thinning.
5. Osseous destruction, periosteal elevation, and soft tissue mass.
1. What is villonodular synovitis?
2. What is PVNS?
3. What are the imaging characteristics of PVNS?
4. What is the DDX of masses within the joint?
1. Proliferative disorder affecting the synovium of joints, bursae, and tendons. When found in tendon sheaths, the disease is termed giant cell tumor of tendon sheath.
2. PVNS is a diffuse form of villonodular synovitis due to extensive deposition of hemosiderin that leads to a thickened synovium that is low SI on both T1 and T2WI.
3.
- Hemorrhagic joint effusion
- Preservation of joint space
- Numerous juxta-articular bone erosions of variable size surrounded by sclerotic rims
- Absence of calcifications
- Low of T1 and T2WI with blooming on gradient echo images.
4.
- PVNS
- Synovial chondromatosis: no joint effusion
- Lipoma arborescens
- Synovial hemangioma
- OA
- RA (rice bodies).
What is a feared complication of ankylosing spondylitis?
- Increased rigidity of the spine renders pts with AS susceptible to minor trauma leading to development of pseudoarthrosis.
- MC, the fx occurs at the level of the thoracolumbar junction.
- Fx line occurs through the discovertebral junction and apophyseal articulation.
2. Differential possibilities include infectious diskitis and transdiscal fracture.
What is the ddx of lytic lesion in the skull?
- Eosinophilic granuloma (beveled inner edge due to asymmetric growth)
- Osteomyelitis
- Mets/myeloma
- Epidermoid inclusion cyst
- Prominent venous lake
1. What is the ddx of periprosthetic lucency?
2. What is a common complication seen after hip arthroplasty and where is it located?
1.
- Infection
- Particle disease
- Insufficient mechanical load
- Implant motion
2. Increased activity after surgery can exert additional forces after a
period of immobilization. Stress fracture in patients who have had a hip arthroplasty usually affects only one side of the pelvis, and these fractures heal without difficulty. The most common site is the inferior pubic ramus, although fracture may also occur in the superior pubic ramus, the superior acetabular region of the ilium, and either side of the sacrum.
What is the ddx of increased signal intensity in the muscle?
1. Infectious myositis
2. Inflammatory myositis
3. Post-traumatic
4. Acute denervation injury
5. Acute compartment syndrome
1. What are the fibromatoses?
2. Wha is the MRI appearance?
1. Group of soft-tissue lesions characterized by fibroblastic proliferation in muscles and connective tissues that
may occur either as a superficial nodular mass or as a deep, infiltrative soft-tissue mass that may mimic a malignancy.
2. Fibromatosis may have a variety of appearances, reflecting the tissue's composition and cellularity. It can be highly aggressive and can infiltrate the surrounding muscles, producing pressure erosions, cortical destruction, and bone lysis.
1. What are the findings of Basal cell Nevis syndrome?
1.
- Skin lesions -- multiple basal cell epitheliomas (as many as 1000).
- Mandibular keratocysts (cystic lesion in the mandible)
- Short 4th metacarpal
- Scoliosis from block vertebrae/hemivertebrae
- Intracranial calcification involving the falx, dura, and tentorium.
- Numerous mesenteric cysts.
1. What is Gorham's syndrome?
1. Massive osteolysis (AKA vanishing bone disease) 2/2 proliferation of angiomatous tissue that results in regional bone lysis, tapering or pointing of the remaining bone, and atrophy of the soft tissues.
2. Process is monocentric and considered benign; however, it is progressive.
3.
- Bone lysis (demineralization)
- Soft tisuee atrophy
- Bone fracture, fragmentation, and disappearance of bone.
What is an elastofibroma?
Elastofibroma is a rare, benign, slow-growing connective-tissue tumor that occurs most often in the subscapular area in elderly women.
- nonencapsu-

lated tumor characterized by varying quantities of fat

and fibrous tissue.
- The etiology of elastofibroma remains unclear, although prevalence is increased in persons who perform manual labor involving the shoulder girdle. Thus, repeated trauma due to mechanical friction of the scapula against the ribs has been suggested to induce this process
1. What are the causes of dense bones?
2. What is erdheim Chester disease?
1. “Regular Sex Makes Occasional Perversions Much More Pleasurable And Fantastic” = Renal Osteodystrophy, Sickle Cell, Myelofibrosis, Osteopetrosis, Pyknodysostosis, Metastases, Mastocytosis, Paget’s Dz, Athelete, Fluorosis

