» Rad_Diff_MSK



MSK NOTES: with sample of multiple MOCK ORALS below.


Bubbly or lytic lesions (FEGNOMASHIC):  fibrous dysplasia (no periosteal reaction, mention adamantinoma if in tibia or jaw; pelvis, proximal femur, ribs, skull, long lesion in long bone, expansile medullary lytic lesion, ground glass, well-defined sclerotic margin, bowing deformities, base of skull sclerotic, hot on bone scan, cherubism in mandible and maxilla, craniofacial in facial and frontal bones, pseudoarthrosis of tibia, Mccune Albright is polyostotic FD with café-au-lait spots with precocious puberty), enchondroma (must have calcifications except in phalanges, no periostitis; tubular bones, chondroid calcifications, endosteal scalloping, pain is malignant, Ollier’s enchondromatosis, Mafucci’s enchondromatosis with multiple ST hemangiomas), EG (age<30; lytic lesion can look aggressive, skull lesion beveled-edge appearance, sequestrum, floating tooth, vertebra plana, lung dz, pituitary, RES), GCT (epiphyses must be closed, must be epiphyseal and abut the articular surface in long bones, eccentric, well-defined but nonsclerotic border except in flat bones; long tubular bone > spine or sacrum, 50% at knee), NOF (age<30, no periostitis, cortically based; metaphysis), osteoblastoma (mention with ABC even if age>30, especially in posterior elements of spine), mets (age>40; renal and thyroid), myeloma (age>40; plasmacytoma in ilium and sacrum, cold on bone scan; vertebral bodies destroyed before pedicles, axial skeleton, long bones, punched-out lytic lesions, generalized osteopenia, skeletal survey more sensitive), ABC (age<30, expansile, eccentric, pain, fluid-fluid levels on MR; posterior elements of spine, metaphysis of long bones, pelvis), SBC (age<30, central, no periostitis; proximal humerus, proximal femur, calcaneus, fallen fragment sign), HPT (brown tumor, must have other evidence of HPT), infection (always mention), chondroblastoma (age<30, epiphyseal), chondromyxoid fibroma (mention with NOF, no calcified matrix)

Automatics (must mention in every case):  age<30 – infection, EG; age>40 – infection, mets, myeloma

Multiple lytic lesions (FEEMHI):  fibrous dysplasia, enchondromas, EG, mets, myeloma, HPT, infection

Rib lesions (FAME):  fibrous dysplasia, ABC, mets, myeloma, enchondroma, EG

Lytic epiphyseal lesion (also apophyseal, carpal and tarsal bones, patella):  chondroblastoma, infection, EG, GCT, geode; age>40 – add mets and myeloma and remove chondroblastoma

Lytic lesion in posterior elements of spine (OAT):  osteoblastoma, ABC, TB

Exclude these lytic lesions if age>30 (CANES):  chondroblastoma, ABC, NOF, EG, SBC

Lesions that have no pain or periostitis (FENS):  fibrous dysplasia, enchondroma, NOF, SBC

Bony sequestrum (FILE):  fibrosarcoma, infection, lymphoma, EG, osteoid osteoma (mimic)

Geodes (CARD):  CPPD, AVN, RA, DJD, trauma

Sclerotic lesion age 20-40:  chondroblastoma, ABC, NOF, EG, SBC, fibrous dysplasia, infection, HPT (healing brown tumor), osteoid osteoma, giant bone island; age>40 – mets

Endosteal scalloping:  fibrous dysplasia, enchondroma, cartilaginous tumor

Wide zone of transition (permeative): mets + myeloma, reticulum cell sarcoma, Ewing’s sarcoma, infection, EG

Malignant bone tumors:  age<30 – Ewing’s sarcoma (diaphysis long bones > flat bones, aggressive, ST mass typical, medullary location), osteosarcoma (poorly defined intramedullary metaphyseal mass lesion extends through cortex, osteoid or chondroid matrix, aggressive periosteal reaction with Codman triangle or sunburst pattern, telangiectatic form purely lytic and simulates ABC, parosteal form is low-grade and seen in posterior distal femur with more mature ossification centrally), mets in children (neuroblastoma, leukemia/lymphoma, Wilm’s); age>40 – mets + myeloma, chondrosarcoma (pain, long bones, pelvis, ribs, clivus, most metaphyseal); age 30-40 – GCT (if lung mets or recurrence), parosteal osteosarcoma (densest calcification is central), fibrosarcoma (almost always lytic), malignant fibrous histiocytoma (mention with fibrosarcoma, aggressive, large soft tissue mass), reticulum cell sarcoma (primary lymphoma of bone, looks like Ewing’s sarcoma, often asx)

Permeative lesion in child:  Ewing’s sarcoma, infection, EG

Permeative lesion in older pt:  infection, mets, myeloma, malignant fibrous histiocytoma, reticulum cell sarcoma

Soft tissue tumors:  MFH, liposarcoma (may or may not have fat), synovial sarcoma (usu extraarticular), synovial osteochondromatosis (multiple Ca++ loose bodies, jt effusion, erosions, destruction; knee, hip, elbow; mimics PVNS if not Ca++), pigmented villonodular synovitis (hemosiderin deposits lining synovium, erosions, jt destruction, no joint space narrowing), hemangiomas (phleboliths, cortical holes, striated vertebral body)

Malignant transformation of bony lesions:  fibrous dysplasia – fibrosarcoma, OSA, MFH; Paget’s – OSA; osteomyelitis with draining sinus – SCC; radiation – OSA, chondrosarcoma, MFH; bone infarct – fibrosarcoma, MFH; Ollier’s – chondrosarcoma; Maffucci’s – chondrosarcoma; osteochondroma – chondrosarcoma

Cortical holes (pseudopermeative lesion):  osteoporosis (metacarpal cortex less then ¼ to 1/3 of metacarpal), radiation, hemangiomas

Focal cortical thickening:  stress fracture, infection, osteoid osteoma

Mets to bone:  PBKTL; P – mostly blastic, B – mixed, K – purely lytic, TL – mostly lytic

Hallmarks of DJD:  joint space narrowing (asymmetric), subchondral sclerosis, osteophytes, subchondral cysts, lack of osteoporosis or erosions

Joints that exhibit erosions with OA:  TMJ, SI, AC, pubic symphysis

Hallmarks of RA:  soft tissue swelling, periarticular and diffuse osteoporosis, joint space narrowing, marginal erosions (including ulnar styloid and triquetrum, proximal distribution (hands), bilaterally symmetric, subchondral cysts, ulnar deviation, carpal instability, rotator cuff tear, distal clavicle resorption, axial migration, protrusio acetabuli, A-a subluxation, may see rice bodies in synovial inflammation; secondary DJD – severe JSN out of proportion to sclerosis and osteophytes

Hallmarks of HLA-B27 spondyloarthropathies:  bony ankylosis, proliferative new bone formation, predominantly axial (spinal) involvement, syndesmophytes

Sacroiliac joint involvement:  AS (bamboo spine, Andersen lesion and pseudoarthrosis), IBD (like AS), psoriasis (distal predominance, sausage digit, pencil-in-cup, acroosteolysis, proliferative erosions, STS, periostitis, bony ankylosis, arthritis mutilans deformities, heel spur with fuzzy margins), Reiter’s syndrome (like psoriasis but feet>hands, IP joint great toe), DJD, infection, gout, HPT; bilateral + symmetric SI jt + marginal symmetric syndesmophytes – usually AS or IBD; unilateral or asymmetric SI jt – exclude AS and IBD and consider psoriasis and Reiter’s

Large joint involvement:  DJD (superolateral migration in hips, medial compartment of knee most affected), RA (axial migration in hips), CPPD, AS (resembles RA), PVNS, synovial osteochondromatosis, infection (Staph aureus most common, Salmonella in SCD, joint effusion, joint destruction, crosses disc space in spine, periosteal reaction, bone destruction, Brodie’s abscess is well-defined lytic lesion with thick sclerotic border, sequestrum), amyloidosis (nodular synovitis with erosions resembling RA), ochronosis (DSN with vacuum, disc calcifications, generalized osteoporosis, secondary OA)

Arthropathy distribution in hands and wrists:  distal – psoriasis, Reiter’s syndrome, osteoarthritis; proximal – RA, CPPD

Bilateral symmetry of arthropathy:  primary OA (middle-aged women in hands only, 1st CMC, gull-wing erosive pattern), RA, multicentric reticulohistiocytosis (multiple erosions predominantly in phalanges without osteoporosis)

Monoarticular arthritis:  CHRIST – crystal arthropathies, hemophilia, RA, infection, synovial (synovial osteochondromatosis, PVNS), trauma

Normal mineralization:  DJD, CPPD, gout, multicentric reticulohistiocytosis, PVNS, synovial osteochondromatosis

Hallmarks of gout:  well-defined erosions often with sclerotic borders or overhanging edges, soft tissue nodules that calcify in presence of renal failure, random distribution in hands without marked osteoporosis, podagra (1st MTP jt), often have chondrocalcinosis, preserved joint space, olecranon/prepatellar bursitis

Hallmarks of CPPD:  pain, cartilage calcification (knee, triangular fibrocartilage of wrist, pubic symphysis), joint destruction from secondary DJD (shoulder, elbow, radiocarpal jt, patellofemoral jt), subchondral cysts, can present as pseudogout

CPPD-associated disorders:  primary HPT, gout, hemochromatosis (DJD 2nd-4th MCP jts with squaring of metacarpal heads with drooping osteophytes, generalized osteoporosis)

Hallmarks of collagen vascular diseases:  osteoporosis and soft tissue wasting in the hands, erosions generally not present; SLE – ulnar deviation of phalanges, nonerosive, resembles Jaccoud’s arthropathy; scleroderma – ST calcifications, acroosteolysis, severe resorption of 1st CMC with radial subluxation of 1st metacarpal; dermatomyositis – widespread ST calcifications, radial subluxation of IP joint of thumb

Charcot joint:  joint destruction, dislocation, heterotopic new bone; causes – DM, spinal cord injury, alcohol abuse, myelomeningocele/syringomyelia

Epiphyseal enlargement and gracile diaphyses:  hemophilia (hemarthrosis, secondary OA, widened intercondylar notch, enlarged trochlear notch, subchondral cysts; pseudotumor – large ST mass with adjacent bone destruction, hematoma, Ca++ common), JRA (diffuse ankylosis of posterior articular joints, periosteal new bone formation, STS, short metacarpals), paralysis

Hallmarks of AVN:  increased bone density at otherwise nl jt; joint effusion, patchy or mottled density, subchondral lucency, articular surface collapse and joint fragmentation, low signal serpiginous border on MR; causes – trauma, steroids, sickle cell anemia, renal disease, collagen vascular diseases, alcoholism, idiopathic; OCD at lateral aspect of medial femoral condyle, talus, capitellum; SONK in elderly at weight bearing medial femoral condyle

Hallmarks of osteomalacia:  osteopenia, Looser’s fxs (femur, pelvis, scapula), epiphyseal flaring and irregularity, bending of long bones

Hallmarks of HPT:  subperiosteal resorption in radial aspect of middle phalanges, medial aspect of proximal tibia, SI jts, distal clavicle resorption, rugger jersey spine, brown tumors, sclerosis, salt and pepper skull, ST calcifications, chondrocalcinosis

Dense bones:  renal osteodystrophy (2o HPT, osteomalacia), sickle cell disease (bone infarcts, dactylitis, H shaped or fish vertebrae, AVN hip, hair on end skull, osteomyelitis, spleen autoinfarction, cholelithiasis, papillary necrosis), myelofibrosis (splenomegaly and extramedullary hematopoeisis), osteopetrosis (“bone in bone, sandwich vertebrae”, erlenmeyer flask, dense base of skull), pyknodysostosis (distal phalanges pointed and dense, tufts absent, widened sutures, straight angle mandible), mastocytosis (thickened SB folds with nodules), mets (breast and prostate), Paget’s disease (bony enlargement, commonly in pelvis with thickened iliopectineal line, lytic phase with flame-shaped or blade of grass leading edge that always starts at end of bone except in tibia, cotton wool skull, 2o OSA, thickened trabeculae, protrusio acetabuli, picture frame vertebral body, ivory vertebral body, osteoporosis circumscripta, diploic widening, bowing of bones), athletes, fluorosis (ligamentous calcification, sacrotuberous ligament) – 3MsPROOF

Periostitis without underlying bony lesion:  trauma, HPO (painful periostitis of long tubular bones; causes – lung cancer, benign fibrous tumor of pleura, mets, mesothelioma, chronic pulmonary infection), venous stasis (lower extremities), thyroid acropachy (occurs post thyroidectomy, metacarpals and phalanges, esp ulnar aspect of 5th metacarpal), pachydermoperiostosis (like HPO but rarely painful)

Periosteal reaction in children:  scurvy (dense metaphyseal lines), Caffey’s (tibia, ulna, mandible), trauma, hypervitaminosis, leukemia, lymphoma, neuroblastoma, infection, physiologic, prostaglandins – SCALP

Don’t Touch” lesions:  posttraumatic lesions – myositis ossificans (peripheral circumferential calcification with lucent center), avulsion injury (cortical irregularity and periostitis at ligament or tendon insertion site, lesser trochanter avulsion suggests mets), cortical desmoid (posteromedial epicondyle of femur), geodes, discogenic vertebral sclerosis (variant of Schmorl’s node), fracture (if not immobilized), pseudodislocation of humerus (inferior subluxation from fracture and hemarthrosis); normal variants – dorsal defect of patella (lytic defect upper outer quadrant), pseudocyst of humerus (lytic area at greater tuberosity), os odontoideum (smooth well-corticated inferior border of dens and hypertrophied densely corticated anterior arch of C1); benign lesions – NOF, bone islands (asymptomatic, usually oblong with long axis in axis of stress, trabeculae extend into nl bone spiculated), SBC (do not prophylactically curettage if in calcaneus), pseudocyst of calcaneus, bone infarct (dense serpiginous border), Pitt’s pit (lytic lesion at lateral aspect of femoral neck); osteoma (facial bones, skull, Gardner’s)

Miscellaneous bone lesions:  achondroplasia (shortened long bones with narrowing of interpedicular distance in caudal direction, posterior vertebral body scalloping), melorrheostosis (thickened cortical new bone like “dripping candle wax”, follows sclerotome), mucopolysaccharidoses (flattened vertebral bodies with anterior beak, flared iliac wings and broad femoral necks, pointed proximal 5th metacarpal base with notch appearance to ulnar aspect, posterior vertebral body scalloping), multiple hereditary exostosis (osteochondromas, metaphyseal, lesion grows away from joint, undertubulation, knees, proximal femur, axial more prone to degeneration), osteoid osteoma (pain, age<30, lucent nidus surrounded by reactive sclerosis in cortex of long bone, can be on concave side of painful scoliosis, “double density” sign on bone scan), osteopathia striata (multiple 2-3mm thick linear bands of sclerotic bone aligned parallel to long axis of bone, asymptomatic), osteopoikilosis (hereditary, asymptomatic, multiple small sclerotic densities on ends of long bones and pelvis), sarcoid (“lace-like” pattern of bony destruction in hands), SCFE (overweight teenage boys, line through lateral femoral neck does not intersect with portion of epiphysis, can be complication of hypothyroidism), DISH (flowing anterior osteophytes at least 4 contiguous vertebral bodies without DSN or sclerosis), reflex sympathetic dystrophy (=Sudeck’s atrophy, severe patchy osteoporosis and STS following minor trauma), acromegaly (skull thickening, enlarged sinuses and sella turcica, hypertrophied terminal tufts with spade appearance, posterior vertebral body scalloping, elongated and widened vertebral bodies, heel pad thickening), transient osteoporosis of the hip (pain, self-limited, low T1 signal, hot on bone scan), tarsal coalition (talar beak, sclerosis of middle facet of subtalar joint), intraosseous lipoma (asx, proximal femur, fibula, calcaneus, may have central calcified nidus); OPLL (C-spine); Poland’s syndrome (absence of pectoral muscles and syndactyly); congenital rubella (“celery-stalk” metaphysis)

Dense base of skull:  fibrous dysplasia, Engelmann’s disease (kids, cortical thickening midshaft of long bones involving both periosteal and endosteal surfaces), Von Buchem’s disease (adults), Paget’s disease, meningioma, pyknodysostosis, osteopetrosis

Lytic skull lesion:  SCD, HPT, Paget’s, FD, TS, infection, mets, myeloma, EG, epidermoid, hemangioma

Wormian bones:  pyknodysostosis, OI, cleidocranial dysplasia (absent distal clavicles, supernumerary teeth), hypothyroidism, pachydermoperiostosis, Down’s – PORKCHOPS

Atlanto-axial subluxation:  RA, trauma, Down’s, Morquio’s, POOF

High-riding shoulder:  RA, CPPD, torn rotator cuff

Distal clavicle resorption:  RA, HPT, osteomyelitis, weightlifting, trauma, scleroderma

Inferior rib resorption:  vascular impression (coarctation), HPT, NF

Madelung’s deformity:  Hurler’s, infection, trauma, dyschondrosteosis, osteochondromatosis, chromosomal anomalies (Turner’s) – HITDOC

Radial hypoplasia:  VACTERL, Holt-Oram syndrome, thrombocytopenia-absent radius syndrome

Ulnar variance:  negative – Kienbock’s; positive – TFCC tear, ulnar impingement syndrome

Distal tuft resorption:  scleroderma, psoriasis, Raynaud’s, vascular disease, frostbite, electrical burns, tabes dorsalis, HPT, pyknodysostosis – PINCH; band-like – polyvinyl chloride, Hajdu-Cheney syndrome

Lytic finger:  enchondroma, glomus tumor (pain, terminal phalanx), epidermoid inclusion cyst, mets, infection, sarcoid, erosive arthropathy

Polydactyly:  familial, chondroectodermal dysplasia, trisomy 13, Meckel-Gruber

Short 4th metacarpal:  idiopathic, pseudohypoparathyroid (brachydactyly), pseudopseudohypoparathyroid, Turner’s, basal cell nevus syndrome (mandibular cysts, dural calcifications)

