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347 Cards in this Set

  • Front
  • Back
Sagittal MR images of the knee. First image shows bowtie. Second image does not; see separate anterior and posterior horns.

Look for displaced fragment in center of joint.

DDx: Developmentally small meniscus
Cartilaginous fragment sitting in intercondylar notch on coronal image
Double PCL sign: Which is the real PCL?
Superior one
ACL origin
Medial surface of the lateral femoral condyle
ACL course
anterior, inferior, and medial
ACL insertion
2 cm posterior to the anterior edge of the tibia, anterior and lateral to the medial intercondylar eminence
PCL origin
Lateral surface of the medial femoral condyle
How do you know which is medial?
Intercondylar eminence is larger on medial side.
PCL course?
PCL insertion?
Posterior aspect of proximal tibia, on a tubercle
Where are cruciate ligaments with respect to knee joint?
Intracapsular but extrasynovial
ACL position on coronal view of intercondylar notch
PCL position on coronal view of intercondylar notch
If you need another way to tell on coronal view of intercondylar notch:
PCL dark signal

ACL lighter signal
Differences between ACL and PCL on sagittal images:
1) ACL runs anteriorly from its origin, PCL posteriorly

2) ACL straight, PCL curved

3) PCL dark signal and thin, ACL lighter signal and fatter
Bone bruise pattern on MRI
If you are looking at lateral femoral condyle and lateral aspect of tibial plateau on a sagittal image, and there is bone bruise they are showing you an ACL tear with translational bone bruise pattern. The bruise does not have to be posterior.

If they are showing you lateral femoral condyle with bone bruise anterolaterally and there is associated bone bruise of the medial facet of the patella and thinning or tear of the medial retinaculum, you are being shown a patellar dislocation/relocation injury pattern
Fracture of intercondylar eminence
The ACL inserts near there, so if you see a fracture there, it is either an avulsion caused by ACL, or a fracture undercutting the ACL insertion
Segond fracture
Avulsion caused by the lateral capsular insertion on the extreme superolateral aspect of the tibial plateau (may also be related to iliotibial band and LCL as well)

IF YOU SEE IT, FIND THE ASSOCIATED ACL TEAR (75-100% association!!!)
Medial meniscus shape
crescentic, with posterior horn larger than anterior
Lateral meniscus shape
Transverse meniscal ligament
Connects anterior horns of medial and lateral menisci
Where is the medial meniscal root?
Central aspects of the posterior (and anterior) horns of the menisci. The anterior roots insert anterior to the tibial spine. The posterior root of the lateral meniscus inserts posterior to the tibial spine and anterior to the posterior root of the medial meniscus, which inserts anterior to the tibial insertion of the PCL.

When a root tear occurs, it acts just like a radial tear, allowing meniscal extrusion to occur, which promotes early DJD
Discoid meniscus -- which side more common
Lateral at least 5X more common
Diagonally oriented structure seen at the posterior aspect of knee
Meniscofemoral ligament names

location of suprapatellar bursa
between prefemoral and quadriceps fat pads
Lump on anterior surface of superior aspect of PCL
Meniscofemoral ligament of Humphrey
Larger meniscofemoral ligament
Location of Wrisberg
Posterior to PCL
Location of Humphrey
Anterior to PCL
Origin of meniscofemoral ligament
Medial aspect of posterior horn of lateral meniscus
Insertion of meniscofemoral ligament
Posterior aspect of lateral surface of medial femoral condyle
What percent of patients have at least one meniscofemoral ligament
On autopsy, 100%

On imaging, 33%
What percent have both a Wrisberg and a Humphrey?
On autopsy 50%

On imaging, 3%
How do you remember which one is anterior?
Humphrey hugs the hole
Which meniscus is more likely to be injured by ligamentous attachments?
Medial, because its attachment to the MCL is tighter than lateral
Where is the popliteus tendon at the level of the knee?
It sits in a recess in the POSTEROLATERAL aspect of the posterior horn of the LATERAL meniscus, aptly named the POPLITEUS RECESS
Blood supply to menisci
Red outer 1/3

White inner 2/3
Functions of menisci
Increases surface area of articulation for femoral condyles

Decreases load on articular cartilages, to limit DJD
histology of menisci

Outer 1/3 with circumferential fibers (hoop strength)

Inner 2/3 with transverse fibers (looser fibers)
Upward sloping meniscus on coronal knee
Posterior root of lateral meniscus as it courses lateral to medial to insert posterior to the tibial spine.
Origin of popliteus
Lateral aspect of posterior surface of femoral metaphysis, above joint capsule.
Course of popliteus
Through posterolateral aspect of knee through popliteus recess within its sheath
Insertion of popliteus
Posterior aspect of proximal tibia
Bow tie on 3 consecutive sagittal images
Discoid meniscus
Best way to visualize meniscal tear
Proton density Fat Sat
High TEs actually hinder diagnosis of meniscal tears, because the fluid in the tear binds to macromolecules which shortens its T2.
Bright linear signal extending to the periphery of a meniscus
Not a tear. The periphery is not an articular surface.
Articular surfaces


Free edge
Anterior on sagittal view
The anterior femur is FLAT

The posterior femur is ROUND with the CONDYLE
why are radial tears so bad?
These injuries are devastating because a full thickness tear destroys meniscal integrity, ie, the ability of the meniscus to distribute hoop stress. Hoop stress is the normal outward force generated in the meniscus in all directions as a result of weight bearing.

Radial tears are also called vertical tears.
Longitudinal tears
Go along the arc of the meniscus.

Bucket handle tears are a special variety of these.
Horizontal tears
Also called fishmouth tears

Usu start on inferior articular surface and propagate in the plane of the meniscus peripherally. May not extend all the way to the base (periphery) but if they do, they transsect that part of the meniscus into a superior and inferior half (or portion)
DDx intrasubstance signal
1) Mucinous, myxoid, or hyaline degeneration (any of these names is ok and means the same thing)

2) Meniscal contusion
High T2 signal between meniscus and joint capsule/ligaments
Meniscocapsular separation
Tx meniscocapsular separation
Nonsurgical. Spontaneously heal due to rich blood supply of periphery of meniscus
Most common meniscus to tear
Medial stabilizer of knee
Covers the MCL insertion
Pes anserinus tendons
Lateral stabilizers of knee
3 layers
Most superficial layer
Has anterior and posterior portions
Anterior portion
Iliotibial band
Posterior portion
Biceps femoris muscle
Middle layer
Inner layer
Lateral joint capsule
Parts of medial collateral ligament
Superficial -- Tibiocollateral ligament

Deep -- Meniscofemoral and meniscotibial ligaments

Superficial and deep layers separated by a bursa
Commonest location of osteochondritis dissecans
Lateral aspect of medial femoral condyle (i.e. closer to notch than edge of knee)
Management of OCD
MRI to determine whether osseous fragment is loose
Vertebral body collapse with air in the collapsed vertebral body
Round lytic defect on articular surface of superolateral pole of the patella.

DDx: Gout, osteochondritis, chondroblastoma, grade IV CMP
What makes appearance pathognomonic for this lesion?
Surrounding sclerosis
When do discoid menisci present?
lateral tibial plateau bone bruise
Look for the ASSOCIATED MEDIAL COLLATERAL LIGAMENT TEAR, as well as for ACL tear and medial meniscal tear (O'Donohue's terrible triad)
DDx multiple small well circumscribed sclerotic lesions
Osteoblastic metastases

Multiple bone islands


Multiple brown tumors now in reparative phase -- when source of hyperparathyroidism is removed, they undergo repair and become sclerotic
Metabolic bone diseases on boards

Osteomalacia (rickets)


Renal osteodystrophy

Hypoparathyroidism, pseudohypopara, pseudopseudo

Thyroid (hyper/hypo)


Most common metabolic bone disease
Most common places for osteoporotic fractures
Proximal femur

Where is DEXA scan performed
Hip or lumbar spine
x-ray with generalized osteopenia
Osteoporosis -- Cortical thinning, resorption of horizontal trabeculae leaving behind primary tensile trabeculae -- thus trabeculae are well defined

Osteomalacia (in peds, usually rickets) -- Everything looks blurry. Trabeculae not well defined.