Hyperparathyroidism = renal cause Small spleen = sickle cell disease Big spleen = mastocytosis or myelofibrosis Bone within bone = osteopetrosis Acro-osteolysis = pyknodysostosis Mixed with destruction = metastases Expanded bone = Paget’s.
2. osteosclerosis of the long bones of the appendicular

skeleton. Involvement of the axial skeleton is uncom

mon. Radiographically, a symmetrical increase in bone

density occurs either diffusely or in a patchy distribu

tion, with associated coarsening of the trabeculation,

sclerosis of the medullary cavity, and cortical thickening

in the diaphysis and metaphysis of the bones. Involve

ment of the epiphysis is uncommon.
Saucerization of the bone caused by mass n the surface of the bone?
periosteal chon-

droma, periosteal chondrosarcoma, periosteal des-

moid, benign osteoblastoma, and ncurofibroma.
1. What is the os trigonum?
2. What attaches to the os trigonum?
1. secondary ossification center which forms from cartilaginous extension from the posterior portion of the talus. It becomes mineralized between the ages of 7 and 13 years and fuses with the talus forming the trigonal process of the talus. It remains a separate ossicle in about 7% to 15% of people, with a cartilaginous synchondrosis existing between the os and the talus.
2. It serves as an attachment site for posterior talofibular and posterior talocalcaneal ligaments.
3. affects people who perform activities that

subject the ankle to extreme plantar flexion (e.g., bal

let). Pain is produced by disruption of the cartilaginous

synchondrosis between the os trigonum and the lateral

talar tubercle, which can then produce compression of the adjacent synovial and capsular tissues against theposterior tibia. It can also cause tenosnovitis of the flexor hallucis.
4. On mag

netic resonance imaging, degenerative changes, fluid, or

both may be evident at the synchondrosis, as well as

bone marrow edema in the os trigonum (as in this

patient). A markedly distended flexor hallucis longus

tendon sheath suggests entrapment.
Pyknodysostosis
Pyknodysostosis is a rare hereditary syndrome (au-

tosomal recessive) consisting of increased bone density,

short stature, frontal and occipital bosselation, hypopla

sia of the mandible, dysplasia of the skull bones, and

hypoplasia-aplasia (or acro-osteolysis) of the terminal

phalanges. An increased tendency toward developing

multiple transverse fractures is characteristic of this con

dition. Although generalized osteosclerosis is a feature

of pyknodysostosis, a bone-in-bone appearance does not

occur, and metaphyseal modeling, if present, is mild,

distinguishing this condition from osteopetrosis. Wor-

mian bones are common in the lambdoid sutures. Men

tation is normal in these patients.
1. What are causes of hemarthrosis?
2. What are the different types of synovial hemangiomas?
1. Synovial hemangioma, pigmented villonodular syno-

vitis, hemophilia.
2. One type presents as a pedunculated synovial

mass and with symptoms that mimic a meniscal tear

(locking and pain). The other pattern is more diffuse

and is associated with synovial proliferation.
3. The radiographic features of a synovial hemangioma

are similar to those of hemophilia. Joint space nar

rowing secondary to cartilage destruction, epiphyseal

overgrowth, and synovial proliferation are common

findings. Conventional radiographs depict phleboliths or bony

erosions in 50% of cases.
Klippel-Trenaunay-Weber syndrome
Varicose veins, soft-tissue and osseous hypertrophy,

and cutaneous hemangiomas.
delayed onset muscle soreness
An increase in both extracellular and intracellular water

content normally occurs in muscles after exercise, the

majority of the increase being extracellular. The pain increases in in

tensity in the first 24 hours after exercise, peaks after

24 to 72 hours, then subsides to normal after approxi

mately 7 days.
Rice bodies
- sequelae of nonspecific synovial inflammation.
- most commonly associated with synovial inflammatory arthritides, such as rheumatoid arthritis and juvenile rheumatoid arthritis and tuberculous arthritis.
- may represent fragments of detached hyperplastic synovium.
- look for numerous tiny, well-defined nodules filling the affected joint and demonstrating low SI on both T1 and T2WI.
- Administration of intravenous gadolinium reveals no enhancement of the rice bodies, although the adjacent synovium enhances brightly.
Synovial sarcoma
malignant soft-tissue tu

