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Glossary of SF MSK

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Sagittal MR images of the knee. First image shows bowtie. Second image does not; see separate anterior and posterior horns.
BUCKET HANDLE MENISCAL TEAR


Look for displaced fragment in center of joint.

DDx: Developmentally small meniscus
Cartilaginous fragment sitting in intercondylar notch on coronal image
BUCKET HANDLE TEAR
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?
Posteroinferiorly
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
LATERAL
PCL position on coronal view of intercondylar notch
MEDIAL
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
circular
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
Meniscofemoral ligament names
Humphrey


Wrisberg
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
Wrisberg
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
Fibrocartilage


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
Why
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
Superior


Inferior


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
Medial stabilizer of knee
MCL
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
LCL
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
AVN (PATHOGNOMONIC) = Aunt Minnie
Round lytic defect on articular surface of superolateral pole of the patella.
DORSAL DEFECT OF THE PATELLA = normal variant


DDx: Gout, osteochondritis, chondroblastoma, grade IV CMP
What makes appearance pathognomonic for this lesion?
Surrounding sclerosis
When do discoid menisci present?
Often in CHILDHOOD
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



Osteopoikilosis



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


Osteomalacia (rickets)


Hyperparathyroidism


Renal osteodystrophy


Hypoparathyroidism, pseudohypopara, pseudopseudo


Thyroid (hyper/hypo)


Acromegaly


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


Spine
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.


Hyperparathyroidism


Multiple myeloma


LOOK FOR THE INSUFFICIENCY FRACTURE
x-ray with osteopenia localized to one area
Disuse


Reflex sympathetic dystrophy


Transient regional osteoporosis


Plasmacytoma
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
NO JOINT SPACE NARROWING

and

NO ABNORMALITY OF THE ACETABULAR SIDE OF THE JOINT


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
Rickets
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


KNEE


WRIST


COSTOCHONDRAL JUNCTION
Bulbous enlargement of anterior ends of ribs
rachitic rosary of rickets

(RR of R)
Causes of rickets
ALWAYS RELATED TO ABNORMAL VITAMIN D METABOLISM


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.
LOOSER ZONE
Osteomalacia in adults
LOOSER ZONES

= 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.

1) BROWN TUMORS ARE NOT COMMON

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
Hypoparathyroidism


Pseudohypoparathyroidism
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


SCFE
Normal looking hand. Then told patient is 13.
Hyperthyroidism
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
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
Osteoporosis


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
Pelkin

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


Syphilis


Neuroblastoma mets


Methotrexate
Bone tumor age 1-5
Eosinophilic granuloma


Neuroblastoma mets
Bone tumor age 5-30
NOF


Solitary bone cyst


Aneurysmal bone cyst


Chondroblastoma


Fibrous dysplasia


Eosinophilic granuloma


Ewings


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


Osteosarcoma
Over 30
Chondrosarcoma


Fibrosarcoma
Over 40
Mets


Myeloma
Diaphyseal
Ewings


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
FEEMHI


Fibrous dysplasia


Eosinophilic granuloma


Enchondroma


Mets/myeloma


Hyperparathyroidism


Infection
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)
AVN
Trauma

Alcoholism


Steroids


Sickle cell


XRT


Lupus


Pancreatitis
staging system
Ficat

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


others,

LOOK AT RESNICKS VIDEO
Arthritis systematic evaluation
Remember your ABCDEs

Alignment

Bone mineral density

Cartilage joint space

Distribution

Erosions

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


Seronegatives


Gout


Synovial osteochondromatosis


PVNS
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


Gout


TB
Classic characteristics of TB arthritis
PHEMISTER'S TRIAD


Juxtaarticular osteoporosis


Peripheral erosions


PRESERVED JOINT SPACE
MCP joint space narrowing with hook-like osteophytes
Hemochromatosis


CPPD
OA
BASAL JOINTS OF THE THUMB AFFECTED
Eccentric lobulated soft tissue mass around a phalangeal joint
Think first of TOPHUS
Calcified tophi
Renal failure related gout
Sausage digit
Psoriatic


Reiters
Eccentric lobulated soft tissue swelling in an arthritis case
Gout


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

Trauma

Burns/Frostbite

Lesch-nyhan

HPT
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
95% CERVICAL SPINE!!!
OPLL association
DISH
DISH criteria
3


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
Neurofibromatosis


Marfans


Ehlers-Danlos


Dural ectasia


Mass lesion
DDx for anterior vertebral body scalloping
Neurofibromatosis


Kid: Neuroblastoma



TB



Lymphadenopathy



Aortic aneurysm



Marfans



Ehrlos-Danlos
Transverse lucency in collapsed vertebral body
INTRAVERTEBRAL VACUUM CLEFT

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

WHEN YOU SEE THIS, IT IS PROOF THAT THE COLLAPSE IS NOT DUE TO INFECTION OR NEOPLASM
Vertebra plana
FLATTENED VERTEBRAL BODY


causes:

Eosinophilic granuloma


Osteoporosis


Tumor (mets, myeloma)


Trauma
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)
Gauchers
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
GAUCHERS


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



Metatarsals



Calcaneus
Appearance of fatigue stress fracture
DENSE SCLEROSIS

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
Neurofibromatosis


Ehlers-Danlos



Marfans



Ankylosing spondylitis



Osteogenesis imperfecta tarda
Ivory vertebral body
Pagets


Osteoblastic mets



Lymphoma
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?
YES

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
BONE WITHIN BONE APPEARANCE OF OSTEOPETROSIS

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

Especially look for SPONDYLOLYSIS
Sclerosing bone dysplasias
Osteopetrosis


Melorrheostosis


Osteopoikilosis


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
PVNS


Hemophilia
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
Density
Disorganization
Dislocation
Debris
Distension
Common joints for neuropathic osteoarthropathy
Foot/ankle


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)
Bilateral
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.
Osteoblastoma
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.
Ochronosis
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.
Achondroplasia
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
Soft tissue OSSIFICATION DDx
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
Low signal on T1W and T2W images, BUT IT IS VERY BRIGHT ON POST CONTRAST IMAGES.
PVNS Tx
synovectomy
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.

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