Multiple myeloma

x-ray with osteopenia localized to one area

Reflex sympathetic dystrophy

Transient regional osteoporosis

RSD appearance
On bone scan, diffuse PERIARTICULAR uptake
Transient osteoporosis of the hip appearance
On plain film, see decreased density of the femoral head/neck on the affected side.

However, even though it may look like it on low quality image, there is



If there truly is JSN or acetabular abnormality, it is another entity such as RA

On MRI, bone marrow edema, which resolves within a few months
Bowing of leg bones

Metaphyseal physeal fraying, cupping, which results in physeal widening. Can be physeal slipping too.

Coarse, ill defined trabeculae. This appearance seen in osteomalacia also.
Bones affected in rickets
Faster growing bones affected more



Bulbous enlargement of anterior ends of ribs
rachitic rosary of rickets

(RR of R)
Causes of rickets

Renal insufficiency resulting in inability to form 1,25 form of vit D

GI malabsorption

Poor nutrition
Linear lucency partially traversing bone with decreased bone density.
Osteomalacia in adults

= Pseudofracture

According to Resnick, it is an insufficiency fracture that PARTIALLY traverses bone.

The bone is weak, gets an insufficiency fracture, which fills in with UNMINERALIZED OSTEOID
Locations for Looser zone
Proximal femur

Lateral scapula

Tibia (less common)
Causes of HPT
Primary -- due to parathyroid adenoma or hyperplasia. The adenoma secretes PTH. PTH has purpose of elevating serum Ca levels. PTH acts in 3 different ways to do this.

1) Acts on OSTEOCLASTS, stimulating them to increase resorption of bone, the main repository of Ca in the body.

2) Acts on kidney, to increase reabsorption of Ca and increase activation of vitamin D to active form.

3) Acts on GI tract to absorb more vitamin D.

Therefore, in primary HPT, we see

1) Decreased bone density (osteopenia). By the same token, we see resorption of bone, which is best visualized in characteristic places: Subperiosteal resorption at radial aspects of 2nd and third middle phalanges, and at medial aspect of proximal tibia. Subligamentous resorption, at the undersurface of the distal clavicle. Subchondral resorption at the distal clavicle and SI joints. Trabecular resorption, best exemplified as salt and pepper appearance in the skull.

2) Brown Tumors -- Because of overstimulation of osteoclasts

3) Soft tissue calcifications -- Because of the chronically elevated serum Ca levels, there is soft tissue calcification, characteristically seen as nephrolithiasis.

SECONDARY -- due to chronic HYPOcalcemic state. Can be renal or GI cause. Renal cause is due to renal failure, which results in inability to activate vitamin D. This causes hypocalcemia, which results in stimulation of PTH release.

The lack of activated vitamin D results in osteomalacia. It also results in secondary stimulation of parathyroid hormone secretion. This combination of factors is RENAL OSTEODYSTROPHY.

It results in one of the changes of osteomalacia: Indistinct trabeculae. It also results in all the changes of primary HPT, with the following notable differences.


2) Overall bone density is variable, and in many cases is actually INCREASED. The combination of thinned indistinct trabeculae with increased density of cortical bone results in the classic RUGGER JERSEY SPINE.

3) Soft tissue calcification is MORE COMMON. Primarily seen as vascular calcifications. But the classic soft tissue calcification in RO is periarticular calcification, which is very prominent, and termed TUMORAL CALCINOSIS.

TERTIARY Hyperparathyroidism is the result of chronic hypocalcemic state such as RO, where the tonic hyperstimulation of PTH release causes development of an autonomously functioning parathyroid adenoma.
Widened SI joints
Could be sacroilitis, but if there is abnormal calcification anywhere on the film, or additional widening of the PUBIC SYMPHYSIS, think immediately that it must be SUBCHONDRAL RESORPTION related to HPT.
Basal ganglionic calcifications

Cause of hypoparathyroidism
Usually post surgical

Pts get hypocalcemic
Findings in hypoparathyroidism
Dense bones -- less resorption by osteoclasts

Soft tissue calcifications -- subcutaneous and basal ganglionic
Short kid, short digits, short metacarpals/tarsals especially
Pseudo or pseudopseudo. Also see the dense bones and soft tissue calcifications.

Obviously, hypo itself is not going to cause short metacarpals, as this is something that happens to kids when they are developing. So it must be due to one of the ones that have a congenital basis.
What is pseudohypoparathyroidism
End organ resistance to PTH
What is pseudopseudo
Look like pseudohypoparathyroidism, but they dont have end organ resistance to PTH. That is why the radiographic findings are slightly different in that there are no soft tissue calcifications in the basal ganglia.
Delayed skeletal maturation
Think hypothyroidism.

Need to know a few other causes of delayed skel maturation
Other findings in hypothyroidism
Delayed skeletal maturation

Intrasutural ossicles = Wormian bones

Coned or fragmented epiphyses

Normal looking hand. Then told patient is 13.
Hyperthyroidism findings
Kids: Accelerated bone maturation

Adults: Demineralization

Thyroid acropachy
Thyroid acropachy patients
After treatment and are no longer hyperthyroid

Only 1% of hyperthyroid patients
Acropachy appearance
Fluffy periostitis with adjacent soft tissue swelling in phalanges
Lateral foot radiograph with thick heel pad
Acromegaly other findings
Spade like phalangeal tufts

Large frontal sinus

Large sella
Spade like tuft -- what is it
Widening of the distal phalanx at both its proximal and distal end
Osteoporosis with lots of periosteal reaction
Scurvy. Probably will be shown in a child.

Osteoporosis is caused by decreased bone production due to decreased collagen synthesis. Dramatic uplifting of periosteum with calcification is caused by subperiosteal hemorrhage.
Findings in scurvy

Dramatic periosteal uplifting with periosteal new bone

Sclerotic appearance of margins of epiphysis (appears that way because of osteoporosis)

Sclerotic appearance of metaphyseal line

Metaphyseal corner fractures/spurs
Sclerotic appearance of margins of epiphysis
Wimberger sign
Sclerotic appearance of metaphyseal line
White line of Frankel
Metaphyseal corner fractures/spurs in scurvy

DDx of non accidental trauma, but not when all of the other associated findings of scurvy
Scurvy appearance DDx
TORCH infections


Neuroblastoma mets

Bone tumor age 1-5
Eosinophilic granuloma

Neuroblastoma mets
Bone tumor age 5-30

Solitary bone cyst

Aneurysmal bone cyst


Fibrous dysplasia

Eosinophilic granuloma


Leukemia (these past 3 are all small blue round cell tumors, and all have that permeative appearance)

Over 30

Over 40


Eosinophilic granuloma
Bone lesion discriminators
1) Pt age

2) Location

3) Pattern of bone destruction (purely lytic, mixed lytic/sclerotic, permeative)

4) Zone of transition (wide, narrow, sclerotic margin)

5) Matrix

6) Mono vs. polyostotic
Multiple lytic lesions

Fibrous dysplasia

Eosinophilic granuloma




Report conclusions for bone lesions
1) Don't touch lesion -- no biopsy or follow up imaging indicated

2) Almost certainly benign -- No biopsy, but follow-up x-rays indicated (fibrous dysplasia, heterotopic ossification)

3) Benign symptomatic lesion -- Surgery for curettage and packing (GCT, chondroblastoma, SBC, ABC)

4) Equivocal -- biopsy indicated (try to keep this group small)

5) Definitely malignant -- (i.e. sunburst in OS)



Sickle cell



staging system

1 -- Normal x-ray, abnormal bone scan or MRI. On MRI, see the dark line separating dead from live bone.

