11. Osteonecrosis Flashcards
Death of osseous cellular components and marrow
Osteonecrosis
mc location for trauma induced osteonecrosis?
intracapsular epiphyses
Osteonecrosis from Alcoholism mc affects the
femoral head
Osteonecrosis from Alcoholism possibly due to
fatty liver releasing fat
emboli, and increased marrow fat
most common theory for Osteonecrosis from Corticosteroids
fatty liver emboli
rapid removal from high pressure environment (diving) which forms nitrogen bubbles in blood vessels causing bone infarction
Caisson’s Disease
extensive epiphyseal and metaphyseal necrosis may occur bilaterally
Caisson’s Disease
mechanical infringement of marrow sinusoids by
lipid-laden histiocytes causing femoral head necrosis
Gaucher’s Disease
RA and SLE due to vasculitis of peripheral blood vessels
causes
vascular thromboses and tissue infarction
Corticosteroids increase incidence of
Osteonecrosis
sludging, thrombosis, and eventual infarction especially in epiphyses and metadiaphyseal regions
Sickle Cell Anemia:
how manuy rads are needed to produce osteonecrosis?
3000
how many rads in children are needed to affect epiphyseal
bone growth
300 - 400
very rarely causes bone infarcts due to fatty emboli
Pancreatitis
medullary and epiphyseal infarcts may occur in 30%
of pts with
gout
anatomically predisposed to osteonecrosis
Intraartcicular epiphyses
AVN usually takes how long to run its course?
2-8 yrs
obliteration of epiphyseal blood supply leading to
death of marrow cells and osteocytes, bone growth stops but the Adjacent articular cartilage continues to
grow
AVN: Avascular Phase
new vessels into necrotic bone causes deposition of new
bone onto necrotic bone, and resorption of dead bone, trabeculae thicken and bone density increases
AVN: Revascularization Phase
Avascular necrosis of the shoulder showing subchondral radiolucent line, aka
crescent sign
deformity occurs due to stress and forces applied during
revascularization and remodeling
“Mushroom” deformity
AVN femoral head
Infarcts heal with calcification
serpiginous configuration of healed infarcts
occurs at area of greatest mechanical stress of cortex indicating localized impaction fracture of weakened necrotic bone (step defect)
Collapse of Articular Cortex from Epiphyseal Infarction
thickened, irregular trabecular pattern causes increased bone density revascularization and repair phases
Mottled Trabecular Pattern:
very common in femoral capital epiphysis and subcortical in areas of greatest articular stress
Subchondral Cyst Formation
due to weakening of subchondral bone
Subchondral Fracture
separates articular cortex from underlying cancellous
bone (rim sign, crescent sign)
Subchondral Fracture
central high signal intensity surrounded by a serpentine, thin low signal margin
MRI of Metaphyseal - Diaphyseal Infarction
Bone scan of AVN: Initially a focal area of decreased activity appears, corresponding to the ________
Later increased activity corresponding to the phase of _________
local ischemia, hyperemia and osteoblastic repair
on MRI for AVN in 80% of patients
Double Line Sign
outer line of double line sign is the
low signal from sclerotic periphery
inner line of double line sign is the
high signal from edema (granulation tissue)
cortical infarction causes widening of small tubular bones of hands and feet
Sickle Cell Anemia
bilateral asymmetrical involvement (50% of cases) buttock, groin, thigh, knee pain gradual increase in pain and decreased ROM
Femoral head AVN
An orthopedic surgeon should perform what before Crescent sign appears
Core Decompression
Drill hole in bone a thin layer is removed which reduces pressure while increasing blood flow
Core Decompression:
After a core decompression healthy bone is transplanted from one part of the body to the diseased area
Bone Grafting
most sensitive and will demonstrate changes of AVN within 1 week after infarction
MRI
at interface of viable and necrotic bone
Double Line Sign (MRI)
arc like curvilinear radiolucency in subchondral aspect
of weight bearing cortex of femoral head that represents a pathologic subchondral fracture
Crescent (Rim Sign)
Crescent (Rim Sign) is best seen on
Frog – Lateral view of hip
can you determine source of AVN by radiograph?
