osteonecrosis

1. Dhanya

2. OSTEOCHONDROSIS-A group of
disorders that share features like –
predilection for the immature
skeleton,involvement of
epiphysis,radiologically characterised by
fragmentation,collapse
sclerosis&reossification.

3. Osteonecrosis – primary-unknown cause
-Secondary –occurs from known
causelike fracture,sickle cell anemia,steroids
 Trauma-simulate ischemic necrosis but lack histo
features .eg;osgood schattler,Blount’s d’
 Growth
variants.eg;sever’sd’s(calcaneal),scheuermann’s
d’s

5. PERTHES’ or LEGG-PERTHES DISEASE
OSTEOCHONDRITIS DEFORMANS
JUVENILIS
COXA PLANA
OSTEOCHONDROSIS OF HIP JOINT

6. Classified as one of the osteochondroses
– group of disorders characterised by AVN
& disordered endochondral ossification of
either primary or secondary centres of
ossification.
AVN of femoral capital epiphysis before
closure of the growth plate.

7. Aetiology remains unknown
Currently accepted that the disorder is due
to interruption of blood supply to capital
femoral epiphysis
Predisposing factors- heredity,trauma,
endocrine d/o,inflammation,nutrition,
altered circulatory haemodynamics.

8. Three primary sources
a. foveal vessels
b. superior & inferior epiphyseal vessels
from medial & lateral circumflex branches
of profunda femoris artery
c.metaphyseal vessels from bone marrow.

9.  During 4-7 yrs contribution by foveal &
metaphyseal vessels negligible.Majority being
derived from epiphyseal vessels esp. lateral
group.
 This solitary source of blood vascularity
predispose the patient to ischaemic necrosis by
not allowing for a collateral supply. Position of
these epiphyseal vessels on the femoral neck in
a subsynovial location renders it vulnerable to
disruption from fracture, intracapsular synovitis
or surgical pinning.

10. An ischaemic episode of unknown cause
occurs rendering femoral capital epiphysis
avascular. Endochondral ossification in
epiphyseal cartilage & growth plate cease
temporarily. Articular cartilage nourished by
synovial fluid continues to grow. Widened
medial jt. space & a smaller ossific nucleus
seen on radiograph.

11. Revascularisation of structurally intact but
avascular femoral capital epiphysis occurs.
Deposition of new immature woven bone
on avascular bone produces increase in
bone mass per unit area – increased
radiodensity of the epiphysis in early
stages.
Deposition of new woven bone &
resorption of avascular bone occur
simultaneously.

12. In subchondral area resorption exceeds
new bone formation. A critical point is
reached when subchondral area becomes
weak biomechanically & susceptible to
pathologic fracture.
Upto this point disease process is clinically
silent & child asymptomatic.
Continuation of this ‘potential’ form of
disease or development of ‘true form’
depends whether or not a subchondral
fracture occurs

13. Potential form – stresses & shearing forces
acting on revascularised femoral capital
epiphysis do not exceed strength of
weakened subchondral area, subchondral
fracture doesnot occur. No subluxation &
no deformity of femoral head.
Subchondral area regains its nl strength &
stability & a ‘head-within-a-head’
appearance seen radiographically. It
represents a growth arrest line that
outlines ossific nucleus at the time of initial
infarction.

14. True form – a pathologic subchondral
fracture occurs.it result from nl vigorous
activity rather than from a specific injury.
Only the true form produces characteristic
clinical and radiographic features.

15.  Subchondral fracture typically begins in the
anterolateral aspect of epiphysis near growth
plate b’coz this area receives max. stress during
wt bearing.Fracture extends superiorly &
posteriorly.
 Revascularised cancellous bone beneath
subchondral fracture undergoes second episode
of local ischaemia secondary to trabecular
collapse & occlusion of ingrowing capillaries.It
can involve either part or all of epiphysis.
 Later entire area is revascularised with
resorption of fibroosseus tissue by a process
termed ‘creeping substitution’. Gradually head is
remodelled depending on epiphyseal stresses
during the whole process.

16. Combined factors of pressure &
asymmetric growth results in a potential for
subluxation of the femoral head & eventual
deformity.