2 -- Mixed lucency and sclerosis on x-ray. If findings are uncertain on x-ray, request MRI, and look again for the dark line separating dead from live bone.

3 -- Subchondral collapse, reflected as subchondral lucency (crescent sign)

Stage 4 -- Actual collapse of the femoral head. No degenerative on the acetabular side yet visible.

5 -- Secondary changes of osteoarthritis.
Treatment of AVN
Stages I and II -- Core decompression

Stage III, (IV) -- Hemiarthroplasty

Stage (IV), V -- THR, as the acetabulum is screwed up also
Types of hip replacement
Hemiarthroplasty -- Used for osteonecrosis of the hip, where there is no damage to the cartilage on the acetabular side. The femoral head is replaced, and articulates with the native acetabulum. A long stem is not necessarily used. In fact, may be able to get away with just femoral head surface replacement.

Total hip arthroplasty -- Both the acetabular and femoral head components are replaced. Can be regular, where both components are cemented, hybrid, where femoral component is cemented but the acetabular is not, or noncemented.
Widened glenohumeral joint space on AP view
Posterior shoulder dislocation

Shoulder should be locked in internal rotation
Normal superior labral anatomy and SLAP
Normal sublabral sulcus goes inferolateral to superomedial, parallel to the biceps anchor.

In a SLAP tear, a line of bright signal perpendicular to the biceps anchor, which goes from inferomedial to superolateral is seen either between the labrum and the bony glenoid or cutting through the labrum (bucket handle tear) depending on the type of SLAP. The tear extends anterior and posterior to the biceps anchor.
Variations of normal superior labral anatomy
Sublabral foramen


Arthritis systematic evaluation
Remember your ABCDEs


Bone mineral density

Cartilage joint space



Soft tissues (swelling, calcification, gas)
Arthritis with osteoporosis
If Symmetric -- RA

If monoarticular -- SEPTIC

If child -- JCA

OR, any with disuse
Arthrist WITHOUT osteoporosis
A more limited differential



Synovial osteochondromatosis

Sclerotic distal phalanx
Ivory phalanx, a reactive sclerotic process in psoriasis
Psoriatic distribution
Hands AND Feet

SI joints, mainly lower 1/3

Spine, with BULKY paravertebral ossification
Where are the syndesmophytes in AS?
In the annulus fibrosis
Differentiating among the spondyloarthropathies
AS and IBD related look very similar, but IBD less severe. Both involve SI joint first, with thin syndesmophytes in the spine. Then they spread to further involve the spine with ankylosis, as well as to involve LARGE PROXIMAL JOINTS, like the HIP and SHOULDER.

Reiters and Psoriatic have hand and foot involvement (Reiters foot > hand), and are distal arthropathies, with less involvement of SI joint and proximal joints. Still involves the spine, but with BULKY asymmetric spurs.
Arthritis with preservation of joint space
PVNS (depending on joint; true for knee and elbow, less so for shoulder, not true for hip)

Synovial osteochondromatosis


Classic characteristics of TB arthritis

Juxtaarticular osteoporosis

Peripheral erosions

MCP joint space narrowing with hook-like osteophytes

Eccentric lobulated soft tissue mass around a phalangeal joint
Think first of TOPHUS
Calcified tophi
Renal failure related gout
Sausage digit

Eccentric lobulated soft tissue swelling in an arthritis case

Amyloid deposition
All connective tissue diseases (scleroderma -- characteristic dense calcifications --, lupus, polymyositis, dermatomyositis)




Ossification seen posterior to spine
OPLL = ossification of posterior longitudinal ligament

Usually asymptomatic, but if bulky enough can cause spinal cord compression and myelopathy.
OPLL location
OPLL association
DISH criteria

Flowing ossification at 4 contiguous levels

Normal disk height (excludes degenerative disk disease)

NORMAL SI joints (excludes AS)
Bone findings in neurofibromatosis
NF I: Multiple NOFs; plexiform neurofibroma

Tibial bowing, fracture, possibly with pseudarthrosis

Scoliosis with or without kyphosis

Anterior vertebral scalloping

Posterior vertebral scalloping

Widening of neural foramina
DDx for posterior vertebral body scalloping



Dural ectasia

Mass lesion
DDx for anterior vertebral body scalloping

Kid: Neuroblastoma



Aortic aneurysm


Transverse lucency in collapsed vertebral body

Results from ischemic necrosis of a vertebral body, with collapse. Lucency may disappear on flexion, and appear on extension views.

Vertebra plana


Eosinophilic granuloma


Tumor (mets, myeloma)

Erlenmeyer flask deformity
Anything that causes marrow expansion at a young age

CHRONIC ANEMIAS (i.e. Sickle cell)

STORAGE DISEASES (Gaucher dz, Niemann-Pick dz) -- both more common in Ashkenazi Jews

Fibrous dysplasia and Pyle disease (metaphyseal dysplasia)
Abnormal accumulation of glucocerebrosides in the RETICULOENDOTHELIAL SYSTEM

Thus, the liver, spleen are enlarged. The fatty marrow is diffusely replaced.
Erlenmeyer flask deformity and AVN

Could also be sickle cell
Types of stress fractures
Insufficiency -- normal stress on weakened bone (osteoporosis, osteomalacia)

Fatigue type -- abnormal stress on normal bone (atheletes)
Typical places for fatigue-type stress fractures
Femoral neck

Anterior tibia


Appearance of fatigue stress fracture

May not be in a linear distribution on the plain film or even on MRI, where you might just see a lot of edema. But the location and age suggest the diagnosis.

DDx: Garre's, Healed NOF, osteoid osteoma without nidus identified on plain film.
Describe Pagets
3 Features

1) Trabecular coarsening

2) Bony expansion

3) Cortical thickening

Lytic phase: Well defined lytic area with non-sclerotic margins and flame shape/blade of grass pointing into the diaphysis
Describe dural ectasia
Ectatic dilatation of the thecal sac in the sacrum.

Defined as diameter of the thecal sac larger at S1 than it is at L4.

Can cause pain symptoms by nerve root encirclement
DDx for dural ectasia



Ankylosing spondylitis

Osteogenesis imperfecta tarda
Ivory vertebral body

Osteoblastic mets

Square area of lucency surrounded by thick square of bone in lateral view of vertebral body
Picture frame appearance of Paget dz in the spine
Amorphous calcifications throughout calvarium
Cotton wool appearance of PAGETS
Pagetic patients susceptible to fracture?

Occur at convex aspect of the bone
Complications of PAGETS
1) Fracture

2) Neurologic compromise in the spine due to bony overgrowth

3) Transformation into osteosarcoma
Lateral view of spine with dense endplates and focal area of increased density within the marrow space

Differentiate from rugger jersey spine by ABSENCE of the bone within bone appearance in renal osteodystrophy
Complications of osteopetrosis

Especially look for SPONDYLOLYSIS
Sclerosing bone dysplasias



ALL due to failure of osteoclast activity
Location of bone islands in osteopoikilosis
Epiphyses and metaphyses -- closer to joints

Not in diaphyses
Lytic lesion in the middle of the distal femoral epiphysis
widening of the intercondylar notch of hemophilia
DDx dark signal areas on MRI

Soft tissue mass causing severe bony erosion in distal thigh
Is patient MALE?