Sclerotic vertebral body:  LIMMP – lymphoma, infection, mets, myeloma, Paget’s

Vertebral body lesion:  Paget’s, osteoporosis, HPT, LIMP, myeloma, hemangioma, SCD, HLA-B27, EG, GCT, osteoblastoma, ABC, TB, osteoid osteoma

Platyspondyly:  diffuse – dwarf, OI, Morquio’s, epiphyseal dysplasia, Cushing’s; solitary or multifocal – EG, infection, trauma, mets, myeloma, lymphoma, leukemia, SCD, osteonecrosis (with vacuum disc phenomenon)

Anterior vertebral body beaking:  Morquio’s (middle), others (inferior) – Hurler, achondroplasia, Downs

Posterior vertebral scalloping:  dural ectasia (NF, Marfan’s, Ehlers-Danlos), syrinx, spinal canal tumor, congenital (achondroplasia, mucopolysaccharidoses, OI), acromegaly

Posterior spinal fusion:  Klippel-Feil, surgical fusion, JRA, HLA-B27

Fused vertebrae:  isolated, trauma, Klippel-Feil

Lytic ilium:  FD, ABC, SBC, hemophilia, mets, plasmacytoma, Ewing’s sarcoma, chondrosarcoma, lymphoma

Lytic sacrum:  met, chordoma (sacrum, clivus, vertebral bodies, expansile lytic lesion with large ST component and variable calcifications), plasmacytoma, chondrosarcoma, GCT

Widened pubic symphysis:  bladder exstrophy, infection, mets, trauma, pregnancy

Widened teardrop in hip:  infection, trauma, pigmented villonodular synovitis (erosions, preserved joint space), synovial osteochondromatosis (multiple calcified loose bodies in jt, mimics PVNS if noncalcified), AVN

Protrusio acetabuli:  RA, trauma, Paget’s, osteomalacia, AS, IBD – PROT A

Femoral head AVN:  alcohol, SCD, exogenous steroids or radiation, pancreatitis, pregnancy, trauma, infection, Caisson, LCP, epiphyseal dysplasia, Gaucher’s (hepatosplenomegaly, osteopenia, AVN, Erlenmeyer flask) – ASEPTIC LEG

Medial tibial spur:  osteochrondroma, Blount’s disease, trauma

Dense metaphyseal lines:  growth recovery lines, lead, healing rickets, scurvy

Erlenmeyer flask:  craniometaphyseal dysplasia, hemoglobinopathies including SCD and thalassemia (marrow hyperplasia, hair-on-end skull, Erlenmeyer flask, extramedullary hematopoeisis), osteopetrosis, Niemann-Pick, Gaucher’s – CHONG

Gracile bones:  NF, immobilization, muscular dystrophy, JRA, OI, dysplasias – NIMROD

Bowed bones:  rickets, NF, OI, FD

Soft bone:  Paget’s, osteogenesis imperfecta, osteomalacia, fibrous dysplasia

Osteopenia:  steroids, osteoporosis, osteomalacia, multiple myeloma

Epiphysis:  chondroblastoma, GCT (after physis closure), EG, chondrosarcoma

Metaphysis:  osteosarcoma, parosteal sarcoma, chondrosarcoma, fibrosarcoma, NOF, GCT (before physis closure), SBC, ABC, osteochondroma

Diaphysis:  myeloma, Ewing’s, reticulum cell sarcoma

Metadiaphyseal:  fibrosarcoma, fibrous dysplasia, enchondroma, osteoid osteoma, chondromyxoid fibroma

Soft tissue mass:  MFH, lipoma, liposarcoma, hemangioma, synovial sarcoma, nerve sheath tumor, mets, hematoma, abscess, rhabdosarcoma, leiomyosarcoma, myositis ossificans, aneurysm

Soft tissue calcification:  tumoral calcinosis, synovial osteochondromatosis, ST tumor, scleroderma, dermatomyositis, myositis ossificans progressiva, HPT, metastatic calcifications, CPPD, calcium hydroxyapatite deposition, hematoma, vascular

Tendon rupture:  steroids, RA, DM, HPT, gout

Heel pad thickening:  >25mm, myxedema, acromegaly, dilantin, callus, obesity, peripheral edema – MADCOP

Periprosthetic lucency:  loosening, particle disease, infection

Massive osteolysis:  palmar fibromatosis (Dupuytren’s contracture), Gorham’s disease (regional lysis by angiomatous tissue, tapering of remaining bone, ST atrophy), mets, aggressive primary bone or ST tumor, infection




Posterior Shoulder Dislocation on XR, start with frontal view

Posterior shoulder dislocations are one of the most often missed diagnoses, which is probably why they love to show it. It is a difficult diagnosis on an AP view, but signs include:

  • 1.The trough sign – A vertical compression fracture of the medial aspect of the anterior humeral head
  • 2.The rim sign – Widening of the glenohumeral joint >6mm
  • 3. The Absent Crescent sign – The same idea, which is that there is separation of the humerus from the glenoid such that the normal overlap is lost.
  • 4. Superior subluxation of the humeral head
  • 5. Disruption of the scapulohumeral arch
  • 6. A film will be labeled external rotation, but it looks like internal rotation, because the patient is unable to externally rotate the arm. If you suspect a posterior dislocation, you need to ask for a “Scapular Y” view. The reason not to ask for an axillary view is that it requires the patient to move the arm which is painful and may dislocate a shoulder that has spontaneously relocated. On the Y view, look for the humeral head to lie posterior to the glenoid, which is the center of the “Y”. CT is needed, not to make the diagnosis, but to look for complications such as a reverse Hill-Sach’s or reverse Bankardt, stripping of the posterior periosteum and a tear of the posterior labrum. Common causes of posterior dislocation are electrocution and seizures (posterior musculature is stronger), and occasionally trauma. See CR p119 c82 (shows trough and superior subluxation), H99 and 100 f5-39 (absent crescent) and 5-41 (“Y” view), C57 f3-29 (trough, >6mm, “Y” view) and ACR disc MSK case 353 (axillary view)



Posterior Hip Dislocation

  • Hip dislocations are usually the result of MVAs.
  • 90% are posterior, +/- posterior wall or column acetabular fracture.
  • Mechanism is posterior force on a flexed hip, like knee against dashboard.


Complications include

  • Sciatic nerve injury (10%)
  • AVN of femoral head,
  • MO, and DJD
  • Occasional femoral head fractures, especially impaction of the anterior aspect.

The femoral head comes to lie superolateral to the acetabulum. Also, the femoral head on the dislocated side appears smaller because it is closer to the cassette and so has less magnification. CT is good for looking for loose bodies in joint. Small loose bodies resorb over time, but large ones need to be surgically removed. See C84 f5-5, ACR case 368.



Lytic Paget’s Disease (blade of grass) of femur or tibia on XR

Paget’s disease starts at the epiphysis and extends up or down the bone. The leading edge is sharp, radiolucent and tapers, like a blade of grass. The lytic phase is almost always hot on bone scan (they may ask this). For typical blade of grass, see C286, H159 f7-29, ACR MSK case 528 & 529.



Soft Tissue Calcification in the Hands

Although many entities cause soft tissue Ca+, the 2 main considerations (that they would be likely to show) in the hands are Hyperparathyroidism and Scleroderma.

Less likely options are burns, SLE, and Dermatomyositis. I will discuss the hand findings in scleroderma and hyperparathyroidism.



The hand findings include:

  • Atrophy and tapering of the soft tissues of the fingers
  • Acroosteolysis
  • Subcutaneous Ca+ or joint Ca+
  • Erosions (late finding) with a predilection for PIPs and DIPs
  • Flexion contractures

A very distinctive feature is severe resorption of the 1st carpometacarpal joint with radial subluxation of the 1st metacarpal. See CR p169, c124 (shows radial subluxation, soft tissue Ca+, acroosteolysis), C219 f12-11, H133 f6-32, ACR MSK cases 225 (F3 note radial subluxation) and 226.



Hand findings in include:

  • The most well known and pathognomonic is subperiosteal resorption along the radial aspects of the middle phalanges, especially the 2nd and 3rd.
  • Brown tumors (lytic lesions)
  • Soft tissue Ca+
  • Acroosteolysis
  • Cortical tunneling
  • Osteopenia
  • Subchondral resorption mimicking erosions
  • Vascular Ca+

See H153 f7-17, CR p115 c79, C277 f15-3, ACR 512, 513 (subchondral), 514 (great case), 515. You gotta look for the subperiosteal resorption, because otherwise scleroderma and hyperparathyroidism are very similar.



Erosive OA in Hands

Erosive Osteoarthritis is an inflammatory form of OA that affects post menopausal middle aged women. It is often limited to the hands (in typical OA locations), especially the PIPs and DIPs, and 1st carpometacarpal and STT joints. The erosions tend to be centrally located, unlike other processes which are marginal. Also, there are marginal osteophytes. The combo of erosions and spurs (mixed erosive/productive) creates the “gull wing”. Ankylosis of IP joints is a feature of erosive OA which does not occur in normal OA. Osteopenia is also a distinct feature. Swelling is common. 15% of patients with EOA go on to develop Rheumatoid Arthritis. Erosive OA may be a feature of Cronkhite-Canada Syndrome. See C234 f13-5, CR p87 c61, ACR case 232.

DDx: PA and Adult Still’s Disease.



Psoriatic or Reiter’s Arthritis of the Hands

Both of these are inflammatory arthritides associated with both erosive and productive changes, which is a unique feature, seen in very few conditions (EOA is another). The erosions have fuzzy margins and wisps of periostitis. They both have distal predominance and soft tissue swelling. In the late phases, ankylosis of joints may occur. Another feature is sausage digit type soft tissue swelling. Very late, there is an arthritis mutilans, with resorption of phalanges. Also the pencil in cup deformity may result (C224 f12-21) Bone density is usually normal except for juxta-articular osteoporosis. Acroosteolysis is another possible feature.

Although there is a lot of overlap, as a general rule, psoritatic favors the hands and Reiter’s the foot. See H126 f6-20, ACR disc 218-222.

DDx in hands includes erosive OA (look for STT and 1st carpometacarpal involvement, and check SI joints), and adult Still’s disease. 3 things that help favor Still’s would be ulnar capping, fever, and predominant pericapitate involvement. Both can involve carpus and distal hand. ½ of PA patients are HLA-B27 positive (Reiter’s =80%).



Renal Osteodystrophy

They start with one of 2 films. Either a spine showing rugger jersey, or a CXR with bilateral clavicular resorption.

Concerning distal clavicle resorption, there are 5 causes total:



  • Trauma(ACR case 347)
  • Mets / Myeloma.

I use the mnemonic either “ChaRM T” or “HuRT My Clavicle”.

However, only 3 of these would be a bilateral process, those being RA, hyperparathyroidism and cleidocranial dysplasia. I think the best next step if they show you distal clavicle resorption is to ask for a hand film, to look for changes of HPT (subperiosteal resorption) or typical findings of RA.

Rugger jersey spine refers to sclerosis of the vertebral body end plates. Three things can cause an appearance of sclerotic end plates, and it is important to distinguish these. These are hyperparathyroidism with “rugger jersey”, osteopetrosis with “bone in a bone”(ACR case 549) or sandwich vertebrae (2 different things), and Paget’s with “picture frame”. Paget’s is easy to tell apart, because it wont involve many levels, and it will enlarge the involved vertebrae. The way to tell osteopetrosis from rugger jersey is that osteopetrosis is both more sclerotic and has sharper borders than rugger jersey. Compare H153 to 157 and C278 to 254. Also see CR p19 c13. Again, if you see the rugger jersey, ask for hand films to confirm diagnosis.



AVN of Hip either on XR or with normal XR and abnormal MRI

There are 5 stages of AVN of plain film, which is called the Ficat’s Classification.

  • Stage 1 is either normal XR or slight increased or decreased density (H142 f6-52). There may be a joint effusion without anything else
  • Stage 2 is mixed osteopenia and sclerosis (C302 L hip)
  • Stage 3 is subchondral collapse (crescent sign, H142 f6-53)
  • Stage 4 is articular collapse (H 143 f6-54, C302 R hip) and
  • Stage 5 is DJD secondary to the AVN.

MRI is much more sensitive for early AVN than XR. On MRI, in the acute phase, bone marrow edema is seen, and there is a long DDX, as this is a very nonspecific finding. Later, the “double line sign” is seen in the anterosuperior femoral head, which consists of an irregular / serpiginous rim of low signal on T1, and paired rims of high and low signal on T2. The inner one is granulation tissue, the outer one is fibrous tissue and cellular debris. See H233, CR p7 c4, C303 f16-18, ACR case 223 (SLE, good case) and case 258.



XR of the L Spine with Syndesmophytes and Asymmetric Sacroiliitis

Asymmetric sacroiliitis is and asymmetric lateral syndesmophytes suggest either Psoriatic Arthritis or Reiter’s. In AS or IBD, the sacroiliitis tends to be more symmetric, but more importantly, the syndesmophytes are delicate and involve the annulus fibrosis, mostly anterior location, vs the bulky lateral syndesmophytes (also known as paravertebral ossification, or PVO) of Reiter’s or Psoriatic which spare the annulus.

As far as distinguishing Reiter’s from PA, this is difficult and sometimes not possible. One of the easiest things is to check the patient’s age and sex. Reiter’s is a disease primarily of young men, so if it’s a female go with PA. Radiographically, Reiter’s tends to favor feet and PA the hands, but this is not a terribly good rule. PA tends to be more severe and mutilating. I think PA is more often associated with the pencil in cup deformity, and on the boards, people asked for hand films, and they were given foot films showing pencil in cup, and they went with PA. However, I am not convinced of this, and I might say Reiter’s if there are plantar or achilles enthesopathies or retrocalcaneal bursitis or calcaneal erosion, which are more typical of Reiter’s (Still should include Psoeriatic, though). The remainder of the foot findings in both are similar to hand findings, with fluffy erosions, periostitis (mixed erosive and productive), mostly normal bone density etc. I guess in the end, Ill try to go with patient sex and age and hand vs foot to distinguish. I don’t think they can fault you too much if you say both in DDx, you probably pass the case.

If they give me a film other than the hands I will ask for patient age and sex and request a hand film. If they start with a hand film, I will ask for patient age and sex and next ask for a foot film. For spine/SI see H125 f6-17, and compare images of syndesmophytes on H122 and 123. For hands and feet, see C224, 225, & 226 f12-23, H126 & 127, CR p53 c39. Compare ACR case 215 to 221 Film 1D. As a final note, remember that spurs in OA are horizontal, while syndesmophytes are vertical.



AS on AP L spine with sclerotic end plates and subtle syndesmophytes

Ankylosing Spondylitis is predominantly a disease of young males. In the spine, it begins in the L/S spine and proceeds north to the C spine. There are XR signs on an AP film which are helpful. The most well known one is the “bamboo spine” from extensive syndesmophyte formation. Another sign is the “trolley track sign” which refers to 3 parallel white lines, the middle one represents ossification of the interspinous ligament, and the outer ones, ossification of the apophyseal (facet) joint capsules. Great image in C221. An earlier sign is the “Dagger Sign”, which is just the middle white line of the ossified interspinous ligament.

Also on the AP L spine film, look for the SI joint erosions/sclerosis/fusion etc, and the abnormal angle of the pelvic inlet (pelvic tilt) which results from loss of the lumbar lordosis. On the lateral film, the earliest vertebral body change is osteitis with shiny corners or reactive sclerosis. Then get squaring (lose the normal anterior concavity, see C221 f12-14) then syndesmophytes. Also see fusion of facet joints (don’t forget posterior elements!). See ACR cases 214 & 215, CR p17 c10.



ABC of fibula on XR f/up by MRI w/ fluid/fluid levels

Know how to tell ABC from Telangiectatic Osteosarcoma, they show both.

Aneurysmal Bone Cysts are primarily seen in patients <30 yo. They are lytic, geographic, with a narrow zone of transition (AFIP 1B lesion) and almost always expansile. They are cortically based, which is a different from Solitary Bone Cysts, which are centered in the medullary cavity. They occur in the metaphyses of long bones, pelvis and posterior elements of spine. 50% occur in isolation, and the other 50% arise in another lesion such as a GCT, NOF, chondroblastoma, osteoblastoma or trauma. Main DDx in long bone are NOF and FBD, and in spine, osteoblastoma.

Treatment is curettage and possible cryosurgery. Low dose rads may also be used. On CT or MRI, a characteristic feature is fluid/fluid levels (from hemorrhage). Although this is not pathognomonic, because other things can cause this, it is still very helpful (For CT see ACR case 157 Film 7, for MRI see H24 f2-29 and ACR case 158 films 8 and 9. Also see Duke 274 just like the boards one).

It is important to distinguish telangiectatic osteosarcoma from ABC.


Telangiectatic Osteosarcoma

A variant of osteosarcoma without any bone matrix, and often without periosteal reaction. To make things worse, it can be largely geographic and even have sclerotic borders, and on MR, it may have fluid/fluid levels. The key is that on XR, there will be at least a portion of the margin which has a wider zone of transition, and there is usually cortical destruction and soft tissue mass. If you see cortical destruction or soft tissue mass, it is NOT an ABC. If they give you an MRI first, and it shows fluid fluid levels, ask for a plain film. Actually, you should never read an MRI with a bone lesion without having a plain film, so if shown one, ask for an XR before you say any sort of DDx.

If you cannot easily tell on XR if there is cortical disruption or just severe thinning, get a CT before bone scan, to check integrity of cortex. For example of telangiectatic osteosarcoma, see C141 f8-4 (skeletally immature) and ACR disc 114. I was shown what I thought was a telangiectatic osteosarcoma. There was absolute destruction of the proximal fibula (about 1/3), the cortex was totally gone, but without any matrix. Since it looked very aggressive, I said I thought telangiectatic osteosarcoma and asked for MR. The MR showed multiple fluid levels, and I said I still thought osteosarcoma.


