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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 â€“ normal or slight increase in space with STS 2 â€“ acromion inferior to to distal clavicle 3 â€“ coracoclavicular separation has also occurred
Synovial osteochondromatosis: most common joint: knee, next most common â€“ hip, next most common â€“ elbow. Same as PVNS. 4th most common â€“ 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 â€“ 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 â€“ 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 â€“ postmenopausal and type II â€“ 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 â€“ 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 â€“ one side of vertebra does not form, congenital block vertebra â€“ 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 â€“ 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 â€“ primary disease of the annulus fibrosus, with osteophytosis and more preservation of disk height. 3) Osterarthritis â€“ 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 â€“ 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 (â€œdeath bringingâ€) dwarfism.
Achondroplasia: causes rhizomelic micromelia â€“ 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 Batsonâ€™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 â€“ 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 â€“ 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 shouldnâ€™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 Mazabraudâ€™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 â€“ 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 â€“ 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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