If yes, could be hemophiliac pseudotumor

Most common locations: Femur, pelvis, tibia
What do PVNS and synovial osteochondromatosis have in common
Normal bone density

Increased joint density

Preserved joint space with erosions

Knee > hip > elbow (bottom of body to top)
DDx for Hypertrophic osteoarthropathy (diffuse periostitis)
Chronic venous stasis

Caffey disease

Scurvy (much more severe)
Tarsal coalitions
Most common : Calcaneonavicular -- look for anteater nose sign, but does not have to be present. Look on oblique RADIOGRAPH. No NORMAL articulation between the calcaneus and the navicular is present, so if they are close together, its a coalition of some type.

Talocalcaneal = Subtalar = Middle facet/sustentaculum tali fusing with the talus. Diagnose with CT. See subtalar joint space narrowing on plain film. See C-Sign. Dana's. The sustentaculum tali fuses with the medial talus. Can be nonosseous and you see DOWNSLOPING of sustentaculum and medial talus
Neuropathic osteoarthropathy
Common joints for neuropathic osteoarthropathy

Shoulder -- think syrinx
Diagnosing neuropathic osteoarthropathy in the foot
Look for widening of the space between the first and second metatarsal bases.

Similar to looking for a Lisfranc, since most patients with a Lisfranc have diabetes anyway
Unilateral erosive and sclerotic changes around an SI joint
SEPTIC arthritis

Psoriatic arthritis and Reiters (they involve SI joints less consistently than AS and IBD arthritis)
AS and IBD

Sometimes, Psoriatic and Reiters can do this, but not commonly like AS (most severe) and IBD (less severe).
Fracture of proximal ulna with radial dislocation types
BADO classification

I -- Radius dislocates anteriorly (65%)

II -- Radius dislocates posteriorly (20%)

III -- Ulna fractures more proximally than others, just distal to coronoid, with lateral radial dislocation.