The Unhappy Triad of O’Donoghue

This refers to a combination of ACL tear, MCL tear and posterior horn of medial meniscus tear. These occur together due to a valgus stress injury to the knee, and there is often also an associated bone bruise involving the lateral tibial plateau. See ACR case 397, F1 shows ACL tear, F2 the MCL tear and lateral plateau bone bruise, and F3 shows PHMM tear.



Joint effusion in a child on XR. MR shows marrow edema

The DDx for a joint effusion in a child includes septic joint, toxic synovitis, Legg-Perthes (in the hip), Hemophilic bleed, JRA and trauma. On XR, the most likely finding is widening of the joint space vs the other side, such as a wide teardrop distance in the hip. Other signs of effusion include displacement of fat planes, such as the obturator in the hip. Other signs of septic joint include cartilage loss and indistinct cortex. Regarding indistinct cortex, the rule I use is that a white line of cortex should surround the bones on each side of the joint. If the line is incomplete, that needs to be explained. See ACR cases 585 and 586 and Donn 205 f7-42. Any effusion must be tapped to r/o septic joint, which can rapidly destroy a joint, and because the hip and shoulder joints extend to the metaphysis so septic joint easily leads to osteomyelitis. Toxic synovitis occurs in 5-10 yo. They develop a limp over a few days, and often have a history of recent viral illness. XR usually shows effusion, and regional osteoporosis.

As far as the MRI, there was an article in Radiology in May of 1999 which showed that septic joints often had altered bone marrow signal, either juxtaarticular or throughout the femoral head and neck (osteomyelitis), whereas transient synovitis did not. Therefore, if they show an MRI with signal changes, favor infection, although some of the other things like Legg-Perthes also can do this, so nonspecific.



Unilateral sacral insufficiency fracture on XR then nucs or CT

Sacral stress fractures are often very difficult to detect on XR. They mostly produce subtle increased sclerosis with a vertical orientation, or smudging of trabeculae (ACR case 305 F1 & 2, H103 f5-45). Bone scan is good for bilateral fractures because it shows the classic “Honda sign” (H103, Mettler 318 f11-38, ACR 305 F3). However, for unilateral stress fracture the bone scan is not as specific, as the appearance could also be from tumor or infection etc. CT is better, because it will usually show the cortical step off (H103 f5-45, ACR 305 F4).



Hardware complications

Loosening, Particle Disease and Infection, XR. See ACR disc cases419-423 and 425 for multiple examples.:



Signs of loosening of hardware on XR include; a lucent zone > 2 mm at cement metal or metal bone interfaces (some say > 1 mm), migration of components from their original position, any lucent gap between cement and metal, cement fracture (refers to a break in the cement, with a piece separating, baby R p185 f20-4 open arrow), subsidence of femoral component with abnormal varus or valgus angulation, and periostitis.See C314, CR p195 c143, baby R 185.



Particle Disease

Refers to osteolysis (lytic lesion) which occurs because of a granulomatous reaction by the body to particles of cement, metal, silastic, bone or polyethylene which shear off from the hardware. This may also lead to loosening. Debris can also spread to lymph nodes. If you see a lytic lesion adjacent to hardware, check for clues of polyethylene break down, such as narrowing of space between metal components. Then you can feel more comfortable attributing a lesion to particle disease. See ACR 422 and 421. If aspirated, the fluid in particle disease will be black in color.



Is actually an uncommon complication of prostheses. It can be difficult to distinguish from loosening and particle disease. They often require aspiration for diagnosis when clinically suspected. If infected, prostheses generally need to be removed. XR signs of infection include a rapidly developing wide cement-bone lucent zone in 1st postop year, endosteal scalloping and periosteal reaction. On arthrogram, an irregular contour to the joint capsule and filling of cavities, sinus tracts and abscesses (baby R 186 f20-6).



Aggressive Lesion in the Femur or Humerus in a Child

Aggressive features include a moth eaten or permeative pattern, a wide zone of transition, aggressive periosteal reaction such as onion skinning, sunburst or Codman’s triangle, and soft tissue mass. In a child, the main 4 things in the DDx are:

  • Ewing’s sarcoma
  • Osteosarcoma
  • EG
  • Infection

Secondary differentials:

  • Lymphoma / leukemia
  • Metastases (mostly neuroblastoma and rhabdomyosarcoma)
  • PNET


Ewing’s Sarcoma

  • Occur mostly in first 2 decades of life
  • Present with pain, swelling, fever, high ESR
  • Mostly diaphyseal or metadiaphyseal in long bones, but also in pelvis, scapula & sacrum
  • Patients are under 30, and great majority are <20.
  • They are central within the bone medullary space.

They are mostly permeative, without a matrix, but they can be partly sclerotic or patchy, so don’t let sclerosis dissuade you from calling it Ewing’s. When sclerotic, they resemble osteosarcoma. However, the sclerosis in Ewing’s is confined to the bone (represents reactive new bone), whereas in osteosarcoma, osteoid matrix will be seen within the soft tissue mass. When lytic without matrix, osteosarcoma is still possible too because can be intraosseous and not have matrix. (see illustration of this point ACR case 131 F1 vs F2 & 3, they stress looking for cortical destruction and soft tissue mass in Ewing’s and not central osteosarcoma). Ewing Sarcoma may have onion skin, or sunburst, or amorphous periostitis. Soft tissue mass very common, but not always obvious on XR. See H45, C152, ACR 131 and 132, Duke 420



This is the most common primary bone tumor in a younger person; (myeloma most common in older patients) it usually occurs in the metaphyseal region, but this is variable. They are permeative, wide ZOT, frequent cortical destruction and soft tissue mass (except intraosseous type), aggressive periostitis, possible mets to lung and bone. Most have osteoid matrix (H40 & 41), but some variants do not, especially the telangiectatic type (H42 f3-10). Also see ACR 103,104,105, C139-141, CR p61 c44.


Eosinophilic Granuloma

This can look like anything, and therefore, EG belongs in pretty much every DDx for a bone lesion in a patient <30yo. It can be lytic or blastic, well defined with narrow ZOT or ill defined, wide ZOT. May or may not have periosteal reaction, which is more often thick and uniform, benign looking, but can be aggressive. It can be monostotic or polyostotic, the only thing that could really help you is if you see a Bony Sequestrum then the DDx is:

  • EG
  • Lymphoma
  • Osteomyelitis
  • Fibrosarcoma / desmoid. (H15, C171)



This, too can have almost any appearance, lytic or sclerotic, monostotic or polyostotic, aggressive or nonagressive. It can pretty much be put into the DDx for any bone lesion, no matter the patient’s age. Bony sequestrum is helpful to narrow DDx. Sinus tract or involucrum (C293 f16-3 and f16-2) is helpful to point to osteomyelitis. See H27 to 29, C292, CR p155 c110.



Congenital Absence of Pedicle with contralateral Hypertrophy

Look for unilateral sclerotic pedicle

A congenitally absent pedicle can occur in the C spine or L spine. It sounds like they showed the L spine, which would have an absent pedicle and overgrowth and sclerosis of the contrlateral one. This is usually asymptomatic. There is usually widening of the neural foramen, which can mimic tumor. The transverse process on the side missing the pedicle is always abnormal in position. See Kirks Practical Pediatric Imaging 1st ed. p145. In the C spine, there is usually a double foramen on the affected side and displacement of the lateral articulating mass, with a small transverse process. The cervical spine ones have symptoms of pain, weakness, numbness. Myelogram would show 2 nerve roots coming out at the level of the absent pedicle.

I am unsure of the sclerotic pedicle part, the recall may be incorrect. Assuming it is correct, the DDx for a sclerotic pedicle in a kid might include osteoid osteoma or less likely chronic osteomyelitis (TB). If the sclerosis is not exactly localized to the pedicle, but is in the pars region, then spondylolysis on one side with sclerosis on the other. In adults, consider blastic met or chronic TB.


Hyperparathyroidism in Hands with Vascular Calcification

This was discussed above in #4. However, one thing they have asked is whether vascular Ca+ is a feature of primary or secondary hyperparathyroidism. The answer is that it is usually seen in secondary hyperparathyroidism from renal failure (ACR disc Case 513 Discussion).

Also, remember that the hands frequently show many types of the resorptive change of hyperparathyroidism, including subperiosteal, subchondral, and cortical. When you see a lot of vascular Ca+, the 2 main diagnoses to consider are hyperparathyroidism and diabetes. However, collagen vascular disease such as SLE or Scleroderma also can cause this.


Sarcoidosis on hand film with Acroosteolysis and then CXR with Hilar Lymph Nodes

Sarcoidosis is one of the many causes of Acroosteolysis, the mnemonic for which is terribly long, “PETER’S DIAPER SPLASH” it is a typical stupid Dahnert mnemonic, and it stands for Psoriasis, Porphyria, Ehler’s-Danlos Syndrome, Wegener’s Granulomatosis (Thromboangiitis Obliterans), Ergot therapy, Raynaud’s, Diabetes, Dermatomyositis, Dilantin, Injury (frost or burn), Arterisclerosis obliterans, PVC worker, Epidermolysis bullosa, RA, Reiter’s, Sarcoidosis, Scleroderma, Progeria, Pyknodysostosis, Leprosy, Lesch-Nyhan, Absence of pain, Syrinx, hyperparathyroidism. This is a ridiculously long DDx, and I hope the case also has the much more typical and distinctive finding of sarcoid, which are the lacelike, reticular lytic lesions. Sarcoid can also cause multiple small lytic lesions or a rapidly destructive process, but I doubt they would show these, unless it was in combo with the lacy lesion There can also be soft tissue swelling.

10% of sarcoid patients get bone disease, and those patients usually also have skin disease. See C244 (nice case of reticular and acroosteolysis & swelling), CR p191 c141, H133 f6-33

Remember to ask for CXR once you suspect sarcoid.



Thalassemia in hand XR

The major sites to look at for diagnosing thalassemia are the hands/feet and skull. In the hands and feet, the metacarpals/metatarsals and phalanges are wide and squared, with thin cortices and abnormal density & coarse trabeculae. See C306 f16-26, Donn 211 f7-50 and ACR cases 580 & 581. The findings are due to marrow packing in an attempt to make more RBCs. The only other thing in DDx is mucopolysaccharidoses, but those should have proximal tapering of the metacarpals.

In the skull, thalassemia shows marked widening of the diploic space, with dense striations which are the stretched, normal bony trabeculae, creating the hair on end appearance. Also, the paranasal sinuses are obliterated due to marrow hyperplasia, and the incisors are pushed forward, leading to the rodent facies appearance (CR p195 c144).



Stress Fracture of the Tibia or Femoral Neck

There are 2 kinds of stress fracture, fatigue is abnormal force on a normal bone; insufficiency is normal stress on abnormal bone.


Stress Fractures

In the femur stress fractures usually involve the femoral neck. Patient complains of hip pain radiating to the knee. If not diagnosed, (often difficult due to osteopenia) and there is continued weight bearing, it may progress to a complete fracture. It is often occult on XR, or just a subtle sclerotic line. Any sclerosis in a weight bearing bone that has a horizontal or oblique configuration is suspect for stress fracture. MRI should be obtained, and T1 may show the fracture line, and STIR or Fat Sat T2 will show the marrow edema. There are 2 types of femoral stress fractures, compressive and tensile.

Compressive stress fractures occur medially, at the base of the neck. This is common in athletes, and is the more common type. There may be focal periosteal thickening. Compressive fractures are treated with non weight bearing. Tensile is less common, and occurs in old people. If a fracture line is visible, it may need internal fixation. See CR p117 c80, H107 f5-55, and 5-56.

In the tibia, stress fractures can be proximal middle or distal. This also is subtle linear horizontal or oblique sclerosis on XR. It may go on to completion with continued weight bearing. See H108 f5-57, and 109, ACR case 425. I was shown a XR without anything obvious, and I missed it. He showed me an MR, and I saw a lot of tibial marrow edema and a linear low signal line, and said stress fracture, and I asked to go back to the XR, and then I found it on the lateral XR.



Osteomyelitis of Calcaneus in diabetic with region of lytic change below an ulcer

The common features in diabetic foot osteomyelitis are Lytic (if acute; sclerotic if chronic) lesion with adjacent soft tissue swelling and possibly ulceration, and associated finding of vascular Ca+ due to the diabetes. Also, the bones are generally osteopenic because of diabetes. Could not find example in calcaneus, for DM foot infection see baby R 658 f59-16.



Type 3 Odontoid Fracture

There are 3 types of dens fracture.

  • Type 1 – Avulsion of the tip (least common)
  • Type 2 – Fracture through base of dens (most common, high rate of nonunion)
  • Type 3 is subdental fracture, through body of C2. Some authors state that this is an unstable fracture, but that it heals well, because it involves cancellous bone, so nonunion is not common. However, others state that it is stable because they only require a halo, whereas a type 2 requires C1/C2 fusion. Therefore, this is not a fair question. I intend to say that the patient needs to be placed in a halo, but does not need fusion, which is all that matters. The “stale/unstable” thing is stupid semantics. See Chew 67 f4-8, CR p145 c103.



Gamekeeper’s Thumb

This refers to a tear of the ulnar collateral ligament of the 1st MCP joint. It is now usually related to skiing injuries (Skiier’s Thumb), with violent abduction of the thumb. It is important to determine if the torn ligament lies deep or superficial to the adductor policis aponeurosis, because those deep to the aponeurosis will heal with immobilization, but when the tendon is ripped, and moves superficial to the aponeurosis, the aponeurosis will prevent apposition of the ligament to the bone, and thereby interfere with healing, and then surgery is the treatment to prevent persistent instability (this is called a Stener’s lesion).

If there is an avulsive injury, then you can see on a regular hand film as a fracture at the ulnar side of the inferior aspect of the 1st proximal phalanx, and you can sometimes tell whether there is a Stener’s lesion. (H89 f5-19 and CR p99 c68). If there is no avulsed fragment, they used to do stress views to show the injury, because the joint would widen with stress (C44 f3-4, ACR case 312) However, we no longer do this because stressing it may cause a Stener’s lesion, and then require surgery, so we do MRI instead.



Segond Fracture on MRI with ACL Tear

A Segond fracture is an avulsion fracture by the lateral joint capsule due to internal rotation of the tibia with the knee in flexion. The avulsion usually occurs about 4mm distal to the femoro-tibial joint line. The importance of the Segond fracture is that it is almost always associated with an ACL tear (100%), and MCL 80%, meniscus 50%, articular cartilage injury 25%. For XR examples see ACR cases 376 & 377 and CR p111 c77. For MRI example, see Internal derangement of joints 656 f16-150 & 657 f16-152.



Double PCL Sign on MRI

This refers to a bucket handle type of meniscal tear (this particular sign only occurs with medial meniscal tear).

Signs of a bucket handle tear on MR include:

  • 1. The double PCL sign-on the sagittal view you see what looks like 2 PCLs. One is the real PCL, but in front of it is a piece of menicus that has torn and flipped into the intercondylar notch
  • 2. You only have one bowtie on sagittals instead of the normal two.
  • 3. The anterior and posterior horns of the medial meniscus may look equal in size, whereas normally the posterior horn is larger.
  • 4. You may see the displaced fragment lying toward the notch on the coronal or sagittal view.
  • 5. The free edge of the anterior or posterior horn appears truncated on the sagittal or coronal view.

These are illustrated in H176 and 177 f9-7 & 9-8, and ACR case 399 F3, CR p99 c69, Beltran 182 f14-5.



Maisonneuve Fracture

Refers to an ankle fracture in which the fibular fracture is quite proximal, near the knee, well above the tib/fib syndesmosis. There is always extensive rupture of the tib-fib syndesmosis in this injury. The key point is that if you have an ankle film demonstrating a medial fracture or widening of the medial joint space or bad soft tissue swelling, or a posterior malleolus fracture, there should always be either a fibular fracture or a disruption of the ankle mortise or both.

This is because the force must somehow dissipate laterally. Therefore, if an ankle film only shows a medial or posterior injury without a mortise or fibular one, you need to ask for a film of the entire fibula and stress views of the ankle to evaluate for Maisonneuve and mortise disruption. See ACR case 405. The Maisonneuve is one type of pronation external rotation injury in the Lauge Hanson classification. It would be a Weber C2 in that classification.



Septic SI Joint

Show unilateral sacroiliitis, then CT with psoas abscess The DDx for a truly unilateral sacroiliitis (other side completely normal)

  • Infection (septic joint)
  • DJD
  • Trauma
  • Possibly RA (some put it in the bilateral category and some in unilateral).

If there is bilateral but asymmetric involvement, then Reiter’s, psoriatic and DJD.

The most important thing on the exam is that for unilateral process you say septic joint first, and say that it needs to be aspirated and sent to the lab, especially if the patient is an IVDA. For examples of sacroiliitis, see H124 and 125, CR p23 c16, C222 f12-18. For nice example of septic arthritis with abscess see baby R p80 f10-17.


Leptomeningeal cyst on skull XR in Child

A leptomeningeal cyst is also called a growing fracture. It occurs in kids <3 yo, when there is a depressed skull fracture with a dural tear. The pia-arachnoid membrane herniates through the dural tear and prevents apposition and healing of the dura. CSF pulsations then fill and enlarge the subarachnoid pouch that extends through the fracture line, eventually expanding the margins of the fracture. It usually is elliptical in shape and has beveled edges because the pulsations erode the inner table more than the outer table. There is often associated post-traumatic encephalomalacia and porencephaly from brain injury due to the original trauma. DDx includes dermoid and Calvarial Epidermoid Cyst, congenital meningoencephalocele, and postsurgical defect. See great case ACR Neuro Disc #812.

If you ask to see prior films (showing a skull fracture), you can seal the diagnosis.



RA of the Shoulder

Findings of RA on a shoulder XR include:

  • High riding humeral head/decreased space between humeral head and acromion (due to rotator cuff tear or atrophy)
  • Osteopenia
  • Resorption of the distal clavicle
  • Mechanical erosion at the medial aspect of the surgical neck (almost pathognomonic)
  • Sometimes erosion at lateral aspect of anatomic neck, & narrowing of the glenohumeral joint space.

A very nice example of all of these findings is in ACR MSK case 204, C216 f12-4, CR p67.