17.  The two ischaemic episodes produce ischaemic
changes in the growth plate also. Chondrocyte
columns of growth plate becomes distorted, do
not undergo nl ossification,resulting in excess of
calcified cartilage in the primary cancellous
bone.
 Sometimes the columns of cartilage extend
unossified into metaphysis producing
radiographic appearance of metaphyseal cysts.

18. Include presence of adipose tissue, osteolytic
lesions, disorganised ossification and extrusion
of growth plate.
Epiphyseal growth plate & metaphyseal
changes alter longitudinal growth of proximal
femur and produce short thick femoral neck
[coxa vara] and enlarged femoral head [coxa
magna]typically seen in Perthes disease.
Greater trochanter continues to grow nlly & may
eventually rise above the level of femoral head.

19. Incidence – 3 -12 yrs.peak 5 - 7 yrs.
M: F – 5 : 1
Bone age < Chronological age by 1-3 yrs.
B/L in 10 %. Two hips are affected
successively, not simultaneously. If b/l
symmetric involvement – other d/s like
hypothyroidism.

20. C/F : vague groin pain , occasionally
extending down to anteromedial knee or a
limp or both. Classic presentation
described as a ‘painless limp”
Abduction & internal rotation of involved
hip invariably produce pain.
C/C cases – prominent atrophy of thigh
muscles.

21. Plain X-ray
US
MRI
Tc-99 bone scan
Arthrography

22. 97% sensitive
78% specific
Limitations – may be entirely normal in
early symptomatic disease

23. Pathologic stage Radiologicfeature
capsular distension
increased jt space
Avascular lateral femoral
stage displacement
[0 – 12 months] small epiphysis

24. flattened small epiphysis
fragmentation
homogeneous sclerosis
[snowcapsign]
Revascularisation increased cortical density
[6 mths – 4 yrs] [head within a head]
metaphyseal cysts
patchy sclerosis
subchondral # [crescent
sign]
wide short femoral neck

25. Repair & remodelling gradualreconstitutionof
[1 – 2 yrs] density & configuration
coxa vara
Deformity coxa magna [enlarged
head]
coxa plana,mushroom
deformity [flattened
head]
large greater trochanter

26. Soft tissue swelling – in intra-articular hip
effusion pericapsular fat lines esp on the lateral
aspect of femoral neck will be convex rather than
the nl concave contour.
Increased medial jt space [waldenstrom’s
sign] – due to lateral displacement of femoral
head epiphysis along with effusion and/or
cartilage hypertrophy.
- evaluated by measuring the distance b/w
pelvic tear drop & medial femoral head [tear drop
distance] & comparing with the other side.

29.  Smaller obturator foramen – due to
projectional distortion of pubis & ischium
secondary to antalgic flexion, ext rotation & slight
abduction of involved hip.
- not a spfc sign, present in any painful
condition of the hip.
 Small femoral head – may be the only
radiographic sign early in the disease. Due to
lack of growth becoz of impaired blood supply.

31.  Wider teardrop size – not a reliable
singular sign of hip d/s but seen in
combination with other changes. Atrophy
of gluteal muscles on the affected side
allows a slight obliquity of the pelvis at the
time of radiographic exposure – widened
teardrop contour.

32.  Fragmentation – radioluscent clefts of
various sizes visible traversing the
epiphysis. Most characteristic is a
curvilinear lucent defect paralleling the
superior wt bearing articular surface
[crescent sign / rim sign].

34.  Sclerosis – of the involved epiphysis is a
manifestation of revascularisation where new
bone is deposited directly over dead trabeculae.
Within the capital epiphysis three patterns of
sclerosis may be seen.
- peripherally at the articular cortex – [head -
within-a-head appearance].
- in patchy segmented sequestered
areas.
- homogenous sclerosis of entire epiphysis
[snow cap appearance].

38.  Metaphyseal widening and shortening -
femoral neck is widened transversely and
decreased in overall length.
 Metaphyseal cysts – represent displaced
uncalcified growth plate cartilage.most
commonly located at the lateral and medial
aspects of the neck & simulates benign
neoplasm.Cystic lesions are found late in the
disease & will eventually disappear. A lucent
defect at the lateral epiphysis & adjacent
metaphysis [Gage’s sign] may occur early in the
disease – indicator of worse prognosis.

42. Enlarged greater trochanter –it is the
result of decreased longitudinal growth of
femoral neck with continued growth of
greater trochanter.