IV -- Who cares
Coned epiphysis
fusion of central portion of growth plate, which causes tethering and cone shape. Also called cupped epiphysis
Lead lines other causes
phosphorous and bismuth (PbPBi)
Types of fibromatosis
same as desmoid tumor. Can be intraabdominal, abdominal, or extraabdominal depending on its relationship to the abdominal wall. 25-35 years of age.
Anterior shoulder dislocation
95% go anterior, inferior and medial to glenoid. Capsulolabral tears very common in young popn, up to 90% acc to chew. In patients over 40, very common to have associated rotator cuff injury
Luxatio erecta associations
80% with rotator cuff or greater tuberosity fracture (similar process since rotator cuff inserts mostly on greater tuberosity). 60% with neurologic compromise.
Subscapularis tendon tears
usually occur after tear of the infraspinatus or supraspinatus
AC separation
1 – normal or slight increase in space with STS 2 – acromion inferior to to distal clavicle 3 – coracoclavicular separation has also occurred
Synovial osteochondromatosis
most common joint: knee, next most common – hip, next most common – elbow. Same as PVNS. 4th most common – shoulder (KHES)
Superior migration of the humeral head
rheumatoid arthritis, resulting in associated chronic rotator cuff tear
DJD of the shoulder in young patient
its not DJD, its CPPD. Could also be posttraumatic DJD.
Where is pes anserinus?
MEDIAL proximal tibia
Calcification around joint
ask if patient on dialysis. Common to have periarticular calcification in dialysis patients. If masslike – tumoral calcinosis.
Osteomalacia appearance in dialysis patient
can be renal osteodystrophy, which causes osteomalacia due to vitamin D deficiency. But can also be due to aluminum toxicity.
Dialysis related bone disease
specifically related to dialysis, not related to the renal failure – tumoral calcinosis/calcification around joints, aluminum toxicity, amyloid arthropathy
C-spine findings in RA
atlantoaxial subluxation (anterior atlantodental interval greater than 2.5 mm in adult, measured at inferior aspect of the arch). Stepladder subluxations. Disk space narrowing affecting mid to upper C-spine also, instead of just lower c-spine like in typical DDD. Ankylosis of facets without enthesophyte formation.
Diffuse ankylosis of c spine
AS and JCA. JCA distinguished by hypoplasia of vertebral bodies and disks. Same appearance if segmental in Klippel-Feil, which is associated with omovertebral bones, and in 1/3 of cases, with Sprengel deformity.
mostly young patients, although older than oo (80% under 30), 50% in spine, most of rest in femur and tibia (spine and lower extremity big bones)
Other cause of DISH like appearance
retinoid toxicity.
DDx severe thoracic kyphosis in kid
Schauermann dz (3 or more vertebral bodies with 5 degrees of incline), e-gran, trauma, postural kyphosis, OI
Vertebral endplate biconcave deformities
consistent with compression deformities of chronic formation. DDx is osteoporosis, osteomalacia, and myeloma. Within osteoporosis category, 95% is involutional, which is broken down into type I – postmenopausal and type II – senile. The other 5% is mainly iatrogenic, such as from hormonal abnormalities such as hypercortisolism from steroid administration. Any patient on steroids should have routine bone density evaluation.
DDx for intervertebral disk calcification
DDD, CPPD, ochronosis, hyperparathyroidism, hemochromatosis, acromegaly and polio. In ochronosis, there is loss of vertebral disk height diffusely, with calcification starting at the PERIPHERY of the disk, instead of centrally as in these other causes.
deficiency of homogentissic acid. Affects spine and other joints. In other joints, looks like DJD, but strange patterns (solitary shoulder involvement, isolated lateral compartment of the knee) and more severe than CPPD.
DDx of soft tissue mass anterior to vertebral bodies, with vertebral body destruction, extending for several vertebral segments
TB, lymphoma, metastases, myeloma, sarcoidosis.
What characteristics define TB from pyogenic disk infection
larger ST mass, involvement of more than 1 segment, DELAYED DISK DESTRUCTION (just like TB in joints, with delayed joint space narrowing), SUBLIGAMENTOUS SPREAD – TB starts out in the subchondral bone just like pyogenic infection, but it is far more indolent, and spreads outward and gets CONFINED by the anterior longitudinal ligament, which it does not destroy, instead it gently asks it to please move out of the way and slips underneath it in order to form its nice fusiform mass.
Spontaneous PTX
LAM, Osteosarcoma mets
DDx for that funky calcified mass with bony spicules in the posterior mediastinum
Metastatic osteosarcoma, extraosseous osteosarcoma, treated Ewings or lymphoma (or other round cell tumor), other metastasis.
Meaning of loss of pedicle on AP radiograph
its metastasis more likely than myeloma. Unless another lesion is very large, it will not destroy the pedicle. Mets preferentially go to pedicle because of bloodflow, so this can be the only abnormality.
Fused small vertebral bodies with scoliosis
congenital scoliosis. Most commonly due to vertebral segmentation abnormalities (congenital hemivertebrae – one side of vertebra does not form, congenital block vertebra – instead of the two hemivertebrae next to each other fusing two at consecutive levels fuse instead, trapezoidal vertebrae, congenital neural arch fusions)
DDx dense small lesion on plain film in spine
Bone island, osteoid osteoma, ALWAYS OSTEOBLASTOMA, unless you see on CT or MRI that it is small. Also osteoblastic metastasis. BUT IF THE PATIENT HAS SCOLIOSIS, WITH THE LESION IN THE CONCAVITY OF THE SCOLIOSIS, IT IS AN OSTEOID OSTEOMA
DDx of ivory vertebrae
2 main are blastic mets and Pagets. But can also be from myeloma, lymphoma, myelofibrosis, chordoma, osteosarcoma,
When Pagets affects the spine, what areas are most common?
Lumbar and SACRAL
Differentiating Pagets from other causes of ivory vertebrae, mainly mets
Look for trabecular thickening, LOOK FOR VERTEBRAL ENLARGEMENT
Chance fracture
occurs at thoracolumbar junction in adults, midlumbar in kids. Begins as a horizontal fracture in the pedicles, which propagates in the axial plane, sometimes through the transverse processes, and also into the vertebral body. There is also commonly an anterior wedge fracture. There is a characteristic hump at the posterior superior endplate.
Degenerative disease of spine subtypes
intervertebral osteochondrosis – abnormality is of the nucleus pulposus. Results in decreased disk height with VACUUM PHENOMENON. If you see vacuum, this type of DDD is the cause. 2) Spondylosis deformans – primary disease of the annulus fibrosus, with osteophytosis and more preservation of disk height. 3) Osterarthritis – facet DJD.
Differential for disk space narrowing
DDD (if you see vacuum this is it), diskitis (poorly defined endplate sclerosis which grades into erosions), Trauma with herniation of nucleus pulposus (look for fracture or other evidence of trauma like anterior bridging osteophytes at those levels only), Neuropathic osteoarthropathy (see disk space narrowing, but also debris, disorganization, etc), RA (typically cervical spine, with stepladder subluxations, atlantoaxial subluxation, and basioccipital settling), CPPD (calcification, fragmentation, narrowing, subluxation), ochronosis, sarcoidosis
Pyogenic diskitis/osteomyelitis
high signal in disk on T2W, erosive endplate changes, enhancement in disk space, subligamentous abscesses, usually confined to single level – can break through into soft tissues as well. LOOK CAREFULLY FOR ASSOCIATED EPIDURAL ABSCESS
Worst complication of AS
Fracture dislocation through the ankylosed spine.
Another more chronic complication of AS
severe spinal canal stenosis, which looks like you cant even separate the spinal canal from the vertebral body caused by ossification of the posterior ligaments. Looks like a ring within a ring (3-42)
Normal appearance of AP lumbar spine
THE PEDICLES GET WIDER AS YOU PROGRESS INFERIORLY. If they get more narrow, in an adult, the only diagnosis is ACHONDROPLASIA. If it is a child, another possibility is thanatophoric (“death bringing”) dwarfism.
causes rhizomelic micromelia – short proximal segments of limbs. Only affects enchondral ossification. Does not affect periosteal bone growth. Thus, shafts of long bones are of normal length, but the metaphyses are FLARED. The calvarium is formed by intramembranous ossification, so it is normal. However, the SKULL BASE is formed by enchondral ossification, and thus there is a SMALL FORAMEN MAGNUM. Autosomal dominant. Heterozygous form is not associated with other congenital abnormalities. HOMOZYGOUS FORM IS LETHAL IN INFANCY and radiologically is indistinct from thanatophoric.
Vertebral hemangioma complications
In pregnancy, especially during 3rd trimester, the gravid uterus compresses the IVC, impairing venous return from the lower body and extremities. A collateral pathway is flow into the valveless Batson’s plexus and if there was already a hemangioma (more common in women to start with), it WILL enlarge. This increased flow coupled with hormonal changes of pregnancy can result in weakening of the trabeculae such that the involved vertebra FRACTURES.
Lateral bridging osteophyte at one or two levels, forming over a period of several weeks, with no history of trauma or preexisting osteophytosis
Psoriatic or Reiters. This appearance is a common EARLY feature in Psoriatic.
DDx of sacral mass (or ANY flat bone)
chordoma (this one only applies to sacrum, clivus, sometimes vertebral bodies – closer to ends more likely since it is notochordal remnant tumor), chondrosarcoma, mets, myeloma, lymphoma, leukemia, infection. Other possibilities include desmoplastic fibroma, giant cell tumor, hemophiliac pseudotumor, brown tumor or ABC.
Desmoplastic fibroma
The ossesous counterpart to extraabdominal desmoid tumor. Desmoid tumors are a type of fibromatosis. ALL TYPES OF FIBROMATOSIS EXHIBIT ENHANCEMENT. It is a benign tumor, but local recurrence is a well documented complication of treatment.
Postradiation changes in spine
Most common – Very bright signal on T1W imaging due to fatty marrow replacement. Can also result in fibrosis, with dark signal on T1W and T2W images. Recurrent or new neoplasm will be bright on T2W imaging, intermediate on T1W imaging.
R/O tumor in spine MRI
If its brighter than other levels on T2W imaging, and darker than other levels on T1W imaging, you might have something to worry about. It shouldn’t be darker than muscle on T1W images or brighter than muscle on T2W images.
Evaluation of DDH
1) look for basic ringers, like femoral head ossification center differences between sides, discrepancy in acetabular angles. 2) Divide the hip into 4 quadrants with a perfectly horizontal line through the triradiate cartilage, and then a perfectly vertical line that tangentially contacts the most lateral aspect of the ossified acetabulum. The normal femoral head ossification center is in the lower inner quadrant. A dislocated one is in the upper outer quadrant, and a subluxed one is in the lower outer quadrant. 3) The angle between the horizontal line through the triradiate cartilage and a line drawn along the angle of the acetabulum should be less than 40 degrees in newborn, 33 degrees in 6 month old, and 30 degrees by 1 year. 4) You should be able to draw a continuous arc from the inferior surface of the superior pubic ramus to the medial femoral cortex.
Normal acetabulum on AP view of pelvis
Superior acetabular margin covers the femoral head, and at its most lateral tip, arches downward.
Acetabulum at its most lateral tip pointing upward
ACETABULAR DYSPLASIA. This is a shallow acetabulum. Since less of the femoral head is covered than normal, more weight bearing takes place through the covered portion, and the person will inevitably develop accelerated osteoarthritis. Treatment is acetabular osteotomy to deepen the socket. Example in book was bilateral.
Slightly higher than fluid attenuation mass in the musculature of thigh or pelvis
DDx is INTRAMUSCULAR MYXOMA, soft tissue sarcoma with myxoid component, neurofibroma. Neurofibroma will homogeneously or inhomogeneously enhance slightly. But the other two cannot be reliably differentiated without BIOPSY. Hey look at that broad over there, her face is a Maza . . .Association between fibrous dysplasia and soft tissue myxomas is Mazabraud’s syndrome.
DDx for early OA of the hip
acetabular dysplasia, other developmental dysplasia (multiple epiphyseal dysplasia, spondyloepiphyseal dysplasia), neuromuscular syndromes (muscular dystrophy, polio), legg calve perthes, SCFE, trauma, post-infectious
Must see trabecular or cortical pattern
post traumatic, burn, paralysis (these three can cause myositis ossificans),
DISH (always enthesal – ligamentous, tendinous, or capsular insertions onto bone)
myositis ossificans progressiva
Bubbles in hip joint after nonpenetrating trauma
indicative of dislocation relocation. Must consider the sequelae – AVN of femoral head, sciatic nerve injury, myositis ossificans, posttraumatic DJD.
Hip dislocation
85% posterior. Most associated with posterior column (more lateral) acetabular fractures. Need CT to look for fragments before reducing.