RA of the Knees on XR

XR findings in RA include:

  • Osteopenia
  • Tricompartmental joint space narrowing
  • Lack of productive changes (note, in late stage, there may be some productive changes e.g. sclerosis and spurs due to secondary DJD, but the joint space narrowing will be out of proportion to those findings, so you know it isn’t just DJD. In the case they have been showing on boards, there are no productive changes)
  • Marginal erosions at the joint and also at the superior patella
  • Mechanical erosion of the distal anterior femur (almost pathognomonic), where the patella impacts it.
  • Also, subluxations and valgus deformities of the tibia due to ligamentous laxity or rupture
  • Joint effusion
  • May get synovial cysts.

Nice case ACR MSK case 202, esp note F3A with arrow to mechanical patellar erosion. Also see C216 f12-5 and H122 f6-11.



Synovial Osteochondromatosis on MRI and then XR. Sometimes in shoulder

Synovial chondromatosis refers to synovial metaplasia with formation of cartilaginous nodules that project into the joint. They can detach and then be loose bodies. They can ossify, and are then called osteochondromatosis.

  • It is usually monoarticular.
  • Most common joints affected are knee, hip, elbow and shoulder.
  • XR reveals numerous small calcified or ossified nodules in the joint space.
  • MR shows additional ones not evident on XR.
  • The cortices of bones may develop pressure erosions, and there is often secondary DJD.

Main DDx is PVNS. The way to tell from PVNS on MR is that PVNS usually has an effusion and SOC does not (PVNS is a chronic synovitis, with inflammation), and the nodules in PVNS are dark on all sequences but have some areas of high signal related to hemorrhage or necrosis, while SOC generally follows marrow signal. If any doubt ask for plain film, because if ossified you know it’s SOC, (but if not ossified then could be either, as logically there is a point at which the metaplastic chondroid nodules in osteochondromatosis are unossified. Pretty damn rare, especially if there is lots of disease, and not one has yet calcified.) Compare ACR case 245 to 246. Also see CR p65.



Multiple Lytic Lesions in Pelvis in Adult

The most likely causes in an adult would be mets and myeloma. The most reasonable thing to do next is SPEP and UPEP to check for myeloma, and a search for a primary tumor, which in adults is most likely to be breast, lung, kidney or thyroid.

The DDx in general for polyostotic lesions is “FEEMHIV” which stands for FBD, EG, Enchondromas, Mets/myeloma, hyperparathyroidism (brown tumors), Infection and vascular tumors (e.g. angiosarcoma). See baby R 597.



Unilateral Facet Dislocation on Lateral C-spine

Unilateral facet dislocation is a Cervical Spine Injury that occurs with a combination force of hyperflexion, lateral bending and rotation. The facet joint on the concave side of the bend is fixed in place while the contralateral articular mass rides forward and up and dislocates into the intervertebral foramen. On XR, you see forward subluxation (anterolisthesis Grade 1 or 2; less than 50%) and rotary misalignment, such that the facets no longer overlap each other at that level. Normally all the superior facets should entirely contact the corresponding inferior facets, but they do not at the involved level. Another clue is that the lower vertebral body at that level looks a bit smaller than the higher one due to rotation. There is often prevertebral soft tissue swelling. Lastly, the disc space and interspinous distance are often widened at the involved level because of hyperflexion. See C71 f4-15, H85 f5-10 & 5-11, ACR cases 427 and 429. I was shown this case in neuro section.


Posterior Vertebral Body Scalloping

This is associated with dural ectasia. Dahnert breaks down the causes into 3 groups. Dahnert gives the mnemonic “DAMN MALE SHAME”.

  • Group 1 is due to increased intraspinal pressure, related to hydrocephalus or Ependymoma.
  • Group 2 is due to mesenchymal tissue laxity, and includes NF, Marfan Syndrome, Ehlers-Danlos, or posterior meningocele
  • Group 3 is related to bone softening from MPS, Acromegaly, AS or Achondroplasia.

With that being said, I think they are most likely to show NF, so I will discuss this a bit. The findings in NF include: posterior vertebral body scalloping from dural ectasia, widened neural foramina, ribbon ribs from dysplasia or compression by intercostal neurofibromas, an acute high thoracic spine scoliosis, dysplastic changes / bowing deformities of bones such as tibia, fibula and clavicles, pseudoarthroses, and multiple NOFs. See ACR case 541, 542 and 543 which show almost all these findings, CR p135, C258, Donn 213.



Brodie’s Abscess in a kid’s femur, humerus or tibia

Brodie’s abscess is a chronic infection that appears as a well defined geographic lytic focus surrounded by diffuse sclerosis. The sclerosis is unique in that it is sharply marginated where it is contiguous with the lesion, but the margins fade out peripherally.

2/3 are metaphyseal and 1/3 are diaphyseal. The abscess is a cavity in the bone lined by inflammatory granulation tissue, filled with purulent fluid. Two distinct features of an abscess are a sequestrum (CR p29 c21) of devitalized bone in the center of it and the involucrum, which is a periosteal shell around the infection (C293 for involucrum). Other features may include a sinus tract to the skin or to the growth plate. Most Brodie’s are in kids, and most are from staph aureus.

The DDx would include Fibrous Dysplasia, EG and perhaps other benign bone tumors.

On MRI, the “double line effect” is seen on T2, the lesion itself is bright, and there is a high signal line of granulation tissue surrounded by a low signal line of sclerosis. On T1 the lesion is low to intermediate, and is surrounded by a low signal line, and there is ring enhancement post Gad. For other examples, see C295, H27 f2-34, ACR case 592. I was shown an osteomyelitis in kid’s tibia. There was permeative lytic lesion with involucrum around it. I said osteomyelitis with DDx of EG, Ewing’s etc


Sickle Cell Bone Findings

There are many findings in Sickle Cell Disease. The most likely they would show is a spine film or CXR PA/lat, which could show the “H” shaped vertebrae with concavity of end plates from infarcts (DDx for this finding is Gaucher’s, see CR p93, H155, Donn 211 f7-50B), infarcts in the humeral head appearing as sclerosis (“snow capping”) or collapse (CR p93, H163 f8-3), and overall either decreased bone density or sclerosis (can cause either). Other findings on a CXR would be cardiomegaly and RUQ surgical clips from cholecystectomy. Classically the spleen is small or absent (autosplenectomy). Other bone findings in sickle include hip AVN (Many of these findings are demonstrated in ACR cases 578 & 579) and dactylitis, (sausage digit) which occurs in 20% of kids with SCD at some point, and presents with painful swelling of a digit with periostitis and abnormal bone density (ACR case 577). Also, sickle cell can be a cause of a widened diploic space in the skull (the hair on end skull) due to extramedullary hematopoiesis.



Jumper’s Knee

Jumper’s knee is a patellar tendinosis that occurs at the enthesis of the patellar tendon in athletes who participate in activities that require repetitive, violent contraction of the quadriceps tendon, such as basketball and volleyball. They present with anterior knee pain. On MRI, there is focal thickening of the proximal third of the patellar tendon. The posterior tendon margin is indistinct, and there may be edema in Hoffa’s fat pad. It does not affect the anterior fibers, which helps distinguish it form a tear. There are ill defined areas of intermediate signal on PD and T2 images, with occasional high signal from cysts. Treatment is surgical. See CR p35.



Supraspinatous Tear on MRI, usually complete

The normal supraspinatous tendon has uniform low signal, although it is OK to have slips of muscle within the tendon. Abnormal signal is defined as higher than muscle, and should be on a T2 weighted sequence, because on T1 may get magic angle effect (55 degrees to B0). The tendon is normally about 3.5 mm thick. 90% of tears are related to impingement by the coracoacromial arch. Tendinitis is represented by poorly defined increased signal oriented along the long axis of a thickened tendon.


Calcific Tendinitis

Is seen as signal voids, with blooming on GRE.


Full Thickness Tear

Is focal high signal traversing the entire tendon substance. These are usually vertically oriented and occur at the critical zone (2cm proximal to the tendon insertion on the humerus. Thi is a relatively avascular plane), or the anterior leading edge. Associated signs may include SST retraction and supraspinatus muscle atrophy, superior subluxation of the humeral head, and fluid in the subacromial / subdeltoid bursa.


Partial Thickness Tears

Are focal fluid signal that do not completely traverse the tendon. They are much more common on the articular surface than the bursal surface. See ACR cases 361 through 365, many nice examples, H196 and 195, B207-210.



Osteopoikilosis of Hips

This is a bone dysplasia with multiple round or oval foci of compact bone within the spongiosa. Osteopoikilosis is asymptomatic, so is an incidental finding. XR shows small, numerous well defined sclerotic foci, from a few mm to several cm in size. They tend to cluster periarticularly, & prefer the epiphysis and metaphysis. May also involve pelvis, carpus, tarsus and scapula. No uptake on bone scan. (The only other thing to consider is diffuse blastic metastasis, but periarticular distribuion is characteristic.) See CR p49, H170 f8-16, C255 f14-4.


MRI with ACL Tear and Bucket Handle Tear

We already discussed bucket handle, so we will discuss ACL tear. The normal ACL arises from the posterolateral aspect of the intercondylar notch of the femur and inserts on the anteromedial anterior tibial spine. It has low signal, but has higher signal striations. 80% of ACL tears involve the femoral origin (except in adolescents).

There are many signs of a complete ACL tear on MRI (they must have shown an MR if the case demonstrated a bucket handle, can’t see that on plain film), some direct and some indirect/associated findings.

  • The direct findings of an acute tear include:
  • Discontinuity in the low signal tendon, with loss of its normally taut parallel margins
  • Mass like configuration to the tendon
  • High signal on T2 in place of the tendon.
  • In chronic tear, there is resorption of the proximal ACL, a horizontal orientation of ACL fibers or fibrosis of ACL to PCL.
  • The indirect signs are evidence of ligamentous laxity, and include:
  • Buckled PCL on sagittal images
  • Visualization of the entire PCL or fibular collateral on a single coronal image
  • A line drawn across the posterior PCL margin not intersecting the femoral medullary cavity
  • The posterior femoral line displaced posteriorly from the tibial surface (see magic notes)
  • Bone bruises in 90% at the anterior aspect of the femoral notch and posterior aspect of the lateral tibial plateau
  • Meniscal tear in 70%, MCL injury in 15%, and shearing injury to hoffa’s fat pad.

For examples of torn ACL, see B183-186, H183, ACR case 399 shows ACL and bucket hande, also 398 & 400, CR p87 c60.


Discoid Lateral Meniscus with tear

A discoid meniscus is a variant with thickening of the free end of the meniscus (the inner arc of the horseshoe). By far a lateral one is more common than a medial one. There are actually six subtypes, but it isn’t very important to know all that. The discoid meniscus is prone to tear. On MRI, you see the bowtie of the lateral meniscus on 3 or more sagittal images. On the coronal view, meniscal tissue extends into the tibial spines at the intercondylar notch, and therefore, the lateral meniscus is not triangular in shape like it usually is (but be careful not to call this on the more posterior cuts, that is a pseudodiscoid meniscus). See H179, CR p21 c15 (with degeneration), ACR case 388.



Meniscal Tear with Meniscal Cyst

A meniscal cyst is caused by decompression of synovial fluid through a meniscal tear. The typical presentation is joint line pain and a mass. On MRI, they are usually located at the joint line, in which case there isn’t much of a DDx. However, they occasionally migrate away from the joint line, and then DDx includes ganglion cyst and synovial cyst, too.

In about 20% of cases the meniscal tear is not identifiable, but in the case on the boards it is. The medial meniscus is involved more often. Pes Anserine Bursitis looks similar, but is located far anteriorly, where the 3 tendons of the pes anserinus insert. See CR p47 c36, ACR case 389, H190 f9-34.


PVNS of hip, XR and MRI

Pigmented Villonodular Synovitis is a proliferative disorder affecting the synovium of joints, bursae and tendons. It mostly affects young adults, presenting with chronic pain, decreased ROM and joint locking. The hallmark is numerous bone erosions, variable in size, with sclerotic rims, localized to a juxta-articular distribution (usually mono-articular, may affect both sides of the joint). There is often a dense (hemorrhagic) effusion. On MR, there are usually areas of very low signal from hemosiderin, as well as brighter areas of more recent hemorrhage or necrosis. See ACR cases 243, 244, & 245, H139 f 6-47, CR p189 c138, C243 f13-21.


Burst Fracture on XR and CT

This fracture is the result of axial loading, usually in a fall from a height, which produces end plate failure and vertebral body collapse. It is an unstable injury because it involves the middle column too, and usually has retropulsed bone, and requires internal fixation. The posterior column may or may not be involved. If it is, then there will be widening of the interpediculate distance on an AP view. One of the most helpful signs of burst on XR is widening of the vertebral body in AP & transverse dimensions.

You should get a CT to evaluate for retropulsed bone fragment compressing on the thecal sac and herniated disc fragments. In a burst, the lack of currently retropulsed fragments doesn’t assure you that fragments weren’t squashing the cord at the moment of trauma, and they just were pulled back mostly into position by the ligaments, so be careful underestimating degree of disease. MR may be needed to evaluate the cord itself. Half of burst fractures have an associated neurologic deficit. See C74 f4-19, CR p91.


Flexion Teardrop Fracture

A flexion teardrop injury is a type of burst fracture in which there is also hyperflexion in addition to axial loading, and the anteroinferior corner of the vertebral body is sheared off. This has a very high rate of neuro injury. See ACR case 444 (teardrop) and 447 shows wide interpedicular distance.


Subcapital Hip Fracture

There are 3 types of hip fracture, intracapsular (37%), intertrochanteric (49%) and subtrochanteric (14%).

  • Intracapsular category is broken down into
  • Capital
  • Subcapital – Highest risk of AVN and nonunion, and the more proximal the fracture the higher the risk
  • Transcervical
  • Basicervical – Most likely of the intracapsular fractures to be a pathologic fracture.

Intracapsular fractures are classified with the Garden’s classification.


Garden’s Classification of Femoral Fractures

Garden 1

Incomplete or Impacted

Garden 2

Complete but Nondisplaced

Garden 3

Complete with Varus Angulation

Garden 4


The higher Garden grades have higher risk of AVN and nonunion. These sometimes require prosthesis rather than pinning. For images of subcapital fracture, see C85 f5-8 (Garden 3), H111 f5-63 (Garden 3), CR p217 (Garden 3) and p117 (Garden 1), ACR case 371.


Trans-Scaphoid Perilunate Dislocation

When assessing the wrist, it is important to evaluate the arcs of Gilula. These are 3 parallel arcs drawn along the proximal articulating margin of the proximal carpal row, the distal margin of the proximal row, and the proximal margin of the distal row (see diagram ACR case 323 F3). Interruption of any arc suggests a dislocation. It is also imperative to check (on the lateral view) the relationship of the lunate to the radius and lunate to capitate, and capitate to radius. Normally, all 3 line up such that a straight line can be drawn connecting them. Lastly, on the frontal view, check the shape of the lunate. It is normally half moon shaped (that’s why it is called lunate).

There are 3 types of carpal dislocation. From least severe to most severe, these are perilunate, midcarpal, and lunate.


Perilunate Dislocation

The perilunate is the most common. It is characterized by a normal position of the lunate in relation to the radius, but dorsal dislocation of the capitate vs the lunate. More often than not, there is an associated fracture, with the fracture most commonly being on the radial side, with more involvement of the ulnar side with progressively worse injury. So, the most likely areas, in order of decreasing frequency, are: radial styloid, scaphoid waist, proximal capitate, base of hamate, ulnar surface of triquetrum and ulnar styloid. The fracture-dislocation is named by listing fracture first, starting at radial side and then once all the fractures are described, state the type of dislocation. So a scaphoid fracture plus perilunate is a transcaphoid perilunate dislocation.


Midcarpal Dislocation

The next more severe injury is a midcarpal dislocation. In this, the radius does not align with the lunate or capitate, because the lunate is tilted/subluxed anterior and the capitate subluxed posterior.


Lunate Dislocation

Most severe is the lunate dislocation injury, in which the capitate does align with radius, but the lunate is completely displaced anteriorly/volar. See C48 for exactly transscaphoid perilunate, and ACR cases 323 – 326, with 325 being transradial transcaphoid perilunate, almost like the boards case. Also see H90. If you see a perilunate, keep looking for fractures! Some were shown a lunate.



Charcot Knee and Spine

Knee: This is usually due to Tabes dorsalis from Syphilis.

Remember the 5 “D’s” 1.Density is increased or nl, 2.Distension – effusion 3.Debris – bone fragments 4.Disorganization 5.Dislocation

Specifically, in a knee, expect lateral translation of tibia vs femur, loss of cartilage/joint space, fragmentation, effusion which may contain debris. A caveat is that 40% of Charcot is the primary atrophic type in which you don’t have the 4 D’s, just resorption of bone so you are missing bone. Charcot is due to combination of loss of pain perception and altered sympathetic control of blood flow. See ACR case 234 (case 235 mixed), H136 f6-37.

Spine – Charcot spine is the result of tabes dorsalis or syrinx. Findings include increased density, deformity, fragmentation, and dislocation. Destruction usually involves the intervertebral disc as well as the vertebral body. See H136 f6-38, and UCSF MSK case 43 fig 15.


Achilles Tendon Tear, partial or complete

The Achilles tendon originates from gastroc and soleus and inserts on calcaneus. Rupture is usually related to strenuous tensile force, either strong plantar flexion or forced dorsiflexion. It can occur in athletes or can occur spontaneously in patients with underlying disease such as RA, gout, renal failure, DM, SLE, hyperparathyroidism.

On MRI, a complete tear shows high signal interposed between the frayed ends of a discontinuous tendon. There is often associated retraction and buckling of the proximal tendon fibers. Tears tend to occur 2 to 6 cm above the calcaneal insertion, a vascular watershed area of the tendon. In partial tears, some fibers are intact, and edema and hemorrhage are confined to portions of the tendon, which may be fusiform/thickened. The need for surgery is determined by whether >50% of fibers are ruptured, and patient age and activity level. For complete tear see CRp157 c112, B198 f15-14 and for partial tear, H216 f12-1.