44. Other manifestations
- widened & irregular physis
- linear radiolucent submetaphyseal
band
- horizontally oriented growth plate
- irregular acetabular roof at its lateral
margin

47. Following completion of the disease
process, the reconstituted femoral head
may take on a number of altered
configurations.
- Coxa magna - overall enlargement
of femoral head
- Coxa plana - flattening of the head
- Mushroom deformity - combination
of flattening & increased transverse
diameter

48. -Coxa vara – decrease in femoral angle
< 120
-Sagging rope sign – a concave, curvilinear
radiopaque line seen superimposed over
the metaphysis caused by tangential
projection of the edge of deformed femoral
head.
- Superimposed degenerative changes –
loss of joint space, sclerosis &
osteophytes.

51. Cessation of growth at femoral capital
epiphysis
Subchondral fracture
Resorption of bone
Reossification of new bone
Residual /Healed stage

52. These x-rays of the hip
show the different
stages of the disease.
At first (stage I), there
are no detectable
changes on x-ray (fig
A). In stage II, there are
some changes but the
surface is still intact
(fig B). As the disease
progresses, the surace
begins to collapse (fig
C) until, finally, the
integrity of the joint is
destroyed (fig D).

53. Catterall
Salter And Thompson
Herring’s Lateral Pillar

54. Based on the radiographic appearance of
femoral head at the time of max.
epiphyseal resorption
Limited prognostic value – difficult to apply
in earlier stages.
Determined from plain AP & lauenstein
[frog leg] lateral views

55. Group I – anterior part of epiphysis involved
- no sequestrum
- no crecent sign
- no metaphyseal reaction

58. Group II – anterior part of epiphysis
involved, intact lateral margin
- sequestrum present
- crecent sign present anteriorly
- metaphyseal reaction localised
to anterolateral aspect

61. Group III – almost whole epiphysis
involved, loss of lateral margin
- sequestrum present
- crecent sign presentanteriorly
& extends posteriorly
- metaphyseal reaction diffuse
in anterolateral area

64. Group IV - involvement of whole epiphysis
- sequestrum present
- crecent sign present anteriorly
& posteriorly
- metaphyseal reaction is diffuse

67. Simplified classification
Based on the subchondral fracture
Dependent on early diagnosis
Prognostically valuable
Determining factor is the presence or
absence of an intact & viable lateral
margin of the capital femoral epiphysis

68. Type A :The extent of subchondral fracture
is < 50 % of the superior dome of the
femoral head - good result can be
expected
Type B : The extent of subchondral
fracture is > 50 % of the superolateral
portion of the femoral head -fair or poor
results can be expected.

69.  Group A: No involvement of the lateral pillar .LP
is radiologically normal. LP height is maintained,
may be lucency and collapse in the central and
medial pillars
 Group B: > 50% of the LP height is
maintained,some radio lucency is present
 Group C: < 50% of the LP height is
maintained,more radiolucent than in group B,
any preserved bone is at a height of < 50%

70.  Caterall’s grp III & IV
 Delayed diagnosis
 Early closure of growth plate
 Elevation of greater trochanter
 Extensive epiphyseal involvement females
 Horizontal orientation of growth plate
 Increased age of onset
 Lateral displacement of femoral head
 Lateral epiphysis outside acetabular rim
 Severe metaphyseal involvement

71.  Findings
 Early signs on CT scans include the following
 Bone collapse
 Curvilinear zones of sclerosis
 Subtle changes in bone trabecular pattern
 Disruption of an area of condensation of bone
formed by a compressive group of trabeculae
(abnormal asterisk sign

72. Late signs on CT scans include the
following:
Central or peripheral areas of decreased
attenuation
Intraosseous cysts
Coronal reconstructions can show
subchondral fractures, subtle buckling, or
collapse of the articular surface

76. Useful in preliminary diagnosis of transient
synovitis of the hip & onset of Perthes
disease.
If there is atleast 3 mm of fluid depth, a
difference between the two sides of 2 mm
& convexity of the capsule
Limitation – hip effusion is non - specific

78. Most sensitive& specific modality.
Typical marrow pattern is seen as
decreased intensity on T1,usually on
anterosuperior subchondral aspect of
femur laterally.
Rim remains low intense on both TI&T2

79. The asterisk sign is defined as findings of areas
of low signal intensity on T1-weighted images
and high signal intensity on T2-weighted
images in marrow.
 The double-line sign occurs in as many as
80% of patients and represents the sclerotic
rim, which appears as a signal void. This sign
is demonstrated as a line between necrotic
and viable bone edges with a hyperintense
rim of granulation tissue

80. Based on appearance of central region.the
area my simulate
1.fat,classA;High intensity on
T1.intermediate on T2.
2.blood,classB;high intensity on T1&T2.
3.fluid,classC;low in T1&High inT2.
4.fibrous tissue,classD;low in T1&T2.