Anterior hip dislocation (10%) occur from forced abduction, external rotation and flexion. The hip capsule is torn, and the dislocation occurs below the strong pubofemoral ligament, with the head coming to rest on top of the obturator foramen. In 10% of anterior hip dislocations, the dislocation occurs above the pubofemoral ligament, and the femoral head comes to rest over the lower abdomen.
Appearance of fluorosis
Increased cortical sclerosis. No cortical or trabecular thickening. Somewhat patchy appearance.
Child with bilaterally widened SI joints, subchondral acetabular sclerosis, and focal areas of growth plate widening on the metaphyseal side
Rickets in an OLDER child (i.e. 8)
What happens in treated rickets?
The unossified matrix suddenly gets ossified rapidly
Bilateral SI joint erosions, sclerosis
AS and IBD only do bilateral. Psoriatic and Reiters also usually do bilateral. BUT, if there is unilateral involvement, psoriatic and reiters are MUCH MORE LIKELY to be the cause than the other two. The biggest differential in bilateral is ALWAYS SEPTIC ARTHRITIS.
Increased signal in one SI joint on fluid sensitive sequence
MOST IMPORTANT DIAGNOSIS IS SEPTIC ARTHRITIS. Bloodflow through the iliac side of the SI joint is slow, thus implantation of infection organisms occurs here first, with spread of the osteomyelitis into the adjacent SI joint. Risk factors include IVDA and HIV.
IBDs associated with spondyloarthropathy
UC, Crohn and Whipple
Mass deep to scapula against chest wall without chest wall invasion. Mass has some fatty components
ELASTOFIBROMA, atypical lipoma, low grade liposarcoma, hemangioma, fibromatosis. Elastofibroma is always located between serratus anterior muscle and the chest wall.
PVNS appearance on MRI
DDx for discrete large erosions in a large joint with or without JSN
PVNS, synovial osteochondromatosis, amyloid, TB.
Differentiator for amyloid arthropathy
involves more than just one joint
DJD appearance of hip, but how can you be sure its DJD
asymmetric narrowing, with superolateral joint space narrowed the most
Protrusio acetabuli
defined as protrusion greater than 3mm in men and 6 mm in women
DDx protrusio acetabuli
RHEUMATOID ARTHRITIS if it is bilateral and symmetric, is by far the top choice. Other possibilities are spondyloarthropathies (should see change in the SI joints or spine), Juvenile chronic arthritis, and osteoarthritis. Any condition that weakens the acetabulum as well, such as osteomalacia, Pagets, OI, and polyostotic fibrous dysplasia.
DDx ankylosis of large synovial joint (hip, shoulder)
Juvenile chronic arthritis, septic arthritis. Differentiate based on bilaterality.
Soft tissue calcified mass near muscle
myositis ossificans (infiltrates, does not displace muscle), leiomyoma/leiomyosarcoma (both can hemorrhage), synovial cell sarcoma, extraskeletal osteosarcoma, extraskeletal chondrosarcoma, mets.
Absent radial head, posterolateral iliac protuberance
NAIL PATELLA SYNDROME. Also has hypoplastic patellae. Usually bilateral iliac horns. Associated with renal disease in 50%. Also eye disease (cataracts, glaucoma)
Diffuse sclerosis of the pelvis in adult
Pagets – most common cause, but must see trabecular coarsening and cortical thickening, mets, lymphoma, leukemia, mastocytosis, myelofibrosis, fluorosis, retinoid toxicity (remember, retinoids are like Vitamin A, and hypervitaminosis A is another cause of bone abnormality)
Replacement of the bone marrow with fibrous tissue. This NECESSITATES EXTRAMEDULLARY HEMATOPOIESIS. What happens is as follows: The fibrotic process begins in the central hematopoietic marrow, so in the pelvis, vertebrae and ribs, the places that actively generate new blood cells. This results in shifting of intramedullary hematopoiesis to the proximal and distal ends of the femora, humeri, and tibiae. Occurs in the metaphyses, but the epiphyses are more resistant to marrow reconversion. But the myelofibrosis progresses into these areas, and then it is time for hematopoiesis to shift to extramedullary sites, which are the PARAVERTEBRAL REGIONS, THE SPLEEN, AND THE LIVER.
Multifocal areas of abnormal trabecular appearance, without cortical thickening seen in Pagets
HEMANGIOMATOSIS, lymphangiomatosis, cystic angiomatosis. On CT or MRI you see cystic spaces in marrow cavity, without cortical disruption or thickening.
Clincal triad of bone lesions, lymphedema, and chylous effusions. Can also look like multiple lytic lesions scattered throughout, involving all parts of bone including epiphyses.
Tumors common to have bone mets
BLT and a Kosher Pickle
Bilateral hip mixed sclerotic and lytic appearance
Soft tissue mass with lytic destructive action on adjacent bone, and sclerotic changes of bone adjacent to the lytic areas
MUCH MORE LIKELY TO BE INFECTION THAN NEOPLASM. DDx of TB, fungal abscesses, pyogenic. CAN’T EXCLUDE neoplasms, though, such as mets, myeloma, lymphoma or leukemia.
Prosthetic hip dislocation
OCCUR LATERALLY. Risk factors are elderly, cerebral dysfunction, and nonunion of the greater trochanter, which results in unapposed adductor action, causing the head to pop out of the acetabular component. Most cases are reduced nonoperatively.
Causes of prosthesis loosening
osteolysis or infection
Diagnosis of prosthesis loosening
Greater than 2mm zone in metal to bone interface if noncemented, or any gap between metal and cement. Other signs are migration of components, cement fracture, and periosteal new bone. Definitive diagnosis is obtained by TAPPING IT.
caused by small particles breaking off from the polyethylene liner that acts as the cartilage space between the mobile components. A granulomatous reaction to the small particles ensues.
Bipolar prosthesis
A type of hemiarthroplasty. Hemiarthroplasties are performed for PROXIMAL FEMORAL disease, NOT HIP disease. Unlike in total hip arthroplasties, where the acetabulum is excavated and a prosthesis inserted or cemented in place, the native acetabulum is left alone. Then a modular femoral head component is inserted (looks like an acetabular component, but it moves with the femur. Then a polyethylene liner is inserted, and then a modular femoral neck component is inserted onto this. Therefore, in the bipolar hemiarthroplasty, there is motion between the native acetabulum and the big femoral head component, as well as between the big femoral head component and the femoral neck component, hence the name BIPOLAR.
Fluid collection near total hip replacement in pelvis
probably abscess. Could be neoplasm if imaging features are consistent. Collection needs to be drained.
Soft tissue mass after trauma
probably hematoma. BUT CANNOT RULE OUT ABSCESS OR NEOPLASM. Look for enhancement or Doppler flow in lesion.
Bilateral femoral head erosive disease, without much acetabular involvement
IS IT REALLY EROSIVE, or are you looking at dense femoral heads? CHECK IF THEY ARE DENSE, because you are missing AVN frequently, thinking it is PVNS or other erosive arthropathy.
DDx AVN hip
Trauma, steroids, alcoholism, sickle cell, pancreatitis, renal transplantation, collagen vascular diseases (lupus, scleroderma), Gauchers.
Thing where femur is partially absent
PFFD – Proximal focal femoral deficiency. Femoral head can be present, and in that case some version of an acetabulum will form. If not, there may be no acetabulum formed at all.
Painful hip with bone marrow edema on MRI
DDX – Must first exclude fracture, either complete or stress. Once that is done, the differential is osteonecrosis, transient osteoporosis of the hip, or reflex sympathetic dystrophy.
Bilateral small flattened femoral heads in a child
DDx is Multiple epiphyseal dysplasia and spondyloepiphyseal dysplasia. Also could be Legg Calve Perthes. JCA has enlarged epiphyses, with eventual ankylosis.
Multiple epiphyseal dysplasia
Defective physeal chondrocytes, resulting in abnormal flattened epiphyses. The acetabuli also appear abnormal, forming around the abnormal epiphysis. The joints most commonly involved are the hip, knee, ankle, shoulder and wrist. There is early OA of weight bearing joints, which is the major cause of morbidity in these patients.
Spondyloepiphyseal dysplasia
similar, with disease of the spine as well
Dense bones with large metaphyses
Osteopetrosis. No ddx when you see large striated metaphyses in dense bones.