Melorheostosis is an idiopathic disorder characterized by thickened cortical new bone that accumulates near the ends of long bones on one side of the bone only, looking similar to dripping candle wax It progresses from an end of the bone to the center. It is usually limited to a single lower limb, and can cause pain, decreased ROM, intermittent swelling, contractures and deformity. H164 and C255 f14-6, CR p69 c51.



Necrotizing Fasciitis in the Thigh

Necrotizing Fasciitis is a rare soft tissue infection accompanied by widespread fascial necrosis, usually in the absence of muscular and cutaneous infection. It is a serious disease associated with systemic infection and death. Predisposing factors are trauma, cutaneous lesions, IVDA, thermal injuries and surgical wounds. It occurs mostly in the extremities, but also can involve neck, face, perineum, genitals, trunk. Most are from strep or staph. XR may show soft tissue gas, which on CT localizes to the fascia. MRI shows T2 hyperintensity in the deep fascia, with or without changes in the adjacent muscle. However, this is a nonspecific finding, and really it is a clinical diagnosis. MRI can be useful for preoperative planning so surgeons know where and how much to debride. See www.uhrad.com/msiarc/msi021.htm


Ollier’s Disease with Degeneration to Chondrosarcoma

Showed multiple lytic lesions in metaphyses of lower extremities in a child. It looked like Ollier’s (no hemangiomas so not Maffucci’s Syndrome) and I did say polyostotic Fibrous Dysplasia would be much less likely. One of the lesions had an irregular cortex, and I brought up degeneration and he asked me how to follow these patients. I said if there was pain to get an XR, but otherwise I wasn’t sure, maybe once a year? Look it up



Showed a large tophus in olecranon bursa. Said gout vs RA. Showed me a foot with tophi and erosions with overhanging edges.



Hypertrophic Pulmonary Osteoarthropathy

Hand with subtle periostits along several metacarpals and phalanges. I said HPO first, but that I would get lower extremity XR because tibias are more commonly involved. DDX including Thyroid Acropachy, which is usually only in hands. Gave HTTPV Ddx.

== Right Humerus Bone Infarct Hard case. XR showed subtle linear sclerosis in proximal R humerus, no periostitis, no soft tissue mass, no cortical destruction. STIR MR showed large lesion, very bright, no cortical destruction or soft tissue mass. I said infarct but wondered about cartilaginous lesion, which can also be bright on STIR. However I asked to see XR again, and there was no cartilage matrix. I said infarct, don’t know if I was right.


DISH with Fracture / Pseudoarthrosis

Anterior C spine. Lateral C spine XR showed thick anterior spurs vs syndesmophytes with fracture or pseudoarthrosis anterior at about C3/4. I originally said AS, but was bothered that the phytes were so thick. He showed me L spine, and there were definite horizontal spurs in addition to the anterior stuff, so I said I favored DISH instead of AS. Both predispose to fracture and pseudoarthosis.



Gaucher’s Disease vs Anemia

showed lateral CXR with “H” shaped vertebral body. I asked if sickle cell history and he said no. I said could be Gaucher’s. He showed me a frontal CXR and there was splenomegaly. I said could still be Gaucher’s, and asked if patient is Ashkenazi Jew, he said he didn’t know. What I probably should of said was other anemias, which also can cause H shaped vertebrae and splenomegaly.




Expansile rib/digit lesion (B9) — enchondroma, fiborous dysplasia


Flat Vertebra in young pt — EG, TB, Leukemia


Expansile/destrucitve bone lesion — Giant cell, TB, ABC


Long Bone findings in Leukemia — subepiphyseal dark line, periosteal Rx, osteopenia


Osteofiborous dysplasia — starts in cortex, present at birth (unlike reg fib dysp)


Osteochondroma = exostosis



Origin    Insertion               Nerve


Iliopsoas               Vertebra                Lesser trochanter                Femoral, lumbar

Rectus femoris    Anterior inferior iliac spine              Patellar tendon    Femoral

Sartorius               Anterior superior iliac spine            Medial tibial head               Femoral

Pectineus              Iliopectineal line Lesser trochanter                Femoral, obturator



Adductors             Ischial tuberosity                Femur (adductor tubercle)               Tibial


Semitendinosus               Ischial tuberosity                Medial tibial condyle         Tibial

Semimembranosus         Ischial tuberosity                Posterior tibial condyle     Tibial

Long head biceps            Ischial tuberosity                Fibular head         Tibial

Gluteus  Ilium, sacrum, ligaments  Femur (gluteal tuberosity)               Gluteal



•              Most prostheses, even from different manufacturers, appear the same radiographically

•              When a complication is suspected and the plain films are unrevealing, a bone scan should be obtained

•              Bone scans are usually positive for 6 months after surgery; after 6 months, a negative scan is good evidence against loosening, infection, or fracture

•              Arthrography may be necessary to aspirate joint fluid for culture and to demonstrate the presence of sinus tracts


Bone densitometry

Predicts the risk for developing fractures. Three methods are available:

•              Single photon absorption

Measures cortical bone density of radial shaft

2-3 mrem exposure

Precision 1%-3%

•              Dual photon absorption with radionuclide or dual-energy x-ray

Measures vertebral and hip done density

5-10 mrem exposure

Precision 2%-4%

•              Quantitative CT with phantom

Measures vetebral body density

300-500 mrem exposure

Precision 5%-25%


Pagets Disease Pearls

•              Bone scans are useful in determining the extent of the disease

•              Lesions in the lytic phase are very vascular: dense enhancement by CT

•              The most serious complication of Paget’s is sarcomatous degeneration; differentiate this from metastases to pagetoid bone

•              Treatment

Calcitonin (inhibits bone resorption)

Diphosphonate (inhibits demineralization)

Mithramycin (cytotoxin)


Distal Radius Fractures: Colles, Bartons (intraarticular Colles), Smiths (volar Colles)



Results from disruption of ulnar collateral ligament; often associated with a fracture of the base of the proximal phalanx.


Bennet’s fracture=First metacarpal fracture

Rolando’s fracture=Comminuted Bennet’s fracture




Rectus femoris









Long head biceps



Ewings will almost always have a soft tissue mass


Tumors by age







Sharply cut off bone with irrgeular perioesteal Rx–think repeated trauma


lucencies around joints in children/atheletes–think hemmoragic cysts


Anterior Atlantodental Ligament AADI = 4-6mm child/ 4mm adult


S.T. thickness in front of the third cervical vert. should not be >5mm

Bone Syllabus (Spirnak


BONE ACR Syllabus 1989




Contrast Congenital enlargement of pedicle has contralateral hypertrophy of pedicle and lamina


Contralateral hypertrophy rules against an osteoblastoma and ABC


two common appearances are those of an osteoid osteoma  and a lytic lesion as in pedicle


similar histology to osteoid osteoma, osteoid osteoma << 1 cm


>90% of patients << 30 yrs





almost exclusively << 30


indistinguishable from osteoblastoma or giant cell tumor if in the posterior elements


Nonexpansile radiographic appearance does NOT exclude diagnosis


NEVER undergoes malignant degeneration



Os Odontoidium


+ associated with atlantoaxial instability


transverse ligament is intact thus os moves with anterior arch of C1


onset of clinical symptoms often preceded by trauma


Hyperplasia of anterior arch of C1 seen in 60%


IMPRESSION:  “Not a fracture however instability is present with an Os odontodium



Rheumatoid arthritis of C spine


atlantoaxial subluxation is m/c finding in c spine of rheumatoids (25%)


atlantoaxial impaction (cranial settling) occurs secondary to destruction of bone and cartilage at occipitoatlantal and atlantoaxial articulation


bony ankylosis is NOT a feature of Rheumatoid (in hand only the proximal carpal row ankyloses)


Contrast this with JRA (Juvenile chronic arthritis with RF and childhood onset)

<>does produce ankylosis


Recall base of skull (clivus) comprised of occipital and sphenoid bones !





Widening of physis is present in all forms of rickets


Vit D resistant rickets has less metaphyseal cupping and flaring and fragmentation than vit D sensitive


Ifosfamide prevents 25 Vit D from being produced in liver


Dilantin and Phenobarbitol decrease production of Vit D Dependent Ca++ binding protein thus lack of intestinal Vit D is seen (similar essentially to lack of bile salts, pancreatic insufficiency and malabsorption)




Blounts disease


Tibia Vara which is a complication to physiologic bowing. Metaphyses under the medial tibial condyle will subside due to increased medial compressive force.


NOT associated with<:f200,BArial,,,> growing pains as it is a slow process


Once medial tibial plateau becomes deformed, stress is self-perpetuating and process will not correct unless bracing or surgery is performed


Dx: characteristic deficiency of medial tibial epiphysis associated with a localized depression of the growth plate and cupping of the medial proximal tibial metaphysis.  Hypertrophic bone is frequently seen.


Ligamentous laxitiy occurs with subluxation of the medial tibial plateau into the interconylar notch later.



Bone Syllabus (Spirnak)



Genu valgum


Valgus trend occurs in kids starting at 18 months straightening the physiologic bowing.


Some patients continue the valgus trend past the

point of straightening representing the genu valgus form which is not related to trauma


>6 degrees of valgus angulation is normal


Should not be treated early in childhood as it often reverses through adolescence



Congenital scoliosis

curvature induced by a congenital anomaly m/cly hemivertebrae or fusion


If no involvement of the growth potential is present, then rapid progression will not occur


Associated with dysraphism: abnormality of midline closure (myelomeningocele in open lesions ranging to closed lesions such as tethered spinal cord, inraspinal lipoma.)


Associated with GU anomalies as 2/3 of patients with vertebral anomaly have a GU anomaly with 1/3 of these having unilateral renal agenesis (epidydimal cysts)


Screening US exam is recommended if child has vertebral anomaly


Surgical intervention discouraged <-#>as this would incur fusion.


Not all congenital scoliotic curvatures progress rapidly and surgical correction should be delayed as long as possible if to be performed at all.



Neuromuscular scoliosis

some degree of scoliosis is NOT the General rule for CP as prevalence overall is 20%.  Severe CP does have scoliosis


Long C-shaped curve with associated pelvic obliquit<-#>y strongly suggests diagnosis of neuromuscular scoliosis


Remember that lumbar contracture induces the pelvic obliquity.


Curvature will  NOT change direction but may worsen during lifetime




Idiopathic scoliosis


>80% of all spinal curvatures (MOST COMMON)


NOT associated with back pain as most of these are diagnosed on routine school exams


Hump seen in severe scoliosis is not due to thoracic kyphosis but rather produced by asymmetry of the ribs and scapulae following rotation


Standard scoliosis view is PA standing without shoes to limit exposure to developing breasts


Back pain should not be taken lightly and idiopathic scoliosis should be reserved as Dx of exclusion


“Osteoid Osteoma presents as a lucency with central nidus (<< 1 cm) centered at concavity (inside) of the apex of the curve



Radiation scoliosis


even will occur with modern techniques


changes are due to growth abnormality and not actual bone destruction


If any of the spine is to be included in Rx, the entire vertebral body should be included<


soft tissues are also affected and will further provide musculoligamentous fibrosis adding to scoliosis



Congenital Kyphosis


most commonly caused by hypoplasia or aplasia of the anterior portion of vertebral body


can also be due to a congenital anterior bar joining and restricting the anterior vertebral bodies


congenital scoliosis also frequently present due to posterior hemivertebrae


can also be found in myelomeningocele patients


likelihood of concomitant GU anomalies present in all spinal anomalies but

highest when cervical region involved<-!>


more common than congenital lordosis which is caused by laminar bars restricting posterior growth



Diskitis (disk inflammation of childhood)


blood cultures usually sterile, possibly due to virus though Staph aureus has been cultured from biopsy specimens


usually << 10 yrs of age


radiographs initally normal until disk space loss presents


If normal plain films, then next step is for bone scan which is + within 2 weeks of sxs


prognosis is quite good with only supportive treatment


This disk inflammation of childhood is to be distinguished from infectious spondylitis of adults where treatment must be very aggressive with IV Abx


Diskitis may be present with a subsequent secondary osteomyelitis leading to more involvement of vertebral bodies




Scheurmann</R>s lesion


Two criteria must be present: intraosseous disk herniation (Schmorl</R>s node) PLUS kyphosis (greater than normal limit of 40 degrees) OR anterior vertebral body wedging (<;>5 degrees)


Schmorl (Not Schmidt) node PLUS kyphosis or anterior wedging!


severe scoliosis NOT seen even when kyphosis is markedly severe


mild back pain is a common presentation, often teenagers


vertebral anterior wedging is due to developmental phenomenon and increased anterior pressure and IS NOT analogous to<:f200,BArial,,,> wedging due to collapse seen in osteoporosis


Etiology not known IDIOPATHIC Scheurmann</R>s lesion    <[>possibly due to abnormal end-plate cartilage]




Supracondylar fracture


Rare in adults and << 2 yrs


60% of frxs in pediatric population


distal fragment usually extends anteriorly or volarly causing ant humeral line to intersect the condyles


posterior fat pad may be normal if joint capsule is torn thus releasing the joint effusion/hemarthrosis


Volkmann contracture is most serious complication (Branchial artery contusion/compartment syndrome)


m/c complication is abnormal carrying angle



Lateral humeral condylar fracture


second m/c frx in pediatric population (15%) compared to supracondylar fractures


Salter Harris IV


pull of extensor muscles which inserton lateral epicondyle displace it distally and posteriorly


displaced fractures almost always require open reduction




Medial humeral Epicondylar fx


Third m/c elbow frx in pediatric population 10% of elbow injuries


Distinguished from a medial CONDylar fracture which is RARE


OPEN reduction is almost always required








Lateral condylar fractures (15%) are much more common than medial and are the second m/c ped inj<:f200,BArial,,,>ury in elbow mostly due to little leaguers elbow injury


Medial epicondylar injuries are third m/c pediatric injury (10%)




Hip fractures

anterior dislocations 10%


hip flexed and abducted with either impaction or posterior force femoral head moves anterior and superior near the anterior iliac spine (iliac type) or inferiorly to obturator foramen (obturator type) which is m/c


Posterior hip dislocation

9:1 more common than anterior


hip flexed and adducted and internally rotated


complications more common than anterior dislocations


AVN of femoral head up to 50% if delayed <;> 24 hrs


Association with Posterior column fractures of acetabulum



Acetabular fractures


Two column classification


Anterior column is iliopubic column extending from iliac crest to symphysis pubis


Posterior column is  from middle of anterior column inferiorly to the ischial tuberosity


Posterior column fractures more common and often associated with posterior hip dislocations


Transverse acetabular fractures cross the innominate bone separating the anterior from the posterior columns creating an inferior ischiopubic and superior iliac segments



Stability of hip fractures


Stable hip fractures do not interrupt the pelvic ring and are more common such as an isolated ischial tuberosity fracture from a fall or avulsion of apophysis such as ant sup (Sartorius and tensor fascia lata) or inf anterior iliac spine

(rectus femoris) in runners


Unstable fractures disrupt the pelvic ring such as a Malgaigne involving both ischiopubic rami or a separation of the pubic symphysis associated with either a fracture about the SI joint or separation of the SI joint




Hyperextension injury

only subtle sign may be a gaseous collection anterior to ALL in front of the disc space


Complex facial fractures and acute cord syndrome


more common in the upper C spine C2-3


Contrast to flexion injuries involving the lower C spine




Spinal infections


In adults it begins in the vertebral body (metaphysel equivalent with sluggish blood flow)


Soft tissues involved early with later spread to the disk due to enzymatic destruction of end plate


Staph aureus most common as was also cultured in kids with diskitis


lumbar spine m/c with least common in C spine (heroin addiction)


TB typically spares the disk space until late in its course, pyogenic progresses rapidly




Anterior column = ALL, vertebral body, Disk, PLL


Posterior column = posterior elements


Instability present if BOTH anterior and posterior columns are involved


Mechanical instability is NOT predictive of neurologic deficit


Thoracolumbar level has a transition from coronal orientation of facet joints to more sagittal orientation at the lumbar level.


The facets of the thoracic spine overlap extensively in a plane which approximates the coronal.  This arrangement changes at the T12-L1 level to a more sagittal orientation.  Superior facets in the lumbar region lie anterol

ateral to the inferior facets of the adjacent vertebra above.




Scaphoid fractures

most common << 30 yrs of age


waist m/c (70%)


blood flow is from distal to proximal therefore AVN m/c proximally


ischemic necrosis occurs in 5 %


Scapholunate space widening occurs in all injuries involving the scaphoid or lunate as rupture of the scapholunate ligament is the first injury in lesser arc injuries.


Inflammatory arthritis may also widen this space with synovitis





more common than VISI


SL angle is > 60 degrees (scaphoid moves dorsally)


Note normal SL angle is 45 degrees (25 – 60 degrees range)




Osteoid Osteoma

cortical appearance is lucent nidus (<<1cm) surrounded by sclerotic reactive bone


Cancellous appearance lack the reactive sclerosis and even share clinical and pathologic features with inflammatory arthropathies when near or in a joint


Rx includes removal of the lucent nidus (dense stain and pooling on angio) and not the reactive sclerotic zone




negative birefringeance


Contrast CPPD which is positively birefringeant


periarticular much more common than intraarticular


secondary causes are HPT, milk-alkalai, idiopathic tumoral calcinosis, paralysis, and hemodialysis


Milwaukee shoulder =progressive destruction with RCT and HADD





Positive birefringeance on polarized light microscopy which means clinician can see these crystals and thus make the diagnosis without seeing calcification on radiographs


Calcification on radiographs is NOT necessary for diagnosis as CPP crystals are seen on light microscopy (positive birefringeance)!