87. Tc scan images of bone depends in part on
blood flow to bone
Avascular areas seen as scan defects
Helps in detection of the disease in the
early stage even before any radiological
abnormality is seen

89.  AVN of 2nd metatarsal head.
 Young adolescent(13-18yrs)
 F:M=5:1
 Pain,swelling,sudden aggravation upon activity.
 AVNsec to trauma or increased stress-
>revascularisation->bone absorption
&deposition->deformity &later degenerative
changes.

90. Articular cortex flattened&collapsed.
Sclerosis &radioluscent foci within head.
Subchrodal fractue-crescent sign
Joint space widened.
Thickened metatarsal cortex.

91.  5 Stage Classification
 Stage 1 Epiphyseal fissure fracture
 Stage 2 Central portion of bone re-
absorption
 Stage 3 Metatarsal head begins to flatten
 Stage 4 Intra- articular loose body
 Stage 5 Complete flattening of the
metatarsal head


92. EARLY STAGE I-II LESION, BEST
SEEN ON AN OBLIQUE
RADIOGRAPH
STAGE III LESION WITH
ADVANCED FLATTENING

93. STAGE IV LESION WITH ARTICULAR
COLLAPSE AND LOOSE BODY
FORMATION
STAGE V LESION WITH ADVANCED
DEGENERATIVE CHANGES INVOLVING THE
METATARSAL HEAD AND PROXIMAL PHALANX

94. BONESCAN - The use of bone scintigraphy has
been described with photopenia in the early stages
of the disease, with intense uptake later as the head
is reconstituted or revascularized
Magnetic resonance imaging (MRI) has been
advocated by some physicians as helpful for
preoperative evaluation, especially if an osteotomy
is planned.

95. Lunate osteochondrosis
Lunate malacia
M;F=9:1
worsoning pain&disability

96.  - stage 1: normal except for the possibility
of either a linear or a compression frx;
- stage 2: definite density changes
apparent in the lunate;
- stage 3: collapse of entire lunate.
- stage 4: stage III with generalized
degenerative changes in the carpus;

97. • Bone scanning may help exclude the presence of
Kienböck disease, but it is not specific enough to
exclude the many other causes of increased
uptake in the area of lunate.
MRI
• MRI is most helpful early in the course of the
disease when plain films are not diagnostic.
• T1- and T2-weighted images reveal decreased
signal intensity..

101.  Painful adolescent selflimiting disorder of the tibial
tuberosity owing to trauma.
 Males commonly.11-15yrs age
 Pain ,swelling,tendorness over tibial tubercle
 The condition is caused by stress on the patellar tendon
that attaches the quadriceps muscle at the front of the
thigh to the tibial tuberosity. Following an adolescent
growth spurt, repeated stress from contraction of the
quadriceps is transmitted through the patellar tendon to
the immature tibial tuberosity. This can cause multiple
subacute avulsion fractures along with inflammation of
the tendon, leading to excess bone growth in the
tuberosity and producing a visible lump.

103.  ACUTE;
 Soft tissue-displaced overlying soft tissue contour
-opacified infraptellar fatpad
-thickened poorly defined patellar tendon
-increased sig intensity within pat tendonT2
weighted
Tibial tuberosity-irregular anterior contour
-multiple isolated ossicles
HEALED;
Normal appearance
displaced skin contour
enlarged irregular tuerosity
persistent free ossicles

106. Llateral radiograph distal patellar tendon
ossification&opacified infrapatellar
bursae(white arrow)

107.  the patellar tendon was noted to attach more
proximally and in a broader area to the tibia in patients
with OS. In the acute stage, T1- and T2-weighted
magnetic resonance images demonstrate increased
signal intensity in the tendon at its insertion site.
Distended deep and superficial infrapatellar bursae are
frequently demonstrated.
 In the late stage, signal intensity in the abnormal
tendon and marrow edema may normalize. In some
cases, thickened cartilage is seen anterior to the tibial
tuberosity.
 Bone scan may demonstrate increased uptake in the
area of the tibial tuberosity .