a heterogeneous group of disorders which all have one common end effect – abnormal activity of osteoclasts. This results in dense bones and abnormal modeling of undertubulated bones, resulting in large metaphyses with striated appearance.
Bubbly lytic lesion in proximal femur
sure it could be a simple bone cyst, but in this location, especially if there is ANY degree of varus deformity, the answer is fibrous dysplasia. You could always do a CT if you need confirmation.
Bilateral enlarged femoral epiphyses, with some deformities such as flattening
DDx is Legg calve perthes and JCA. In JCA there should be some other evidence of arthritis.
Legg calve perthes
Normal initial growth of the femoral epiphyseal ossification center, so acetabuli are relatively normal compared with the abnormal appearance of the involved epiphysis later in life. The disease starts between 2 and 13 years, average of 7. There is diminished blood supply to the femoral epiphysis, but the articular cartilage, nourished by synovial fluid continues to grow.
In a young patient, if imaged at this stage, which is usually preclinical, you would see a small femoral epiphysis for age and widened joint space. Then there is reperfusion of the femoral head, and ossification then begins CENTRIPITALLY, from centers not contiguous with the original central ossific nucleus. If imaged at this stage, the appearance is of fragmentation of ossification. This bone forms fast and in a somewhat disorganized fashion, resulting in 1) LARGE FEMORAL HEAD (coxa magna) – this does not occur in older children, who already have formed most of their epiphysis, instead they just get DENSE OSTEOSCLEROTIC FEMORAL EPIPHYSIS, which is not enlarged greatly, 2) Weaker bone with abnormal weight bearing from the big size of the head, resulting in compression fractures of the femoral head. This is when clinical symptoms usually start, and patients get imaged.
Treatment is to image the patient with MRI to see how much of the femoral head is uncovered by the acetabulum. The goal of treatment is to cover as much of the femoral head as possible during the reossification phase, so that it will model the femoral head into an appropriate shape. This can be done with a brace to put the hip in valgus, or a varus osteotomy of the proximal femur, which also puts the hip in valgus.
Any cause of osteonecrosis will cause the same appearance
Affects boys more than girls 4:1. Bilateral in 20%.
Causes of femoral head osteonecrosis in child
legg calve perthes, septic arthritis, trauma, sickle cell, gauchers
Multiple sclerotic lesions
metastatic disease, osteopoikilosis, mastocytosis, occasionally lymphoma
Make the diagnosis by periarticular distribution, uniform size, well defined margins, oval shape oriented along the axis of the long bone. Can sometimes show activity on bone scan.
Diagnosing SCFE
Draw line along femoral neck – it should intersect some part of the femoral epiphysis. Widened growth plate. Irregularity of zone of provisional calcification. Posteroinferior slippage of the epiphysis. Tx is nailing, without reduction. Complications are dysplasia of hip and early OA. The most devastating complication is osteonecrosis, however, which tends to occur in acute slips more than the chronic indolent ones.
Patient with SCFE
CHECK THE OTHER SIDE!!! 50% are or will be BILATERAL.
Fatty replacement of muscles diffusely
POLYMYOSITIS, DERMATOMYOSITIS, paralysis, muscular dystrophy, corticosteroid excess, arthrogryposis. Differentiate paralysis by history and maybe decubitus ulcers. Differentiate muscular dystrophy and arthrogryposis by joint and bony deformities. To clinch diagnosis of polymyositis or dermatomyositis, would also want to see deep or superficial soft tissue calcification. If there is a rash or dermal calcification, that clinches dermatomyositis.
Intertrochanteric hip fracture treatment
ORIF with dynamic hip screw
MRI showing extensive marrow edema with uplifting of the periosteum by fluid intensity and with surrounding fluid intensity
could be osteomyelitis, but could also be a stress fracture. In kids, MRI can make the lesion look worse, because the periosteum is loosely adherent in young people. Thus its easier to uplift with fluid.
Patient with dense sclerotic bones and opening on the cortical surface
chronic osteomyelitis with cloaca. Look carefully for the sinus tract extending from the cloaca through the soft tissues to the skin.
Chronic osteomyelitis
must be treated with surgical excavation and drainage and bone chip packing to promote healing after drainage. COMPLICATION IS SQUAMOUS CELL CARCINOMA, which occurs because of initial epithilialization of the sinus tract followed by neoplastic transformation due to the chronic irritation.
Differentiate osteomalacia from osteoporosis
in osteoporosis, you see cortical thinning with increased prominence of the tensile trabeculae. There is preferential resorption of the nontensile trabeculae. In osteomalacia, all the trabeculae become indistinct. There are bowing deformities. There are incomplete fractures = LOOSER ZONES, which can have periosteal new bone forming adjacent to them. Osteomalacia is caused by a deficiency of available Ca or P. Most commonly this is due to vitamin D deficiency. The bodies response to this is to increase PTH production to mobilize more Ca to raise the serum Ca so the person doesn’t go into tetany and die. This is the secondary hyperparathyroidism that is seen whenever there is vitamin D deficiency. The two go hand in hand to cause osteomalacia, as there is decreased Ca available to form bone, and then the bone is further being told to rev up osteoclast activity to free up more calcium.
Collection of amorphous calcifications near a joint
Tumoral calcinosis
Hydroxyapatite deposition into cystic spaces NEAR a joint. In aqueous suspension like milk of calcium, so they can layer out on CT and upright radiographs. RELATED TO DIALYSIS. Treatment is modification of the dialysate.
Sclerotic diaphyseal lesion replacing medullary cavity and mildly expanding bone in child
MUST RULE OUT OSTEOSARCOMA. Up to 20% can be epiphyseal or diaphyseal without metaphyseal involvement. May not have periosteal reaction or visible cortical destruction. The presence of a SKIP LESION hands you the diagnosis. Ewings can have skip lesions, but would be more permeative and have periosteal reaction. Lymphoma would too.
Numerous lytic lesions
mets, myeloma, but don’t forget about LYMPHOMA too.
Most common sites: Vertebral bodies 66%, Ribs 45%, Skull 40%, Shoulder girdle 40%, Pelvis 30%, Long bones 25% of patients. Myeloma is PURELY LYTIC, and well marginated lesions. The appearance may be multifocal lytic lesions, moth eaten, or permeative. It may be so uniform as to just cause osteopenia, and is a big cause of GEOGRAPHIC OSTEOPOROSIS appearance. It can also just look normal. However, it also can break through the cortex and cause LARGE SOFT TISSUE MASSES. BONE SCAN IS NOT A GOOD WAY TO LOOK FOR MYELOMA INVOLVEMENT. CURRENTLY, THE BEST MODALITY TO LOOK FOR INVOLVEMENT IS MRI, which shows the marrow replacement.
Swelling, fever and pain with periosteal reaction on xray in child
Can occur in any bone, but MOST occur in sacrum, innominate bone, and long bones of lower extremity. Diaphyseal and metadiaphyseal most common, but can be metaphyseal. MOST COMMON BONE TUMOR OF FIRST DECADE. Second most common in second decade. 75% occur before age of 20. Can occur at any age, though. Treatment is radiotherapy, with adjuvant surgical or chemo tx.
Ossification originating in cortex and wrapping around bone
PAROSTEAL OSTEOSARCOMA. There are 3 varieties of surface osteosarcomas. Parosteal, periosteal, and high grade. Parosteal is densely ossified, but may have unossified portions. It tends to wrap around the bone, and a cleavage plane between the tumor and native cortex can be seen where the wrapping is occurring. Periosteal is not densely ossified. High grade are like intramedullary lesions, just occurring on the surface. The definition of all of these lesions is that the medullary cavity is not involved, at least initially, with the center of the lesion in the cortex. Parosteal is low grade. Periosteal and high grade are high grade lesions.
Chondroid lesion for biopsy
Needle biopsy can be misleading, because behavior of chondroid tumor is based on its highest grade part, regardless of the size of that part relative to the size of the whole tumor.
Children and young adults