50 % of patients are asymptomatic


scalloping of the anterior surface of the distal femur from the patellar surface is classic finding


Can also lead to multiple CPP loose bodies in knee joint or popliteal fossa (osteochondromatosis)





decrease in bone mass with normal mineralization of the bone which is present


Since the bone which is present has normal mineralization, the cortices and trabeculae are thinned but well defined


CONTRAST osteomalacia which has a normal amount of bone matrix but it is inadequately mineralized.  Therefore the cortical and trabecular elements of osteomalacia are indistinct and not well defined]


Peripheral bone loss occurs at the <+#>endosteal surface<-#> maintaining the periosteal distance from side-to-side


ie the external bone diameter remains unchanged but the medullary canal diameter increases


serum levels of calcium and alkaline phosphatase are NORMAL


ie osteoporosis is a <+#>silent killer just like CAD as there are no serum markers to follow severity<-#> or presence


recall alk phos levels reduced in hypophasphatasia and alk phos levels elevated in Pagets]


Unlike osteomalacia which has a uniform pattern of involvement in the vertebral bodies, Osteoporosis has a nonuniform pattern of involvement with each vertebral body being affected to a different degree<:f200,BArial,,,><:p >



Brown tumors are seen more in secondary HPT due to improved renal dialysis therapy prolonging life


chondrocalcinosis is seen in 12% of patients with HPT but without the characteristic subperiosteal bone resorption findings.  Therefore the statement is true that chondrocalcinosis without specific bone changes may be consistent with primary HPT






inadequate quantities of mineralized bone (unmineralized bone is referred to as osteoid and therefore osteomalacia has osteoid seams or bars)  These are not specific for osteomalacia however!


Looser zones or pseudofractures are focal accumulations of osteoid and reflect a systemic process therefore they are bilateral and symmetrical


When osteomalacia occurs in an immature skeleton, Rickets is dxed


Most productive yield of rachitic changes are 1) costochondral junctions of the midddle ribs, 2)distal femur, 3) proximal humerus and 4) both ends of the tibiae


Since osteomalacia has decreased mineralization,

serum Ca and Phosphorous are reduced and alkaline phosphatase is increased trying to work overtime to increase the mineralization of bone


Dilantin Rx causes osteomalacia due to enzymatic inhibition in hepatic microsomes and reduced intestinal absorption of Vit D due to lack of Vit D dependent Ca++ binding protein


Tumoral Osteomalacia<-!>


Osteomalacia can be seen in some benign and malignant bone lesions such as fibrous dysplasia, nonossifying fibroma, hemangioma a nd hemangiopericytoma.  Etiology possibly due to increased phosphate excretion and thereby creating a hypohosphatemic form of osteomalacia in adults and Vit D resistant rickets in childhood




Specific radiographic findings in osteopenic disorders


HPT: subperiosteal bone resorption radial aspect of middle phalanges


Osteomalacia: bilateral and symmetric Looser</R>s lines or pseudofractures


Rickets: growth plate changes reflecting osteomalacia in unfused skeleton



Osteomalacic-Rachitic syndromes WITHOUT associated ABNORMALITIES of Vit D, Ca or Phosphate


Axial osteomalacia, hypophosphatasia, metaphyseal chondrodysplasia (Schmid type)


Hypophosphatasia is auto recessive deficiency of serum, bone and liver alkaline phosphatase


Precursor to alkaline phosphatase is phosphoethanolamine which accumulates in urine of patients with hypophosphatasia




Serum chemistries


Alk phos low = hypophosphatasia with increased urinary phosphoethanolamine


Alk phos high = osteomalacia with reduced Ca and Phos


Alk phos, Ca and Phos NORMAL = osteoporosis




Regional migratory osteoporosis

M > F


lower extremities more common than UE with knee, foot, ankle more common than hip




transient synovitis on histopathology


bone scan is increased uptake in involved osteoporotic joint


local pain and swelling which occurs acutely, last months then resolves only to recur at another site


Radiologic changes are osteopenia and are similar to RSD and transient osteoporosis of the hip associated with pregnancy


Paget Disease (osteoporosis circumscripta


measles of osteoclasts (viral)


AV shunts are not present<-#> but rather increased blood flow (hyperperfusion)


Rx:  calcitonin and diphosphanates used to reduce bone pain and reduce progression on radiographs


Rx (Didronel) may lead to osteomalacia if prolonged beyond 6 months


malignant transformation occurs << 2 %


Lytic phase has circumscribed regions osteoporosis circumscripta in skull and blade of grass in long bones


Mixed followed by sclerotic phases follow


Begins at ends of long bones (epiphyses) except for tibial diaphysis which may extend in either direction


Pagetoid bone fractures more easily however fracture healing is not abnormal compared to normal bone


Protrusio acetabuli and basilar invagination occur due to the softened bone


Giant cell tumors can occur via transformation in the skull or facial bones


Multiple (benign) Giant Cell Tumors in the skull of facial bones should alert one to the possibiltiy of Paget</R>s


OH-Proline in Urine and Elevated alkaline phosphatase in serum




Mixed Connective Tissue Disease


mixture of collagen vascular radiographic appearances and clinical presentations


POSITIVE antibody to  RNP (ribonucleoprotein) component of ENA (extractable nuclear antigen)


Prognosis is good with often sustained remission





PVNS m/c in knee


NOT CALCIFIED (calcification ONLY reported in ONE patient – idiot!)




Joint space loss NOT a feature (Gout also preserves space) since the PVNS changes form at the chondro-osseous margin of the intracapsular joint inciting a periarticular erosive process (NOT articular process)


Synovial reflection is the region of initial involvement and therefore causes erosions in the bare area similar to any synovitis such as RA


Juxtaarticular osteoporosis is NOT a feature of PVNS which helps distinguish it from RA




Synovial Osteochondromatosis


m/c in knee




2/3 of osteochondroma bodies are calcified and visible on plain films


M > F


Osteochondral bodies arise from synovial lining resulting in chondroid metaplasia


THUS osteochondral bodies DO NOT arise from articular cartilage<-#> (thus it is named SYNOVIAL OSTEO…)


If they arose from articular cartilage they would be called “loose bodies

of Secondary Osteochondro…


Joint space is also maintained like PVNS




Secondary Osteochondromatosis


similar histologically to the primary synovial form (Note: Synovial vs Secondary)


econdary to trauma, osteonecrosis, arthritis


Identification of an osseous donor site may be the only clue to distinguishing primary Synovial osteochondromatosis from Secondary Osteochondromatosis




PVNS and synovial osteochondromatosis are monoarticular processes


Both maintain joint space


If sclerotic erosions are seen in more than one joint space, consider RA


2/3 of osteochondroma bodies are calcified and visible on plain films<:f200,BArial


TWO Atypical presentations of RA


Cystic RA: subchondral cysts predominate appearance possibly due to decompression of joint space with elevated intra-articular pressure


Rheumatoid Nodulosis: soft tissue nodules predominate appearance


In both, the classic findings of RA such as osteopenia, marginal erosions, joint space loss are less prominent!




Calcific loose bodies in the knee DDx


CPPD with loose calcific bodies, look for other evidence such as scalloping of anterior femoral surface


Secondary Osteochondromatosis (NOT primary Synovial osteochondromatosis) look for donor sites



Soft tissue calcification


Metastatic: deposition of calcification in soft tissue (visceral or nonvisceral) with an elevated CaxPO4 product <;> 70.   THUS either high Ca or high PO4 or both


Dystrophic: deposition of calcification in necrotic tissue with normal serum calcium and PO4 levels



Myositis ossificans


Congenital Myositis ossifican progressiva (Fibrodysplasia ossificans progressiva)]


Myositis ossificans circumscripta


most commonly after trauma (up to 75%)


25% havedisorder known to produce heterotopic ossification (head injury, paraplegia, surgery, burns) with the remainder


spontaneously occurring after trauma


Serum Ca and PO4 are normal


zonal findings include a peripheral trabecular zone, central zone has necrosis which may be similar to sarcoma if biopsied


separated from adjacent bone by a lucent zone soft tissue zone.   This distinguishes parosteal and periosteal osteosarcomas from MO


Acute Paraplegia results in heterotopic ossification in up to 50% (example in Syllabus has bridging ossification of hip as well as bladder calculi)


Heterotopic Ossification seen in head injury, paraplegia, surgery, burns



Milk-alkali syndrome


usually occurs secondary to ulcer therapy with milk and alkali antacids


original description described 6 men with chronic renal insufficiency and peptic ulcers  treated with large amounts of milk and alkali antacids


elevated CaxPO4 product (<;>70) at which time metastatic calcification usually ensues


Chronic renal insufficiency leads to impaired urinary excretion of calcium (normal calciuria) with subsequent hypercalcemia due to increased ingestion of milk and antacids


Predisposed is renal patient who develops an ulcer




Idiopathic Tumoral Calcinosis


Black men who are otherwise healthy


Extra-articular deposition of calcium salts which do not limit ROM since they are extra-articular!


May grow and ulcerate skin leading to intermittent discharge of white chalky material


NO OTHER VISCERAL OR SKELETAL ABNORMALITIES PRESENT distinguishing this idiopathic tumoral calcinosis from other processes with metastatic calcification (hyperphophatemia may be present)


Diagnosis of exclusion first ruling out other sources of metastatic calcification such as milk-alkali, HPT, Hyper Vit D, or collagen vascular disorders




Secondary HPT follows chronic renal failure.  Following renal transplantation, 1,25 OH Vit D is produced again and it is not uncommon to have a persistent parathyroid adenoma.


Tumoral calcinosis (extra-articular) can occur when Ca x PO4 product <;> 70, but when this level is reduced as with a parathyroidectomy the tumoral calcinosis deposits will disappear.


Example in text is bilateral tumoral calcinosis of AC joints in patient with neck dissection clips with followup films showing resolution of tumoral calcinosis and residual resorption of the distal clavicles.


Osteomalacia (rickets in kids) also occurs due to lack of Vit D producing a picture of osteomalacia (generalized osteopenia affecting all vertebral bodies similarly) which also improves with therapy producing a osteosclerosis such as a rugger jersey spine




Ankylosing Spondylitis


syndesmophytes are ossifications of the outer fibers of the anulus fibrosus connecting vertebral borders of adjacent bodies


Syndesmophyte formation is preceded by osteitis of the anterior corners which produces a shiny corner Squaring occurs due to reparative sclerosis of the corner erosions (Romanus lesions)


Bamboo spine results with multiple levels


Ossification begins at T-L or L-S junctions


Spinal ascent occurs in some but not all


syndesmophytes of AS are identical to those of IBD


HLA B27 antigen + in 90% (+ HLA B27 in 8% of population)


Sacroiliitis bilateral and symmetrical similar to IBD as well


SI involvement almost always precedes spine syndesmophytes





ossification of at least 4 contiguous bodies, relative preservation of disk space


ABSENCE of intervertebral or SI joint bony ankylosis, erosions or sclerosis


SI joints are involved though without ankylosis or erosions.  SI joints  also have para-articular osteophytes bridging the inferior margin of the joint.


association with ossification of PLL


Ossification of other ligaments such as sacrotuberous ligaments




DDx of enthesopathic changes




X-linked Hypophosphatemia



Cadmium poisoning


Vit A poisoning


Idiopathic Hypo PTH








Parathyroid disorders

Primary HP (lack of parathyroid tissue 3 & 4 pouches)


* Low PTH


** Rad normal in adults (kids have Ca++ in soft tissues and BG)


Secondary HP (Surgery m/c)


* Low PTH


PseudoHP (PHP) End organ unresponsiveness


* Elevate PTH,  HypoCa++,  HyperPO4


PseudoPseudoHP (PPHP)

Patients who have “rescued themselves from their unresponsiveness to PTH


**Rad short MC, MT AND Phalanges [>PPHP <;> PHP]


** Rad coned epiphyses and soft tissue and BG Ca++ [>PHP <;> PPHP]




Prosthetic Hip Loosening


Bone scan should be normal 6-9 months s/p replacement


Signs of loosening on Bone scan include increased activity about femoral shaft especially at the prosthetic tip


Radiographic loosening: 1) increasing lucency at bone-cement interface or <;> 2 mm, 2) scalloping of endosteal surface of femur or acetabulum, 3) femoral cortical thickening about femoral prosthesis, 4) increasing lucency at prosthesis-ceme

nt interface (weaker than bone-cement interface), 5) subsidence of femoral component into femur


Normal limits of NM arthography = opacification of 1 cm or less of the bone-cement interface at lateral margin of acetabular roof or inferior margin of acetabulum.  And opacification of femoral component within a few mm of bone-cement inter

face at proximal femoral stem is also normal.


Positive arthrographic findings much more important than negative findings as a FN exam may be due to fibrous adhesions at bone-cement interface which obstruct flow of contrast down the bone-cement interface


Bone scan positive findings indicate either loosening OR infection and cannot distinguish between the two!  Further evaluation with Ga-67 or In-111 WBC should follow a positive bone scan.




Femoral neck fractures


Intracapsular (aka subcapital)








Extracapsular (aka intertrochanteric)






AVN higher in intracapsular frxs (25%) compared to extracapsular frxs due to increased distension of capsule compressing retinacular vessels


Extracapsular (intertrochanteric) frxs affect older individuals with muscular weakness and osteoporosis


Intertrochanteric frxs produce a varus deformity with instability indicated by comminution of the medial femoral cortex


Heterotopic bone formation predispositions s/p hip replacement


DISH patients


second revision or prior surgery in that location


Prior evidence of heterotopic bone formation


Presence of OA in joint


Nonunion of fracture sites


Osteoporosis is NOT a predisposition to delayed or nonunion!


Two types of nonunion 1) Hypertrophic with callus buildup or 2) Atrophic with necrosis of bone


Nonunion defined as a situation in which the fracture healing process has ceased completely and the fragments remained nonunited.





occurs in up to 10% of patients with NF1


form fruste of NF1 if congenital pseudoarthrosis is present ?


m/c involves tibia (anterior bowing of distal1/3) but also upper extremities


Histologic exam nonspecific for NF1 and show a mass of fibrous tissue and

NOT a neurofibroma


Spontaneous healing and operative results are POOR possibly due to

underlying defect in mesoderm


Giant cell tumor


hypervascular AND is the tumor rarely seen to transform in skull and facial bones in patients with Paget.


Recall that m/c malignancy associated with Paget is osteosarcoma.


Paget is hypervascular with markedly increased flow and therefore it makes sense that Giant cell tumors are hypervascular and can be seen in the facial bones of patients with Paget Disease!



Gaucher disease

abnormal glucocerebroside-filled RE cells result due to deficient glucocerebrosidase in RE cells


Ehrlenmeyer flask metaphyseal modeling defect is seen though is not specific as any marrow expanding disorder can cause it (Niemann Pick disease


Skeletal mets

infrequently cause periosteal reaction


do not characteristically have a sequestrum


All mets to vertebrae start at posterior body (NOT pedicle), plain film reveals pedicle involved because that is what is apparent on the plain film, not the body.





Brodie abscess

children <;> adults


Staph aureus m/c


50% are sterile on culture!!!!


Periosteal rxn in form of Codmans triangle is NOT commonly seen though it is

potential manifestation


Involucrum is the reactive new bone with granulation tissue – chronic osteomyelitis (thickened new bone)


Sequestrum is the necrotic dead bone in center


Garre sclerosing osteomyelitis = nonpurulent osteomyelitis with sclerotic features


Resorption of the white cortical line within a joint space strongly suggests pyoarthrosis




Skeletal TB

children almost always have an abnromal CXRAY however adults may have a normal cxray with skeletal TB


Vertebral column, hip and knee are the three m/c sites


most often epiphyseal +/- intraarticular extensions with diaphyseal involvement exceedingly rare


Bursa involement is common especially involving erosions of the greater trochanter


Phemisters triad and TB


1) juxta-articular osteoporosis


2) peripheral bone erosions


3) slowly progressive joint space narrowing


Cystic TB is rare though m/c seen in children with multiple lytic nonsclerotic lesions in long bones, adults with cystic TB is even rarer and usually has a sclerotic border


Skeletal Coccicioidomycosis


Think of Cocci for a specific infection with multiple lytic lesions (bilateral & asymmetric)


Skeletal sites are about the chest where the disease is often manifest (vertebral bodies, ribs & pelvis)


Prominate predilection for bony prominences (patella, tibial tuberosity, ulnar olecranon, calcaneus) which is true of all fungal infections the m/c of which is probably Cocci especially in endemic regions


Metaphyseal involvement is m/c in long bones like any other infection (except for TB which involves epiphyses)


Primary Cocci may have a self-limited migratory polyarthritis (desert rheumatism) seen in 1/3 of patients


Phemister triad may also be seen however it typically is seen with TB as joint involvement is late in TB




Skeletal Bronchogenic mets

all cell types are predominately lytic


If a osteoblastic (sclerotic) lesion is seen, think adenoCa or small cell


50 % of all destructive lesions to hands or feet are bronchogenic in origin


Bony prominences are not typically involved (this pattern is typical of fungal especially Cocci)


Subperiosteal deposits with cortical destruction is suggested (cookie-bite)




Skeletal Sarcoidosis

osseous involvement in 5%


typical sarcoid age range (20 – 40</R>s)


Bone lesions rare in absence of skin lesions (E nodosum)


80-90 % with bone lesions have pulmonary  involvement


Osteopenia, lacework trabecular coarsening, cystic lesions


Lacking periosteal reaction


Hands and Feet (short tubular bones) with predilection for middle and distal phalanges (acroosteosclerosis)


Vertebral involvement also seen and should be included in DDx vertebra plana sparing disk space




Conjoined Nerve Root

two adjacent nerve roots within common arachnoid sheath


1 – 7 % of population


Almost ALL involve L5 and S1 nerve roots


Not associated with spinal anomalies or symptoms


Incidental findings





Most occur posterolaterally


only 10 % occur midline due to reinforcement of the PLL


HNP normally has attenuation similar to normal HNP, however extruded material is often lower in attenuation and may mimic nerve roots or blood vessels




Spinal stenosis


Narrowing of sagittal dimension of canal and is multifactorial


<10 mm is absolute stenosis, though sxs vary


Congenital (developmental) nonhereditary with exception of Achondroplasia (also have narrowed interpedicular distances) and manifest sxs also later in life with DJD changes compromising an already compromised canal


Acquired stenosis has two major categories: lateral and central both of which manifest later in life due to DJD encroaching upon the nerve roots.