109. MRIMAGE NORMAL STRIATED
QUADRICEPS(LARGE BLACK)
MRIMGE SHOWINPATELLAR
TENDON
THICKENING&HETEROTOPIC
OSSIFICATION(BLACK
ARROW)

111.  Scheuermann disease refers to
osteochondrosis of the secondary ossification
centers of the vertebral bodies. The lower
dorsal and upper lumbar vertebrae are
involved initially. The process may be limited
to several bodies or may involve the entire
dorsal and lumbar spine.
 Male>F;13-17yrs
 Mostcommonly middle &lower thoracic region

112.  The vertebral bodies are separated by a cushion, called an
intervertebral disc. Between each disc and vertebral body is a
vertebral end plate. Sometimes one or more discs in patients
with Scheuermann's disease squeeze through the vertebral
end plate, which is often weaker in patients with
Scheuermann's disease. This forms pockets of disc material
inside the vertebral body, a condition called Schmorl's nodes.
 A long ligament called the anterior longitudinal ligament
connects on the front of the vertebral bodies. This ligament
typically thickens in patients with Scheuermann's disease.
This adds to the forward pull on the spine, producing more
wedging and kyphosis

114. • Wedge-shaped vertebral bodies
• Arcuate and rigid kyphosis
• Narrow intervertebral disc spaces with
calcifications
• Prominent irregularities of the vertebral surfaces
• The vertebral plates are poorly formed and
develop multiple herniations of the nucleus
pulposus known as Schmorl’s node

115. Radiologic criteria for the diagnosis of
Scheuermann kyphosis:
• Hyperkyphosis greater than 40°
• Irregular upper and lower vertebral endplates with
loss of disc space height
• Wedging of 5° or more in 3 consecutive vertebrae

117. Lateral radiograph of thoracic spine
shows endplate irregularity and
vertebral wedging characteristic of
Scheuermann's disease

118. OCD is a form of
osteochondrosis limited to
the articular epiphysis.
Articular epiphyses fail as a
result of compression.
Both trauma and ischemia
probably are involved in the
pathology. Trauma is most
likely the primary insult,
with ischemia as secondary
injury

119. 11-20yrs
Mc in knee&ankle
M>F

120.  Knee: In the knee joint, the medial femoral
condyle is the most commonly involved.
Potential locations are the lateral aspect of
the medial femoral condyle (75%), the weight-
bearing surface of the medial (10%) and
lateral femoral condyles (10%)
 Elbow: In the elbow joint, the most common
site of OCD occurs in the anterolateral aspect
of the capitellum
 Ankle: In the ankle joint, OCD occurs more
frequently in the talus

121. Radiographic classification of osteochondral
lesions
 Stage I - Normal radiograph
 Stage II - Partially detached osteochondral
fragment
 Stage III - Complete, nondisplaced fracture
remaining within the bony crater
 Stage IV - Detached, loose osteochondral
fragment


123.  CT classification of osteochondral lesions of the
talus :
 Stage I - Cystic lesion of the talar dome with an
intact roof
 Stage IIa - Cystic lesion with communication to the
talar dome surface
 Stage IIb - Open articular surface lesion with an
overlying, nondisplaced fragment
 Stage III - Nondisplaced lesion with lucency
 Stage IV - Displaced osteochondral fragment


126. MRI classification of osteochondral lesions
Stage I - Bone marrow edema
Stage II - Subchondral cyst &Incomplete
separation of the osteochondral fragment
Stage III - Fluid around an undisplaced
osteochondral fragment
Stage IV - Displaced osteochondral
fragment

129. sonographic appearance of OCD
Stable - Localized, subchondral bony
flattening and normal articular surface/ with
nondisplaced osteochondral fragment
Unstable - osteochondral defect with
loose intra-articular fragment/ with slightly
displaced osteochondral fragment