NO
Fractures that occur in the subchondral bone may be recognized by a
crescent lucent zone
NEW NAME for Spontaneous Osteonecrosis of the Knee (SONK)
Subchondral Insufficiency Fracture
Subchondral Insufficiency Fracture mc affects
medial femoral condyle of 60+ adults
Subchondral Insufficiency Fracture usually progresses to collapse, fragmentation and loss of joint space suggesting
Charcot’s joint
5 Stages Subchondral Insufficiency Fracture
Stage 1: Normal plain films, abnormal bone scan or MRI
Stage 2: Subtle flattening of femoral condyle
Stage 3: Area of radiolucency surrounding sclerotic area in subchondral bone
Stage 4: Radiolucency surrounded by a sclerotic halo
Stage 5: Secondary changes of DJD
decreased medial tibiofemoral joint space subchondral cysts, sclerosis, osteophytes, chondrocalcinosis, and
varus deformity
Progressive DJD from Subchondral Insufficiency Fracture
will permanently arrest growth at physis
1800-2600 Gy
radiation changes in Adult Bone
3000 Gy = threshold for bone cell death
5000 Gy = definite bone cell death
AVN of femoral capital epiphyses prior to
closure of growth plate (peaks 5-7 yo)
Legg-Calve-Perthes Disease
Legg-Calve-Perthes Disease on Bone scan shows _______ uptake in femoral head
decreased
increased medial joint space of hip
“Waldenstrom” Sign
sclerosis indicates revascularization (cap entirely sclerotic)
widening and shortening of femoral neck
Snow Cap Appearance
lucent defect at lateral epiphysis and adjacent metaphysis that indicates poorer prognosis
Gage’s Sign
Snow Cap Appearance and Gage’s Sign
Legg-Calve-Perthes Disease
overall enlargement of femoral head
Coxa Magna
flattening of femoral head
Coxa Plana
flattening of femoral head and increased transverse
dimension
Mushroom Deformity
flattening of femoral head and increased transverse
dimension
Mushroom Deformity
AVN of a metatarsal head (mc 2nd), females (13-18yo) with tenderness and pain over MT head
Freiberg’s Disease
AVN of carpal lunate with radiating wrist pain, swelling, entrapment neuropathy and DJD
Kienbock’s Disease aka Lunate Malacia
may cause mechanical stresses between lunate and
radius disabling vascular supply in up to 75% of cases
Negative ulnar variance
advanced scapholunate collapse & chronic instability of wrist (Lunatotriquetral ligament may also be damaged)
SLAC lesion
Sclerosis, irregularity and collapse of the lunate
Kienbock’s Disease
common, painful, self limiting disorder involving patellar
tendon-tibial tubercle complex in adolescents
Osgood - Schlatter Disease aka Traction Apophysitis
Do not confuse avulsed fragment with
multiple ossification centers of tibial tuberc
- overlying edema displaces soft tissue anteriorly
- thickening of patellar ligament
- poorly defined margins of patellar ligament due to edema
- blurring of infrapatellar fat pad
- distended infrapatellar bursa (MRI)
- increased signal at site of insertion of patellar tendon
Soft Tissue Changes in Osgood - Schlatter
traumatic growth arrest and growth plate fractures
(Schmorl’s nodes) during adolescent growth period that mc affects mid and lower TS
Scheuermann’s Disease
adolescent disorder that may cause spinal pain, cosmetic deformity, and predispose pt to thoracic disc
herniation and premature DJD
Scheuermann’s Disease
pain, fatigue, defective posture increased TS kyphosis
Scheuermann’s Disease (not AVN)
- irregular endplates disc space narrowing and fibrosis - increased TS kyphosis - multiple Schmorl’s nodes - anterior vertebral body wedging (5 degrees or more per vertebral body) - Limbus bones superimposed DJD scoliosis
Scheuermann’s Disease
Scheuermann’s Disease is thought to be due to a
growth abnormality of the vertebral body (anterior growth plage stops)
small necrotic segment of subchondral bone (Joint Mouse) mc in knee with clicking, locking, pain, joint effusion
Osteochondritis Dissecans
The Osteochondritis Dissecans Defect may contain
fibrous and fibrocartilaginous tissue
Osteochondritis Dissecans is mc in lateral aspect of
medial femoral condyle
MRI is helpful to assess Osteochondritis Dissecans lesion for
stability, detachment,
AVN, and loosening of fragment
Affects medial (MC) and lateral aspects of dome of talus active pts 20-40 yo
Osteochondral Lesions of Talus
fragment from medial posterior aspect of talus
due to
shearing force of distal tibia
forceful inversion that compresses the lateral talar border against the adjacent fibula and creates a small, thin, wafer shaped fragment is difficult to
identify
Lateral Talar Osteochondritis Dissecans
may involve any joint that is traumatized with a shearing-compressive force
Osteochondritis Dissecans
disease involving capitellum of distal humerus that produced changes similar to those observed in Legg Calve Perthes disease.
Panner’s Disease / Osteochondrosis
Panner’s should be distinguished from
osteochondritis
dissecans (which occurs in 13 + years)
Panner’s is caused by an interference
in blood supply to growing epiphysis
in patients under 20 years of age, capitellum is only supplied by
end arteries entering posteriorly
AVN of navicular
Kohler’s disease
Kohler’s Disease Treatment
soft longitundinal arch supporters, medial heel wedge, and limitation of strenuous activity
delayed (usually two weeks) vertebral body collapse due to ischemia and non-union of the anterior vertebral body wedge fractures after major trauma
Kummel disease
calcaneal Apophysitis from mechanical irritation
Sever’s Disease
Painful inflammation of the calcaneal apophysis
Sever’s Disease