Most frequent cause of the “failed back surgery syndrome


Synovial cyst (intraspinal

low density mass adjacent to a degenerated facet joint and contains calcification in the wall


Almost ALL cases are at L4-L5 level


Recall that conjoined nerve roots almost always involve L5 and S1 whereas intraspinal synovial cyst are at L4-L5!


Recall that perineural cysts aka Tarlov cysts m/c occur at S2 and S3]


Synovial cyst formation most likely due to DJD of the facet joints with subsequent herniation of synovium through rents in the joint capsule




PAIN is the main symptom probably related to the facet DJD rather than nerve root compression


Classic Hx is LBP withOUT associated neural levels by motor or sensory exam or DTR



Soft tissue Sarcoma

1/3 arise in the thigh (most common)


Calcification is not specific nor does it differentiate between subtypes


Margins seen on CT do not reliably indicate benign or malignant nature (Margin characteristics are usually the key finding in delineating benign from aggressive lesions hwoever this is not the case with soft tissue sarcomas)




Clavicular HPT findings

Similar to subperiosteal bone resorption and intracortical tunneling seen in the hands though findings often found in the clavicles AFTER findings manifest in the hands


resorption at ligamentous attchments including the conoid (coracoclavicular) and AC ligaments


Clavicle (proximal and distal) affected to a far greater degree than acromion which can distinguish RA




Post-Traumatic Osteolysis of the clavicle

bone resorption of distal clavicle weeks to years following minor or severe trauma


Repair follows with cessation of activity though resection of distal end also helps


Self-limited process so long as inciting activity is discontinued


Residual radiographs reveal increased AC joint space and sxs are usually absent when radiographs indicate healing of the process


Ddx: RA, HPT, Scleroderma, Gorham</R>s disease (massive osteolysis) and cleidocranial dysostosis




Gorham disease

Massive Osteolysis “Vanishing Bone Syndrome

soft tissue hemangiomas without Ca ++


frequent hx of prior trauma



any bone without respect for joints and may involve all bones within an area





RA erosions



Less common site though characteristicly involved is the superior surface of posterior


ribs 3 – 5



Possibly due to friction from the overriding scapula



DDx of superior rib notching = RA, Scleroderma, Polio, HPT, Marfan</R>s syndrome (anuloaortic ectasia)






Diaphyseal Bone Infarcts



Gout possibly due to associated hyperlipidemia or  DM



SS anemia = bone infarcts



Cooley anemia  (B thalassemia major) does NOT produce bone infarcts, rather leads to hyperplastic marrow


Endosteal scalloping seen with central Chondrosarcoma and NOT bone infarcts




Peripheral vs central (medullary) types based on location in

individual bone


Peripheral is therefore often secondary in that it occurs following dedifferentiation of existing exostosis or enchondroma


Central is within the medullar canal with chondroid matrix and endosteal scallopping


Recall Bone Infarcts do NOT have endosteal scallopping)


Dedifferentiated Chondrosarcoma m/c in iliac bones


stability of lesion does NOT necessarily imply benignancy as these lesions are typically slow growing




Trevor disease


Osteochondroma-like growth from one side of the epiphysis into joint space


m/c in tarsus, carpus, ankle, knee


2 – 4 yrs m <;> F


may be associated with hemihypertrophy


Dysplasia Epiphysealis Hemimelica




Synovial cell sarcoma



Include in DDx of popliteal mass (Bakers cyst)


Malignant tumor near (not within) joints


94 % occur in extremities


Highly aggressive tumors! Enlarging mass in popliteal fossa (painful) which

does not communicate with joint space like a Bakers cyst is highly suspicious




Knee Joint

Suprapatellar pouch is first to accumulate fluid


when width of base of pouch is <;> 10 mm, <;> 10 cc present in joint


when width 5 – 10 mm, 1 – 9 cc


Density of suprapatellar pouch is similar irregardless of fluid type present




Patellofemoral relationships


ratio of legth patellar tendon to patellar length (LT/LP) is @ 1.0 (equal) with knee in mild flexion


abnormally high patella (ratio  1.3) aka patella alta associated with recurrent patellar subluxation, chondromalacia, Sinding-Larsen-Johanssen syndrome (Osteochondrosis of inferior patellar pole) and Cerebral Palsy


Lateral patellar views should be performed at 30 degrees and quadriceps relaxed


Sunrise view assesses patellar tracking within the trochlear groove (flexed at 45 degrees) AND the congruence angle and the patellofemoral index


Congruence angle  16 degrees to the lateral = chondromalacia patella


Patellofemoral index << 1.6 (medial patello femoral distance / lateral patellofemoral distance) = chondromalacia patellae


Chondromalaica patellae results in lateral tracking of patella within trochlear groove and therefore manifests as decreased lateral patellofemoral joint space (index) and outward positioning  (congruence)


Chondromalacia patellae can only be accurately assessed on sunrise view and NOT lateral view




DDx of Patella Alta


recurrent patellar subluxation, chondromalacia, Sinding-Larsen-Johanssen syndrome (Osteochondrosis of inferior patellar pole) and Cerebral Palsy



Sickle cell disease



clinically worse combination is SC disease


Infarctions involve diaphyses of tubular bones (hand foot syndrome) and in femur is contrasted in location with the normal location of metaphyseal for pyogenic infections



Dactylitis (hand-foot syndrome) can result in premature fusion of bones <[>ie markedly shortened metacarpal or isolated phalanx not following pattern seen in HypoPTH (short MC phalanges or Turner with short MC alone]


Premature fusion occurs in the central physis as the peripheral receives some nourishment from the synovium, thereby resulting in a “coned epiphysis</T>


Salmonella in up to 50%


Obliteration of the sinuses due to marrow hyperplasia and the hair on end appearance is more commonly seen  in thallasemia


Occipital bone has no marrow elements therefore no hair on end appearance is present in occipital bone




DDx of coned epiphysis

PseudoHP, PseudoPHP


Sickle cell disease



Myeloid metaplasia

Splenomegaly with dense bones though a generalized osteopenia may present due to marrow packing of hyperplasia,  This is replaced by fibrosis and may present with focal osteolytic lesions representing islands of fibrous tissue deposition


Bone infarction does not occur

recall that bone infarcts occur with sickle cell and gout within the diaphyses of long bones]





Endemic water has the same end radiographic result as industrial where fluorsis is acquired by inhalation


Similar appearance to DISH


Hyperostosis, enthesopathy, osteosclerosis and osteophyte formation


Skull is spared








mast cell accumulation in tissue (ie skin and bone)


associated with leukemia


splenomegaly, skin lesions, pancytopenia, lymphadenopathy


Osteoporosis due to heparin production of the mast cell


scattered sclerotic / lytic foci in bone due to fibroblastic and granulomatous rxn from the mast cell


skin pigmentation evident half of patients


Extramedullary hematopoiesis




Cerebral Palsy = Upper Motor Neuron lesions = spasticity


Long C-shaped curve with associated pelvic obliquity strongly suggests diagnosis of neuromuscular scoliosis


femoral neck valgus and dislocations and GI ileus and fecal impaction other associated signs


Perinatal anoxia is major cause


Muscle groups involved do not progress beyond first few years of life thus neuromuscular sequelae are defined when the diagnosis is made.


Asymmetrical involvement of  the anoxia of upper motor neurons results in muscle imbalance causing scoliosis and pelvic obliquity.  Hip dislocations are typically unilateral involving the hip which is elevated.


Femoral neck valgus and hypertrophy of the lesser trochanter are due to the muscle spasticity and can be indicative of muscle imbalance even if hip dislocation is not present


Surgical release of iliopsoas tendon on the lesser trochanter can be performed to relieve the spasticity and sequelae may be a calcified iliopsoas tendon with hypertrophied lesser trochanter


Unbalanced muscle pull can also be seen in patella alta (possibley with avulsion of inferior pole), halux valgus or flat feet


Scoliosis seen in 39% of bed ridden patients and only 7 % of ambulatory patients



Muscular dystrophy = Lower Motor Neuron lesions = flaccidity and paralysis


Duchenne m/c variety


X-linked (boys affected)


Pseudohypertrophic dystrophy due to fatty accumulation of muscle


muscle weakness results in characteristic stance with lumbar lordosis, and weight placed on one leg with slight flexion.  Hip flexion contractures result from maintained tension on the tensor fascia lata (not due to spasticity seen in UMN lesions such as cerebral palsy)


Hip dislocations do not occur due to lack of muscle strength<-#> to dislocate the femoral head


femoral neck retains valgus deformity like CP however lack of activity prevents a varus deformity of the hips from developing whichwould be expected with the erect imbalanced posture


Death is @ 25 yrs from cardiac or respiratory failure


cardiomegaly seen after teenage years






level of spinal dysraphism (involvement) does not predict level of neurologic dysfunction as  spinal tracts are asymmetrically involved and skip areas are seen.  Bladder findings cannot be interpretted either!


asymetric involvement may lead to muscle imbalance (flexors functioning with impaired extensors) often leading to hip dislocations


Kyphosis present in 15% of patients with apex located at widest interpediculate distance


Fractures of LE have increased incidence due to muscle weakness


Neuropathic joint may also exist


(also spinal cord injury, polio = anterior horn cell disease, and peripheral neuropathies)




Radiographs + in 75% of lesions


Bone Scan + in << 50% of lesions


30 % of lesions detected ONLY on Radiographs


10 % of lesions detected ONLY on Bone Scan


Skull and Mandible


Sclerotic type (1-3 %) associated with POEMS (polyneuropathy)


POEMS = Polyneuropathy, Organomegaly, Endocrine, M-protein, Skin changes



Skeletal Mets detected up to 45 % by bone scan alone


Skeletal Mets detected 10 % by Plain film alone





Physaliferous cells


Hematogenous dissemination uncommon (10 %), most commonly, if occurring, to lung


Sacrum = 50 %, Cervicobasilar = 35 %



Congenital Hip Dysplasia

F > M due to  maternal hormones = ligamentous laxity

Breech more often than vertex deliveries


L <;> R


Rx  Pavlik harness




Deprivational dwarfism


causes widened cranial sutures during recovery phase due to rapid brain growth


etiology includes malnutrition or prolonged illness




Congenital Syphilis




Metaphyseal bands


Lytic lesions (Wimbergers sign = lucent lesions in medial proximal tibial metaphyses)


Periostitis (mataphysitis or diaphisitis)


Epiphyses usually spared as are synovial membranes




Caffey Disease


Case: 7 week old with swelling of face (mandible), ulna and clavicle with diaphysitis




Diaphyseal periosteal rxn


Less common in current times (? etiology)


DDx :  Neonatal/Idiopathic, High Frequency Ventilation, Infection, Vitamin A, Trauma (Incidental)



Marrow infiltrating disorders


Leukemia, Lymphoma, Mets, Myeloma


Replacement of high SI on T1 with low SI


enhancement on T1 with Gd BUT this may be obscured by fatty marrow signal


STIR sequences have increased intensity and is highly recommended by Moss and Gamsu !!!!


Marrow edema such as in RSD (low T1, High T2 and High STIR)


Hemangiomas are exception as they are HIGH on T1 and remain high on T2 and STIR


MIMICS of marrow disease


Gauchers with Erlenmeyer flask (nonspecific) has low SI on T1 and high SI on STIR due to Kerasin


Sickle cell dz, Thalassemia, hemolytic anemias, polycythemia, Langerhans cell histiocytosis


Transient marrow edema of the femoral head which is similar to AVN except for absence of predispositions and HOT Bone Scan [>Now referred to as Transient Marrow Edema Syndrome because 3 of initial 10 patients lacked osteopenia on plain films !!!!!!!!!]


Heterogeneous SI in distal femurs frequently seen in Young females and athletes !!!


Interpret SI of distal femur in Knee “r/o meniscal injury in this athlete</T> with caution to avoid overcall !!




MRI of Knee normal variants


Transverse Geniculate Ligament runs anterior to Hoffa fat pad connecting lat and med menisci anteriorly


Menisco-Femoral ligaments connect lateral meniscus to medial femoral condyle


Wrisberg is posterior to PCL (33 %)


Humphry is anterior to PCL (33 %)


* Both are seen concomitantly in only 3 % of exams


* Do not mistake for intra-articular fragments


Popliteus Tendon simulates tear of posterior horn of lateral meniscus






Lisfranc frxs include TMT joint and are Homolateral or Divergent


Chopart frxs include intertarsal (Talo-Navicular joint)


Segond frx = avulsion of lateral femoral condyle implying internal derangement (Rec MRI)




DDx Enlarged digit in child


Macrodystrophia lipomatosa  (Note this is not Lipodermatoarthritits aka Multicentric Reticulohistiocytosis)






Neural Fibrolipoma (median nerve – 2nd and 3rd digits)









Soft Tissue Masses




Definition of Soft tissue = Non-epithelial extraskeletal Tissue


Big Picture:

Young:   Rhabdomyosarcoma (10 yrs) or Lipoblastoma


Young:   Synovial Cell Sarcoma (25yrs)


Adult:   MFH  or  Liposarcoma





Well-Differentiated –   100% fatty (aka Atypical Lipoma)


Myxoid  –  most common (40-50%)


Pleomorphic  –  highly vascular


Excluding well-differentiated varieties, 50% of liposarcomas have ZERO FAT!





Liposarcoma equivalent in kids


Of 2500 liposarcomas, only 2 presented in children << 2 yrs


*  When mature, lipoblastoma will become LIPOMA (BENIGN)<-#>



Giant Cell Tumor of Tendon Sheath = PVNS equivalent of tendon or ligament!




DDx Low density lesions of scapula and axilla



Elderly pt, CHEST WALL (scapula) low density mass


From mechanical friction




YOUNG (20s)


“Brown Fat</T> tumor


+ Highly vascular


Not malignant




DDx  Macrodactyly f 2nd & 3rd digits (median nerve distribution m/c)


Neural Fibrolipoma


(aka Lipomatous Hamartoma of Nerve)




Hemangioma or vascular tumor


Macrodystroophia lipomatosa (increase in all elements of digits)







Osteopetrosis:  “Bone within a Bone


Melorheostosis:  Familial boney excrescences unilateral limb (“candle drippings


Gaucher Disease:  “Ehrlenmeyer Flask metaphysis with osteonecrosis


Osteopoikilosis:  “chicken pox in bone (multiple focal densities in bone)


Multiple Myeloma:  multiple punched nonsclerotic skull lesions

Skull and Mandible


Sclerosing variety << 3%


Associated with POEMS (polyneuropathy, organomegaly, endocrinopathy, M protein, skin changes)




Sequestrum DDX= FOOGEIL


Fibrosarcoma (equivalents), Osteoid Osteoma (nidus), EG< Infection, Lymphoma (11% in AFIP series)






Osteomalacia (Rickets): poor quality bone (smudgy trabeculae)


Osteoporosis: insufficient quantity of bone (fine trabeculae preserved)




Osteomalacia (Dilantin, Ifosfamide, Heparin (Mastocytosis), Hemangiopericytoma)


Dilantin and Phenobarbitol decrease intestinal absorption of Ca++ by decreasing activity of Vit D dependent Ca++ binding protein




CPPD (primary)


HPT (primary)



Dialysis and skeletal abnormalities<-!>


* Amyloid arthropathy caused by deposition B2-microglobulin of amyloid

* Aluminium: secondary to intake of oral phosphate binders to control hyperphosphatemia






deficiency of alkaline phosphatase (bone, liver)


wormian bones


metaphyseal lucencies


Urinary excretion of phosphoethanolamine


Pagets Disease

Urinary excretion of OH Proline





Endocardial cushion defect (Goose Neck appearance of LV outflow tract)


double ossification ofthe sternum


relative increased height of vertebral bodies in lumbar spine




large flared ilia


flattening of the acetabular angle


reduction of iliac index ( iliac index = acetabular angle + iliac angle) normal <;> 72 (72-95 degrees)


Crunched down pelvis flattening acetabular angle and iliac angle (reduced iliac index therefore)




Trisomy 18


small pelvic wings appearing rotated anteriorly (opposite of large flared ilia in downs)


Antimongoloid pelvis




Turner syndrome (XO)


aortic coarctation


positive metacarpal sign (line drawn through heads of 4th and 5th MC will normally not intersect 3rd)


ie SHORT 4th metacarpal


does not apply if 3rd is also shortened.


phalanges are not shortened (distinguishing this from pseudohypoPTH)




Pseudohypoparathyroidism or PPHP<-!>


Short 4th and 5th metacarpals with SHORT distal phalanges as well


(contrasted with short 4th metacarpal with preserved distal phalanges seen in Turner syndrome)


PseudohypoPTH is a systemic disorder therefore there will be more widespread involvement than XO!






low tissue and serum alkaline pohophatase with excess phophoethanolamine in the urine


irregularity or metaphyses of various bones similar to rickets however abnormalities


are more punchd out and discrete than in rickets




Pes anserinus = GSS (both have  in them!)


three muscles attached: Gracilis (inf pubic ramus), semitendinosis (ishchial tuberosity), sartorius (ant sup iliac spine)


Semimembranosus attaches to medial tibial condyle from origin on ischial tuber  Membranosus=Middle of tibial condyle




Looser lines (pseudofractures)


lucent lines in cortices with or without evidence of fracture healing (periosteal bone reaction)


May or may not involve the entire cortex


Osteomalacia (concave side) and Paget (convex side) also OI


Soft bone of osteomalacia bends at outer convex side


Brittle bone of Paget breaks at convex side


Recall that Pagetoid bone and osteoporotic bone have normal fracture healing inspite of having a tendency to fracture in the first place (Osteoporosis is also NOT at risk for nonunion)




Vitamin A


Skin changes


Case: Polar bear meat induced GI symptoms and NO Abnormal radiographic findings in adults


children have premature fusion of physes and thinning of calvarium diploic space c/w increased ICP


Distinguish from Caffey disease (infantile cortical hyperostosis) which has diaphyseal subperiosteal bone formation sparing the metaphyses and epiphyses


seen in kids treated for Ichthyosis





osteolysis of the terminal phalanges Thumb most commonly affected





radiodense lines at metaphyses of growing bones.


