2. MSK p218-226 (Hip arthroplasty complications, Marrow, Metabolic/Misc)

Question 1

Total Hip Arthroplasty - complications (5)

Answer 1

Loosening.
Particule disease.
Stress shielding.
Wear patterns (Polyethylene Wear, Creep)
Heterotopic Ossification

Question 2

Loosening (3)

Answer 2

Most common indication for revision.
>2mm at the interface is suggestive on X-ray.
Migration of the component (including varus tilting of femoral stem) is diagnostic

Question 3

Particle disease (3)

Answer 3

Any component of the device that sheds particles will cause an inflammatory response.
Macrophages will try to deal with the particles.
Most commonly in non-cemented hips.
Tends to occur 1-5 years post op

Question 4

Particle disease - imaging (3)

Answer 4

X-ray: smooth endosteal scalloping (differs from infection).
Produces no secondary bone response.
Can be seen around screw holes (particles are transmitted around screws)

Question 5

Stress shielding (3)

Answer 5

Stress is transferred through the metallic stem, so the bone around it isn’t loaded.
Unloaded bone just gets resorbed (Wolff’s law)
Happens more with uncemented arthroplasty.
Increased risk of fracture

Question 6

Wear patterns (2)

Answer 6

Axial thinning of the area of weight bearing is normal (Creep).
Polyethylene wear is pathological if seen at the superior lateral aspect

Question 7

Heterotopic ossifications (3)

Answer 7

common (15-50%) and usually asymptomatic.
Hip stiffness is the most common complaint.
Seen more often in Ank Spond patients, who are generally prone to heterotopic ossifications, such that they’re given low dose prophylactic radiation prior to THA.

Question 8

Components of bone marrow (3)

Answer 8

Trabecular bone (support structure)
Red marrow (for haematopoiesis)
Yellow marrow (fat, purpose unknown)

Question 9

Bone marrow conversion (normal) (4)

Answer 9

Yellow marrow increases with age in a predictable, progressive way. usually completed by mid 20s.
Born with all red marrow, which converts to yellow from the extremeties to the axial skeleton.
Within each long bone, progression occurs from epiphyses/apophyses to diaphysis to distal metaphysis to proximal metaphysis.
Red marrow can be seen in humeral and femoral heads as a normal variant in adults

Question 10

Bone marrow - trivia (5)

Answer 10

Yellow marrow increases with age (replacing trabecular bone as that decreases with osteoporosis).
T1 MRI: Yellow is bright, red is darker than yellow (iso to muscle).
Red marrow should never be darker than normal disk or muscle on T1.
Red marrow increases if there is a need for more haematopoiesis (reconversion occurs in opposite order to conversion)
Marrow turns yellow with stress/degenerative change in spine.

Question 11

Leukaemia - bone marrow (4)

Answer 11

Proliferation of leukaemic cells results in replacement of red marrow.
Marrow will look darker than muscle (and normal discs) on T1. May be higher than muscle on STIR due to increased water.
T2 is variable but often looks like diffuse red marrow.

Question 12

Typical leukaemia appearances (2)

Answer 12

Lucent metaphyseal bands in child
T1 MRI showing marrow darker than adjacent discs and muscle.

Question 13

Infiltrative bone marrow conditions (3)

Answer 13

Most affect marrow diffusely.
Exceptions are Multiple Myeloma (focal deposits) and Waldenstrom’s macroglobulinaemia (infarcts)

Question 14

Chloroma (3)

Answer 14

Aka granulocytic sarcoma
“Destructive mass in bone of leukaemia patient”
Type of colloid tumour

Question 15

Calcium Hydroxyapatite (2)

Answer 15

Most pathologic calcification in the body is calcium hydroxyapatite, also the most abundant form of calcium in bone.
Causes calcific tendinitis.

Question 16

Calcific tendinitis (3)

Answer 16

Calcium is deposited in tendons around joints, most commonly shoulder, specifically supraspinatus tendon, usually at the insertion near the greater tuberosity.
Longus Coli muscle is also a common location on multiple choice tests.

Question 17

Calcific tendinitis - causes (5)

Answer 17

Can be primary (idiopathic) or secondary:
- Chronic renal disease
- Collagen-vascular disease
- Tumoural calcinosis
- Hypervitaminosis D

Question 18

Osteopoikilosis (3)

Answer 18

Bony islands, usually in epiphyses (differs from blastic mets or osteosarcoma mets)
Can be inherited or sporadic.
Osteopoikilosis tends to be joint centred, sclerotic mets are randomly distributed.

Question 19

Osteopathia striata (2)

Answer 19

Linear, parallel and longitudinal lines in the metaphysis of long bones.
Usually no clinical significance, can sometimes cause pain.

Question 20

Engelmann’s disease (6)

Answer 20

aka progressive diaphyseal dysplasia or PDD
Fusiform bony enlargement with sclerosis of long bones.
Bilateral and symmetric
Likes long bones, commonly tibia
Hot on bone scan
Can involve skill and cause optic nerve compression
Starts in childhood.