132.  The common denominator in tibia vara cases is abnormal
stress placed on the posteromedial proximal tibial epiphysis
that leads to growth suppression. Predisposing factors for the
development of the condition include obesity, early walking,
and black ancestry
 Altered mechanical forces in the proximal tibia lead to
abnormal axial loading, which results in a change in direction
of the weight-bearing forces from the perpendicular to the
oblique. The oblique angle tends to displace the tibial
epiphysis in a lateral direction, overloading the posteromedial
segment and inhibiting its growth. A cycle of further
longitudinal growth is established, and this results in
progressive varus deformity

134.  Sex
 The infantile type of Blount disease demonstrates
female predominance, whereas the late-onset
types demonstrate a male predominance.
 Age
 There are 3 age peaks in persons with tibia vara:
 The infantile type occurs in patients aged 1-3
years.
 Late-onset juvenile type occurs in persons aged 4-
10 years.
 Late-onset adolescent type occurs in persons aged
11-14 years

136. Stage 1:progressive incr in varus
 -irregularity of growth plate
 -beaking of medial metaphysis
Stage2:wedging of epiphysis
 -depression of medial metaphysis
Sage3:metaphyseal beaking deepens
Stage4;cartilagenous gr plt narrows
Stage5:deformed articular surface
Stage6:grw plt fuses medially,lat nl growth

138. Left: Toddler with infantile Blount's
disease involving the left lower extremity.
Right: Radiograph of the left knee
demonstrates the Blount's abnormality of
the proximal tibia

139. MRI can demonstrate the extent of the physeal bar to
quantify the percentage of physeal involvement. On a
T2-weighted image, an open physis is bright and the
physeal bar appears black.
role for MRI in differentiating physiologic bowing from
Blount disease. Children who eventually had Blount
disease were found to have a depression of the medial
physis and abnormal signal intensity in the metaphysis
in addition to the lesion in the epiphysis. In
comparison, children with physiologic bowing were
found to have high signal intensity only in the
epiphyseal cartilage

141. Blount disease, increased uptake occurs
medially in the tibial plate, and
scintigraphic changes may also be seen in
the distal femur

142. physiologic bowing
 congenital bowing
 rickets
Trauma

143.  Difficulty may be encountered in differentiating infantile tibia vara
from physiologic bowing of the legs. However, the proximal tibial
angulation is acute in Blount disease, occurring immediately below
the medial metaphyseal beak. This feature results in a metaphyseal-
diaphyseal angle greater than 11º. In physiologic bowing, angular
deformity results from a gradual curve involving both the tibia and
the femur.
 Congenital bowing must be considered. The angulation may occur in
the middle portion of the tibia, with a normal-appearing distal femur
and proximal tibia.
 Rickets affects the skeleton in a generalized and symmetric fashion,
with loss of the zone of provisional calcification in the physis. In
addition, the typical biochemical abnormalities of rickets help
differentiate the conditions.

144. Calve's disease
Osteochondritis due to eosinophilic
granuloma of a vertebral body
Spontaneous collapse of vertebral body
due to AVN.

145. Avn involving tarsal navicular bone
M>F
Around 5yrs
Xray-naviculum shows sclerosis ,collapse
&fragmentation.
Joint spaces are preserved as a reflection
of cartilage noninvolvement.

147. AVN of capitellum of distal humerus
Males(5yrs)
Radiologically capitellum shows sclerosis
fragmentation collapse &reossification.

148. AP RADIOGRAPH OF THE ELBOW
DEMONSTRATES ABNORMALLY
INCREASED RADIODENSITY IN THE
CAPITULUM
T1-WEIGHTED MR IMAGE DEMONSTRATES
ABNORMAL LOW SIGNAL INTENSITY IN THE
OSSIFIED PORTION OF THE CAPITULUM

149. Calcaneal apophysitis
Radiologically apophyseal irregularity

151. The etiology appears to be a traction
tendinitis with de novo calcification in the
proximal attachment of the patellar tendon,
which had been partially avulsed
Males(10-14)yrs

153. an osteochondrosis involving the
phalanges of the hand and typically
occurring in young men between the ages
of 11 and 19 years. This disorder is also
known as epiphyseal acrodysplasia
Xray-irregularity ofepi of phalanges esp
middle finger&also shows sclerosis&
fragmentation->joint space narrowing.
HAAS’S DISEASE-juvenile avn of humeral
head