mor,
- affects

patients between the ages of 18 and 35 years,
- fewer than 10% of

tumors are intra-articular. These sarcomas may also arise

from a tendon sheath.
- sharply marginated soft-tissue mass that may be lobu-

lated and quite large. Calcifications within the tumor

are evident in 20% to 30% of cases. Erosive changes in

the adjacent bone and periosteal reactions
synovial sarcomas demonstrate low

signal intensity on T1W images and heterogeneous to

intense high signal intensity on T2W images. Fluid-fluid

levels may occur secondary to hemorrhage. Administra

tion of intravenous gadolinium demonstrates prominent

enhancement, indicative of the hypervascular nature of

the tumor.
Cppd
- arthralgia caused by shedding of calcium pyrophate dihydrate crystals into the synovial fluid of affected joints.
- tophaceous pseudogout = massive periarticular soft-tissue crystal deposition in patients with CPPD.
- Associated with: Hyperparathyroidism, Hypothyroidism, Hemochromatosis, Hypomagnesemia
- Chondrocalcinosis involves both hyaline and fibrocartilage.
- Can appear similar to osteoarthritis (subchondral cysts, etc.)
- Involves the annulus fibrosis of the spine, but never the nucleus pulposis as in ochronosis
Gracile bones
- NF
- Immobilization
- Muscular dystrophy
- JRA
- OI
- Dysplasia
IV drug abuse
Get septic arthritis n unusual joints.
Soft tissue calcifications
- Dermatomyositis
- SLE
- Scleroderma
- Hypervitaminosis D
- Hyperparathyroidism
- Pseudohypoparathyroidism
- PseudopseudohypoPTH
- Parasitic infection
Early osteoarthritis
- Hemophilia
- CPPD (Milwaukee shoulder)
- Alkoptonuria (Ochronosis): calcification of the intervertebral disk
- Acromegaly
1. What is the DDX of diffuse cortical thickening?
2. What is mixed sclerosing bone dystrophy?
1.
- Melorheostosis
- Engelman Disease: AKA Progressive Diaphyseal Dysplasia (PDD) results in heavily thickened bones, especially along the shafts of the long bones
- Osteopoikilosis
2. Presence of melorheostosis, osteopoikilosis, and osteopathia striata
Gaucher disease
Erlenmeyer flask deformity of the femurs.
AVN
Lincoln llog (fish mouth vertebral bodies) can also be seen (mimics sickle cell disease which is very uncommon in whites).
Neurofibromatosis I
spenoid hypoplasia, macrocranium, orbital enlargement sharply angled kyphoscoliosis posterior scalloping of vertebral bodies “ribbon ribs”, chest wall masses destroying ribs pseudoarthrosis after bowing fracture multiple nonossifying fibromas
Terminology for osteomyelitis
- Sequestrum: dead, sclerotic bone that is separated from living bone by granulation tissue.
- Involucrum: granulation tissue surrounding the dead bone.
- Cloaca: penetrates the involucrum through which pus and the sequestrum may be expelled to the skin surface through a draining sinus tract.
Lymphoma
- Both Hodgkin and NHL can affect the bones in both primary and widespread disease.
- Look for an osteolytic lesion wiht poorly defined margins.
- Sequestrum can be seen (more common in HL than NHL)
Multiple lytic bony lesions
Mets
Myeloma (if solitary = plasmocytoma)
LCH (button sequestrum, beveled edges, vertebra plana)
Lymphoma
Fibrous dysplasia
CRMO
Sequestrum
Osteomyelitis
LCH
Osteoid osteoma
Lymphoma
Fibrosarcoma/MFH
Fibrosarcoma/MFH
- osteolytic foci with a geographic, moth-eaten, or permeative pattern of bone destruction.
- Minimal or absent osseous reaction despite bone destruction.
Chondrocalcinosis
CPPD
- most commonly affects the knees, wrists, and pubic symphysis
- isolated disproportionate involvement of patellofemoral compartment.
- Wrist = predilection for radiocarpal joint; can lead to SLAC
HYPERPTH:
- look for additional findings of hyperPTH -- bone resorption, soft tissue calcifications, brown tumors.
HEMOCHROMATOSIS
- beak like osteophytes of MCP joints (also seeen in CPPD).
- tends to affect all MCP joints, whereas CPPD tends to spare the fourth and fifth joints.
WILSON DISEASE
- resembles CPPD and hemochromatosis.
chondrosarcomas
findings that suggest chondrosarcoma over enchondroma:
- size > 6cm
- rapid growth
- cortical breakthrough
- deep endosteal scalloping (> 2/3 of the overlying cortex)
- PAIN
Soft tissue calcifications
HEMANGIOMA
- look for phleboliths (round calcifications with central lucency)
- usually intramuscular with reactive overgrowth of fat.
- may contain flow voids, avidly enhance, hyperintense on T1 and T2
SCLERODERMA:
- look for acroosteolysis
- sharply marginated calcifations in a subcutaneous and periarticular distribution.
MYOSITIS OSSIFICANS
- aka heterotopic ossification
- 2/2 trauma or immobility
- cloud like calcification with peripheral maturation to cortical bone.
ARTHROPATHY WITH CALCIFIED SOFT TISSUE NODULE
- synvoial osteochondromatosis
- gouty tophi can also calcify in the setting of renal failure.
SOFT TISSUE SARCOMA
- synovial sarcoma, extraskeletal osteosarcoma, chondrosarcoma.
- extraskeletal OSM have central calcification.
TUMORAL CALCINOSIS
Synovial sarcoma
- Mass with amorphous calcifications in close proximity to a joint.
- "triple signal intensity" is seen due to hemorrhage, fibrous tissue, and cystic components often containing fluid fluid levels.
Thickening of the anterior tibial cortex
Osteofibrous dysplasia
- less than 10 years of age
Adamantinoma:
- greater than 20 years of age
- affects the anterior cortex of the tibia
Gorham’s Dz (massive osteolysis)
“vanishing bone dz”; regional bone osteolysis/destruction