Question 21

Pituitary gigantism (3)

Answer 21

“Widening of joint space in adult hip”
Late stages, cartilage outgrows it’s blood supply, causing collapse and early onset OA.
Formation of endochondral bone at existing chondro-osseous junctions results in widening of osseous structure.

Question 22

PVNS - intra-articular disease imaging (4)

Answer 22

Plain film:
- Joint effusion with/without marginal erosions.
- Osseous erosions with preservation of joint space
- Normal mineralisation.
Cannot distinguish PVNS from synovial chondromatosis on plain film.
MRI shows blooming on gradient echo.

Question 23

Pigmented Villonodular Synovitis (PVNS) (2)

Answer 23

Rare, benign neoplastic process that may involve synovium of joint diffusely, or focally.
Can also affect tendon sheath.

Question 24

PVNS - intra-articular disease (3)

Answer 24

Basically synovial proliferation + haemosiderin deposition.
Knee is most commonly affected (65-80%).
Rx: Synovectomy (20-50% recurrence)

Question 25

PVNS - trivia

Answer 25

Unusual in kids, but when present it’s usually polyarticular.

Question 26

Giant Cell Tumour of Tendon Sheath (4)

Answer 26

PVNS of tendon.
Usually found in palmar tendons of hand.
Can cause erosions of underlying bone.
Soft tissue density, T1 and T2 dark (unlike T2 bright glomus tumour)

Question 27

Primary Synovial Chondromatosis - (6)

Answer 27

Primary and secondary (due to degenerative changes in joint).
Metaplastic/true neoplastic process (not inflammatory), resulting in multiple cartiilaginous nodules in the joint synovium, tendon sheaths and bursae.
Nodules eventually progress to loose bodies.
Usually affects one joint (70% knee), usually in 40s-50s.
Joint bodies (multiple, uniform) may demonstrate ring and arc calcifications, characteristic of chondroid calcification.
Rx: Removal of loose bodies, with or without synovectomy.

Question 28

PVNS vs Synovial Chondromatosis (3)

Answer 28

Both benign neoplasia.
PVNS associated with haemarthrosis, never calcifies.
Synovial chondromatosis not associated with haemarthrosis, may calcify.

Question 29

Soft tissue haemangioma - imaging (5)

Answer 29

Can look like phleboliths on plain film (characteristic of cavernous subtype).
CT: Intralesional fat.
MR: T1 and T2 bright, intralesional fat.
Well defined with lobulated border and heterogenous features.
Enhance avidly and may have blooming due to phleboliths.

Question 30

Lipoma aborescens (Imaging) (3)

Answer 30

MRI: T1 and T2 bright with response to fat saturation (like fat). Fat-fluid interface causes chemical shift artefact on gradient.
US: Frond-like hypoechoic mass with associated joint effusions.

Question 31

Secondary synovial chondromatosis (3)

Answer 31

Secondary to degenerative change, usually seen in older patient.
Extensive degenerative changes, fragments are usually fewer and larger compared to primary.

Question 32

Diabetic myconecrosis (4)

Answer 32

Infarction of muscle in poorly controlled T1DM.
Commonly affects thigh (80%) or calf
MRI: marked oedema with enhancement and irregular regions of muscle necrosis.
DONT biopsy, delays recovery and high complication rate.

Question 33

Soft tissue haemangioma (3)

Answer 33

Benign vascular tumour, comes in several types
Commonest is capillary.
More common in women and can enlarge during pregnancy.

Question 34

Lipoma aborescens (5)

Answer 34

Affects synovial lining of the joints and bursae.
“Front-line” depositions of fatty tissue.
Seen in late adulthood (50s-70s), most commonly in suprapatellar bursa.
Often associated with OA, chronic RA or trauma.
Usually unilateral

Question 35

AVN of hip - Causes (5)

Answer 35

• Perthes in kids
• Sickle cell
• Gaucher’s
• Steroid use
• Femoral neck fractures (more displacement/disruption of retinacular vessels = more risk)

Question 36

AVN of hip - imaging (6)

Answer 36

Typically affects superior articular surface, beginning more anteriorly.
Double line sign: Best on T2, inner bright line (granulation tissue) with outer dark line (sclerotic bone)
Rim sign: Best on T2: High T2 signal line sandwiched between 2 low signal lines, represents fluid between sclerotic borders of an osteochondral fragment. Implies stability (Stage III).
Crescent sign: X-ray (ideally frog leg): subchondral lucency seen more frequently anteriolateral aspect of the proximal femoral head. Indicates imminent collapse

Question 37

Stages of osteonecrosis (5)

Answer 37

0 = normal.
1 = Normal x-ray, oedema on MRI
2 = Mixed lytic/sclerotic
3 = Crescent sign, articular collapse, joint space preserved
4 = Secondary OA

Question 38

Thalassaemia (5)

Answer 38

Defect in Hb chain (alpha or beta, major or minor).
“Hair on end” skulls
Expansion of facial bones.
Rodent faces.
Expanded ribs “Jail-bars”
Frequently associated with extra-medullary haematopoiesis.
Will obliterate sinuses, unlike sickle cell