Maily metaphyses of long bones and posterior elements of vertebrae
Epiphyseal ABC

Most commonly in association with Giant cell tumor or chondroblastoma.
Predominantly lytic lesion in proximal femur with no cortical thickening or bony expansion in middle age patient
Liposclerosing myxofibrous tumor of bone

Look a little like fibrous dysplasia, a little like pagets, a little like ABC, and even may have some chondroid elements.

These tumors have a variety of patterns, and are grouped together into this subheading.

They are hamartomas.
Large soft tissue mass in the thigh with some calcifications
Synovial sarcoma




Extraskeletal OS

Extraskeletal CS
Soft tissue calcifications with central lucencies
Phleboliths. Probably soft tissue hemangiomas.
Peripheral calcifications around soft tissue mass
Myositis ossificans
Osseous masses with cortex and medullary space

Myositis ossificans progressiva
Calcifications in soft tissues with uniform density and shape
Cystic/milk of calcium calcifications
Tumoral calcinosis

Seen periarticular in dialysis patients only
Reticular/linear soft tissue calcifications
Calcification of muscular fascial layers

Dermatomyositis or collagen vascular disease
Most common soft tissue sarcoma in young (20s) patient
Synovial sarcoma

Well encapsulated soft tissue mass
BOTH MALIGNANT AND BENIGN MASSES MUST BE CONSIDERED, unless the lesion has some special characteristic, i.e. lipoma, myositis ossificans
Soft tissue mass bright on T2WI with central hypointense area
Look for other features of NEUROFIBROMA because this is a typical feature of them.
Noncalcified thigh soft tissue mass
Soft tissue sarcoma (MFH, synovial cell, or lipo)

Extraabdominal desmoid (fibromatosis)




Nerve sheath tumor
Soft tissue malignancies that COMMONLY calcify
Extraskeletal OS and CS

Synovial sarcoma
Thickening of disphyseal cortices of long bones diffusely
Camurati-Engelmann disease

Not pagets, because Pagets would begin at ends of bone (except in tibia) and spread toward diaphysis.

Not Hypertrophic osteoarthropathy, because that would not cause narrowing of the medullary cavity. Only periosteal bone depositon.
Camurati-Engelmann disease
Endosteal and periosteal depositon of new bone

Bone infarct


MFH (primary or secondary in previous bone infarct)
Can be primary in bone

Secondary in bone to:

Dedifferentiation of chondrosarcoma

Malignant differentiation of lipoma, infarct, radiation, or Pagets
Radiation change
Looks like patchy sclerotic appearance, not unlike bone infarct
Calcifications adjacent to the epiphysis of a long bone in a child
Trevor's disease = articular chondroma
Trevor's disease
Epiphyseal form of osteochondroma. There is overgrowth of the cartilage of the epiphysis, with formation of a secondary ossification center.

It occurs at the medial portion of the epiphysis of a long bone, usually of the lower extremity.

Lytic lesion in the epiphysis of the proximal femur
Common location for Clear cell chondrosarcoma
Lytic lesion in the epiphysis of the proximal humerus
Common location for Clear cell chondrosarcoma
Aggressive malignant permeative metaphyseal long bone lesion in young child (5 or 6)


Osteosarcoma -- can occur in very young patients

Neuroblastoma or Wilm's mets
Sclerotic trabecular thickening with cortical destruction and soft tissue mass in femoral metaphysis in 35 year old patient

Looks like Pagets with malignant transformation, but the patient is much too young.
Focal area of reactive sclerosis in long bone metaphysis

Infection (subacute Garre)


Widened intercondylar notch, DDX

Juvenile chronic arthritis
DDx widening of growth plates in 8 year old

Metaphyseal dysplasia (rare)

So, basically if you see diffusely widened growth plates, you know its going to be rickets
Erlenmeyer flask

Neimann Pick

Chronic anemias
Adolescent with meniscal tear
Child with diffuse osteopenia
Look for overgrowth of epiphyses

Its probably JCA
Signs of JCA
JCA involves mainly the large joints, unlike RA

May just see inflammatory changes (STS, effusion)

But a very important finding is either epiphyseal overgrowth or undergrowth.

In the knee, where the disease predominantly involves hyperemia, there is overgrowth because of the hyperemia.

In the wrist, where there is erosion of cartilage and epiphyseal destruction by pannus, undergrowth is what occurs.
Bony ankylosis of the knee in 18 year old

If it is present, kid has JCA

If it is not, still could be JCA, but could consider AS (although it would be really early for ankylosis)
DDx for ankylosed large joint


Septic arthritis

Associated with hyperparathyroidism, hemochromatosis, osteoarthritis, diabetes, and just plain aging.

CPPD crystals are generated locally in the joint, and are then deposited within cartilage (both hyaline = articular, and fibro = menisci), joint capsules, tendons, ligaments. Also deposited in intervertebral disks. These are evident radiographically as chondrocalcinosis.

Tendinous and ligamentous deposition explains the propensity of these patients to rupture said structures.

Sometimes these deposits rupture through the articular cartilage or joint capsule into the synovial fluid, which results in a SYNOVITIS = PSEUDOGOUT.

Also, the chronic deposition, rupturing of cartilage, and resultant synovitis finally result in pyrophosphate arthropathy, which radiographically looks like OA, except that different parts of the joints are involved vs. OA (i.e. patellofemoral involvement)

So, the 3 manifestations of CPPD that are evident radiographically are:

1) Chondrocalcinosis

2) Crystal-induced synovitis (Pseudogout)

3) Pyrophosphate arthropathy
3 compartment severe degenerative arthritis

Secondary OA after septic arthritis or infection

CPPD with pyrophosphate arthropathy
Difference between dermatomyositis and polymyositis
DDx muscular atrophy, muscular/muscular fascial calcification, subcutaneous calcification


Obliteration of intercondylar notch
Paget phases


The space between the femoral condyles. So its posterior. That is why hemophila widens it, because as you know hemorrhage into the origins of the cruciate ligaments, which occurs at the medial aspects of the . . .
salter harris injuries
I -- Widening and soft tissue swelling

II -- Avulsion of the growth plate, with the fracture line then extending into the adjacent metaphysis

III -- Vertical fracture through the epiphysis into the growth plate, without involvement of the metaphysis

IV -- Same as III, but the vertical fracture goes right through the physis, continuing into the

V -- Crush injury to the physis
Discrete fluid collection adjacent to PCL

Can also be next to ACL. Or anywhere, in fact the ddx for a baker's cyst is ganglion. Make dx of Bakers by location and hopefully even presence of a neck extending into the joint
Small Baker's cyst with fascial fluid distal

Cyst gets smaller sometimes, but fascia fills with fluid, and infiltrates distally, because of gravity
Linear calcification at medial aspect of distal femur
= Calcification of injured origin of MCL

MCL edema and discontinuity

BUT, you cannot stop there. These injuries are caused by valgus stress, so you immediately must look for the following:

1) If you have a radiograph, look for a segond fx

2) Valgus stress is associated with the whole triad of MCL tear, medial meniscal tear and ACL tear. The reason for the meniscal tear is that the MCL has both superficial and deep fibers. The deep fibers consist of meniscofemoral and meniscotibial components. Thus they are intimately associated with the meniscus. So if you tear the MCL, you will likely tear the meniscus too.

The same is NOT true on the lateral side, in which there is no significant connection between the lateral ligaments and the lateral meniscus
Fragmentation of inferior patellar pole in a 70 year old

Apparently jumper's knee can happen in old fogies too