Abdominal radiographs in children should be performed to evaluate for ingestion




DDx Dense mataphyseal lines




stress / illnesses


heavy metals


healing stages of scurvy or leukemia


Hyper Vit D




Hypo PTH





thickened skull with chronic ingestion


osteopenia  (osteomalacia or rickets if growth plates open)





cortical hyperostosis can be either outside bone or endosteal


Candle drippings


regional involvement related to sclerotomes (zones of skeleton supplied by spinal sensory nerves)






AVN vs Transient Marrow  Edema


AVN has focal reactive interface between live and necrotic tissue.  Early Fatty marrow changes not seen on SE MRI.  Stage when it becomes evident not known.


T1 Interface has low SI band with sharp inner face and blurred outer face.


T2 interface has Double line sign (2 = Double)


Double line sign = High signal band = hydrated cellular marrow; Low signal band = peripheral sclerosis VS chemical shift artifact due to reversal of bands when  requency -encoding gradient is reversed.


Transient Marrow Edema has Ill-defined marrow findings of edema (high SI on T2)


Both can lead to  epiphyseal fractures and linear areas of low SI may  indicate impacted fracture


Ref = Radiographics 13: 501-519, (May) 1993






Fracture Healing


Peezoelectric Effect


Tension side (c<:f200,BArial,,,>onvex) + charge attracts Osteoclasts


Compression (concave) – charge attracts Osteoblasts



First evidence of fracture healing is widened fracture site due to necrotic bone resorption


Callus formation

Internal Endochondral Ossification


External Intramembranous Ossification (periosteum)





Delayed > 6 months


Nonunion > 9 months


Hypertrophic has exuberunt callus


Oligotrophic has small callus


Atrophic has no callus






Predispositions to Nonunion


Inadequate reduction


Inadequate immobilization




Decreased blood supply





Muscle Trivia



Plantaris and Gastrocnemius do not insert on Tibia or Fibula but rather originate on distal femur (condyles) and insert on calcaneus by calcaneal tendon




Soleus does insert on fibula and tibia




Three muscles on Coracoid process:




Biceps brachii (short head)


Pectoralis minor





Originates on humerus and inserts on coronoid process of ulna




Four muscles of forearm flexors<-!> (Four fingers on antecubital fossa)


Index finger = Pronator Teres  <[>Median nerve]

Median n runs between two heads


Middle finger = Flexor Carpi Radialis  <[>Median nerve]


Ring finger = Palmaris Longus  <[>Median nerve]  Absent in 11 % of population


Little finger = Flexor Carpi Ulnaris  <[>Ulnar nerve]

Ulnar n runs between two heads






Only muscle in body to insert and originate on distal ends of bones


Origin on distal humerus and Insertion on distal radial styloid





Flexors of the arm innervated by Musculocutaneous nerve


Extensors of the arm innervated by Radial nerve


Flexors of forearm innervated by median except for


Flexor Carpi Ulnaris (Ulnar nerve)


Brachioradialis (Radial nerve)


Flexor Digitorum Profundus 4th and 5th digits (Ulnar nerve)


Extensors of forearm innervated by Radial nerve




Shoulder Rotation

External Rotators:  Rotator Cuff muscles EXCEPT for Subscapularis


Supraspinatus, Infraspinatus, Teres Minor


Internal rotators of humerus include Latissimus, Subscapularis, Teres Major, Pectoralis Major




Psoas Major

Originates T12 – L5


Inserts on Lesser Trochanter with Iliacus




Psoas Minor


Originates T12 and L1


Inserts Pectineal line and Iliopectineal Emiinence (superior aspect of lateral superior pubic ramus)


Absent in 40 % of bodies (love that gross anatomy term – “bodies</T>)


Does NOT insert on Lesser Trochanter






Posterior Scalloping Vertebral Body<-!>




Intramedullary:  Astrocytoma, Ependymo, Hemangioblastoma, Syringohydromyelia


Intradural Extramedullary: Meningioma (though usually cord sxs first), Neurofibromatosis, Mets


Extradural: Arachnoid cyst, Mets, Hematoma


CT Disorders:  Marfans,  Mucopolysaccharidoses, Ehlers Dahnlos, Osteogenesis Imperfecta


Growth Disturbances<-:  Achondroplasia, Acromegaly, Hyopothyroidism




Beaked Vertebrae




Growth Disturbances (Achondroplasia, Hypothyroidism)


Mucopolysaccharidoses (Hurler</R>s,  Morquio</R>s)


Neuromuscular Disorders (Kyphotic curvature-related, NiemanPick,Werdnig-Hoffman, Phenylketonuria)






Metaphyseal densities<-!>


Normal Variant


Lead Poisoning


Heavy Metal (Bismuth, Arsenic, Fluoride, Mercry, Lithium, Radium)


Healing Rickets


Healing Scurvy


Healing/Treated Leukemia


Growth Arrest Lines (Chronic disease)


HyperVitamin D / Hypercalcemic states / HypoPTH


Infection (Torch and Syphilis)





Metaphyseal Lucencies<-!>


Normal Variant






Leukemia and other Systemic Illnesses


Metastatic Neurblastoma


Infection (TORCH)




Metaphyseal Dysplasia




Vertical Striations<

Congenital Rubella (Celery Stalk)


Osteopathia Striata



Periosteal Reaction


HO (Lung/Pleura/mediastinal CA, COPD, Chronic lung diseases, Cyanotic CHD, CF)


Abdominal (biliary cirrhosis, UC, Crohn</R>s Pancreatitis)


Trauma (stress, Trauma X)


Phsiologic of Newborn (ventilator)


Thyroid Acropachy






Caffey</R>s Disease (Infantile Cortical Hyperostosis)




HyperVitaminosis A


Congenital Syphilis


Hand- Foot Syndrome


Healing Scurvy or Rickets


Vascular Stasis (venous insufficiency)<+!>




Outer Clavicle Destruction<-!>




RA, Scleroderma


Neoplasm (Mets, Myeloma, EG, Lymphoma)


Cleidocranial Dysostosis




PostTraumatic Osteolysis, Trauma




Hurlers Syndrome




Holt-Oram Syndrome


Trisomy 13/18






Thermal Injury (Burns, Frostbite, Electrical)




Scleroderma, Psoriatic arthritis, Sjogren</R>s syndrome


Neurotrophic (Syrinx, meningocele, DM, Charcot joint, Congenital Indifference to Pain,Leprosy, Tabes)


PVC (middle of phalanx)




Lesch-Nyham Syndrome


Familial acro-osteolysis







Arthritides Three Types]


1)  Degenerative (OA with or without erosions)


2)  Inflammatory


Rheumatoid Factor Positive


Spondylonegative Arthropathies





Ankylosing Spondylitis


3)  Crystal Deposition Diseases


Calcium PyroPhosphate Depostion




Gout (primary or secondary)


Hemochromatosis (primary or secondary)



Ochronosis (alkaptonuria)

B O N E   A N D   J O I N T   D A T A



Scleroderma – appear bitten off

Psoriasis – usually w/ nail changes of pitting & ridging

Hyperparathyroidism – other resorptive changes



Occlusive vascular disease

Polyvinyl chloride poisoning




– 30% show bone changes

– chondrocalcinosis

– brown tumors

– high serum ca# – low PO4

– 80% due to parathyroid adenoma – also hyperplasia, carcinoma


– sclerosis

– soft tissue calcification, tumoral calcinosis

– subperiosteal resorption

– in response to chronic low vitamin D – low serum ca# – high PO4


– autonomous parathyroid gland

Other findings

– salt & pepper skull

– rugger jersey spine

– nephrocalcinosis

– vascular calcifications



Hyperaparathyroidism (most important to exclude)

seen mostly in primary HPTH



Pseudogout (CPPD)


Wilson’s disease






Congenital syphilis

Battered child


if metaphyses appear like celery stalk – suggests TORCH infections



Wide epiphyses – cupped & frayed metaphyses

Wide, poorly calcified zone of provisional calcification

Rachitic rosary on CXR

Triradiate pelvis

Bossing of skull



Vitamin D deficiency

– poor dietary intake

– no sun exposure


Malabsorption of vitamin D

– liver disease

– biliary atresia


Vitamin D resistant

– inherited

– Dilantin tx


Renal rickets

– Renal failure

– RTA (distal type)


Neonatal rickets


lack of calcium – poor mineralization of matrix



Generalized osteoporosis

Thin cortex

Subperiosteal hemorrhages lead to periosteal reaction

Pelken spur – corner fracture leading to splayed metaphyses

Trummelfield zone – zone of attrition at metaphyseal end

Ring epiphysis



Colitic spondylitis

Ankylosing spondylitis

Reiter’s syndrome

Psoriatic arthritis

Infection (Tb)



The SI joints show bridging in DISH



Age of patient

Location in bone (M-D-E)


Matrix (Fibrous-Chondroid-Osteoid)

Periosteal reaction

Codman’s triangle



Primary bone tumors are rare. Mets are 200 times more common

PBKTL are those tumors tending to metastasize to bone

prostate, breast, kidney, thyroid & lung



Cortical destruction

Soft tissue mass

Periosteal reaction

Ill-defined margins

Rapid growth

Lack of bone deformity – no remodelling


This category includes malignant bone tumors, infection

and agressive benign tumors such as eosinophilic granuloma



0- 1  Neuroblastoma

5-10  Eosinophilic granuloma

5-15  Ewing’s

10-20 Osteosarcoma

30-40 Fibrosarcoma

Parosteal sarcoma

Giant cell tumor


>40 Met

Multiple myeloma





Eosinophilic granuloma


Clear cell chondrosarcoma



Non-ossifying fibroma

Unicameral bone cyst

Giant cell tumor



Ewing’s tumor



Unicameral bone cyst


Fibrous dysplasia



Giant cell tumor

Aneurysmal bone cyst

Nonossifying fibroma

Chondromyxoid fibroma




Benign                            Malignant

– Osteoid osteoma          – Osteosarcoma

– Osteoma

– Osteoblastoma



Benign                            Malignant

– Osteochondroma          – Chondrosarcoma

– Chondroblastoma

– Enchondroma

– Chondromyxoid fibroma



Benign                                   Malignant

– Parosteal desmoid               – Fibrosarcoma

– Fibroxanthoma (NOF)        – Malignant fibrous histiocytoma

– Unicameral bone cyst




– Myeloma

– Reticulum cell sarcoma



Benign                                   Malignant

– Hemangioma                     – Angiosarcoma

– Glomus tumor

– Hemangiopericytoma



Benign                                   Malignant

– Giant cell tumor                – Adamantinoma


Remember to consider metastasis, lymphoma and infection

Vascular lesions can occasionally appear tumor-like

– Infarct

– Hemophilic pseudotumor


– Brown tumor of hyperparathyroidism


– Paget’s disease

– Eosinophilic granuloma



Infection -Tb/pyogenic

Pigmented villonodular synovitis

Hemophilia – due to intraarticular hemorrhage, synovial hyperemia

Synovial sarcoma – usually away from joint

Rheumatoid arthritis/JRA

Synovial osteochondromatosis





Fibrous dysplasia

Gaucher’s disease

Brown tumors



Eosinophilic granuloma








Osteoblastic metastasis

Osteoid osteoma

Sclerosing osteomyelitis

Healing benign lesion (FCD-NOF-bone cyst)


Bone island

Bone infarct

Avascular necrosis


Paget’s disease



Paget’s disease


Fibrous dysplasia


Osteogenesis imperfecta


Chronic osteomyelitis can develop squamous cell ca of sinus tract



Giant cell tumor

Aneurysmal bone cyst










Fibrous dysplasia


Eosinophilic granuloma

Aneurysmal bone cyst

Chondromyxoid fibroma




Giant cell tumor


Brown tumor of hyperparathyroidism

Benign fibrous histiocytoma


Eosinophilic granuloma



Patella is epiphyseal equivalent




Steroid therapy



Sickle cell anemia

Gaucher’s disease



Caisson disease

Occlusive vascular disease

Radiataion therapy



dense bone, fragmentation and compression

may see subchondral crescent



Fibrous dysplasia – polyostotic

Osteogenesis imperfecta


Enchondromatosis – Ollier’s disease – not hereditary

– malignant change in 25%

Gaucher’s disease – AVN + wide medullary cavity

Thalassemia – marrow packing, gallstones, extramedullary hematopoesis

Hemangiomatosis / lymphangiomatosis




– Osteogenesis imperfecta

– Scurvy

– Leukemia

– Steroid therapy

– Juvenile osteoporosis


– Postmenopausal

– Cushings disease

– Acromegaly

– Thyrotoxicosis

– Osteomalacia – bone softening, Looser’s zones

– Multiple myeloma

– Hyperparathyroidism

– Gonadal deficiency




Osteoblastic metastases (prostate, breast)

Paget’s disease – usually multifocal – cortical thickening




Renal osteodystrophy




Paget’s disease


Progressive diaphyseal dysplasia





Glycogen storage disease

Sickle cell anemia




Normal neonate

Hypervitaminosis D


Phosphorus ingestion




Bone tumors


Subperiosteal hemorrhage (trauma – hemophilia)


Histiocytosis X

Vascular stasis




Rheumatoid arthritis



Cleidocranial dysostosis

Eosinophilic granuloma

Post-traumatic osteolysis / stress osteolysis



Joint space narrowing



Soft tissue changes




Subchondral sclerosis

Cartilage calcification



Look at least destroyed but affected joint

Check 1st MCP for OA, ulnar styloid for RA




Rheumatoid arthritis

Pyogenic arthritis

Tuberculous arthritis

Reiter’s syndrome



Psoriatic arthritis (acute)





Psoriatic arthritis (chronic)


Neuropathic joint



Rheumatoid arthritis

SLE – no erosions

Jaccoud’s – no erosions – hx of rheumatic fever

Charcot joint



Rheumatoid arthritis (acute) – esp JRA

Psoriatic – “fuzzy wuzzy” periosteal reaction

Reiter’s syndrome

Pyogenic arthritis





– Hypertrophic pulmonary osteoarthropathy

– Pachydermoperiostosis

– Venous stasis

– Fluorosis

– Thyroid acropachy


– Physiologic periostitis of newborn

– Battered child syndrome

– Syphilis

– Scurvy

– Hemophilia

– Caffey’s disease – infantile cortical hyperostosis

– mandible & clavicles Leukemia



PYOGENIC            TB

Osteopenia           Early                      Late & extensive

Cartilage loss       Early                      Late, at periphery

Bone destruction                 Weight bearing    Nonweight bearing

Bony debris          Removed               Not removed




Rheumatoid arthritis



Ankylosing spondylitis


Down’s, Morquio’s




JRA – posterior elements

Ankylosing spondylitis – anterior & posterior

Myositis ossificans progressiva – posterior

Reiter’s – severe



Rheumatoid arthritis

SLE – Reiter’s

Ankylosing spondylitis


Down’s – hypoplastic peg



Ankylosing spondylitis





Calcification in paravertebral soft tissues due to inflammation



Degenerative disc disease





Wilson’s disease



Neurogenic tumor

Spondylitis (decreased disk space)

Trauma – hematoma

Metastasis – check pedicle

Extramedullary hematopoesis


Neurenteric cyst






Lead poisoning

Growth lines (stress)

Normal zone of provisional calcification

Healing rickets

Protracted anemia

Treated leukemia








Infection – chronic Tb

Normal asymmetry



Gaucher’s disease

Eosinophilic granuloma








Steroid therapy

Osteogenesis imperfecta




Osteoid osteoma




Unilateral pars defect on other side (stress)






Paget’s disease





Syringomyelia – 75% upper extremity

Tabes dorsalis – 80% lower extremity

Meningomyelocele – lower extremity

Diabetes – feet

Spinal cord tumors

Analgesics, anti-inflammatory Rx

Congenital insensitivity to pain


Fragmentation, bony debris, eburnation, dislocation – no osteoporosis



Nonunion of fracture



Osteogenesis imperfecta

Fibrous dysplasia

Ankylosing spondylitis

Cleidocranial dysplasia



Congenital – due to vertebral abnormalities such as hemivertebra

Idiopathic – most common – may progress

Neurofibromatosis – sharp angle scoliosis with kyphosis

Due to osteoid osteoma of neural arch

Paralytic – due to polio, cerebral palsy, syrinx



Hemoglobinopathies –  Sickle cell, Thalassemia

Metastatic neuroblastoma

Polycythemia vera



Idiopathic (familial)

Turner’s syndrome

Kleinfelter’s syndrome

Myotonia dystrophica



Renal failure


Milk-alkali syndrome

Hypervitaminosis D


Dystrophic tumor



Flexion teardrop/Extension teardrop

Hangman’s fracture (extension)

Jefferson bursting fracture (compression)

Bilateral interfacetal dislocation (flexion)

Hyperextension fracture/dislocation (extension)


Anterior subluxation though initially stable

shows 20% delayed instability



Grade 1 – Globular – not adjacent to an articular surface

– early degeneration

Grade 2 – Linear – not adjacent to articular surface

– extensive mucinous degeneration

Grade 3 – Linear – does extend to an articular surface

– true tear




Colle’s – Fracture of distal radius with dorsal angulation

Smith’s – Fracture of distal radius with volar angulation

Monteggia – Fracture of proximal ulna with disloc proximal radius

Galleazi – Fracture of distal radius with distal r-u disloc

Reverse Monteggia – Fx ulna w/ posterior dislocaton of proximal radius

Barton’s – Fracture distal radius with interarticular extension


GRUMP – Galleazi – Radius, Ulna – Monteggia – Proximal



Chance – Horizontal fracture of vertebral body & posterior elements

Lisfranc – dorsal & lateral dislocation of tarsometatarsal joints

Gamekeeper – disruption of ulnar collateral ligament of 1st MC

Bennett – base of thumb

Boxer – metacarpal shaft – usually 4th or 5th

Jones – base of 5th metatarsal



Lunate disloc – lunate dislocated volar directon

Perilunate – lunate w/ radius – carpals dorsally displaced

Rotary sublux of scaphoid – Terry Thomas sign, signet ring sign

Scaphoid waist fx-avascular necrosis proximal frag

50% in nondisplaced – 100% in displaced



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