Osteonecrosis, also known as avascular necrosis, occurs when bone loses its blood supply and dies. It most commonly affects the femoral head. Early symptoms are often absent. As collapse occurs, pain and loss of function increase. Risk factors include alcoholism, corticosteroid use, trauma, and idiopathic causes. MRI is the most sensitive imaging test, showing changes in signal intensity and double line signs. Staging systems evaluate extent of involvement and prognosis. Treatment depends on stage, with core decompression or hip replacement for late stages with collapse.

1. Osteonecrosis
Under the guidance of
Dr. Sanjay singh sir
Dr. C.D. Sahu sir
Dr. Amit Kumar sir
Presented by
RAVISH KUMAR

2. Avascular necrosis
 Also known as osteonecrosis ,aseptic
necrosis, bone infarction
 Implies that a segment has lost its
blood supply so that cellular elements
within it die.

3. Anatomic predisposition for
osteonecrosis
Femoral head,
Humeral head,
Distal femur

4. Clinical presentation
Usually non-specific and depend on the cause and
location.
Early phase symptoms are variable and often absent or
relatively minor. This clinical latent period may range
from a few weeks up to 1 year in duration
Evident, particularly when the articular surface
collapses, altering joint function.. As progressive
collapse of the joint surface occurs, greater pain and
debility are to be expected.
localized and referred pain, antalgia, reduced and
painful ranges of motion,and adjacent muscle atrophy.
Metaphyseal and diaphyseal infarcts -completely
asymptomatic to acutely symptomatic.

5. Etiology
 Unilateral Bilateral
Common
 Spontaneous (idiopathic) Alcoholism
 Surgery Corticosteroid
therapy
 Trauma (fracture, dislocation) Spontaneous
(idiopathic)
Uncommon
 Gout Arteriosclerosis
 Hemophilia Caisson’s disease
 Infection Cushing’s disease
Gaucher’s disease
Hemoglobinopathy
Lupus
erythematosus
Pancreatitis

6. pathology
 Ischemia results to death of all component of bone
cell
 Revascularization is seen at the live marrow and
dead marrow interface.
 Necrotic zone is invade by capillaries , fibroblasts
and macrophages
 Fibrous tissue replace dead marrow and may
calcify.
 New osteoblast lay down fresh woven bone on
devitalise trabeculae
 Neovascularisation and ossification-creeping
substitution(Phemister)
 Bone ends and cartilage recieves nutrition from
synovial fluid.

7. Osteonecrosis- femoral head
VASCULAR SUPPLY: FEMORAL HEAD. There are two
sources of blood supply:
profunda femoris (1)and ligamentum teres (2). From the
profunda femoris the circumflex vessels (3 and 4) provide the
medial and
lateral epiphyseal arteries (5 and 6). It is probable that the site
of precipitating occlusion is at the lateral epiphyseal vessels.

8. Radiological features
 Anterosuperior location
 Cortical collapse (step defect)
 Cystic radiolucencies
 Degenerative joint disease
 Fragmentation
 Periosteal bone apposition
 Sclerosis (snowcap sign)
 Subchondral fracture (crescent, rim sign)
 Trabecular alteration
 Wedged or semilunar shape (bite sign)

9. EPIPHYSEAL INFARCTION: GENERAL
FEATURES.
F
A. Collapsed Articular Cortex. Observe the sharp, angular deformity (arrow) in the
weight-bearing cortex (step defect). Sclerosis of the femoral head is also evident.
B. Epiphyseal Fragmentation. Note that multiple cystic and linear lucencies
produce a mottled, fragmented appearance to the femoral head. This is owing to a
combination of fractures, subchondral cysts, and localized repair response.
C. Subchondral Fracture. Note the thin curvilinear radiolucency (arrow) just
beneath the weight-bearing articular cortex (crescent sign).

10. HIP AVASCULAR NECROSIS: PROGRESSIVE
ARTICULAR COLLAPSE
. A. Initial Film. Note the two sharp, angular deformities (step defects) at the weight-
bearing superior articular cortex (arrows). A slight increase in density is visible in the
femoral head.
B. 12-Month Follow-Up. Note that greater collapse is evident.Degenerative
changes have also intervened, with loss of joint space and osteophyte formation.
C. 18-MonthFollow-Up. Note that severe collapse and fragmentation have
occurred, with considerable lateral displacement of the femur.

11. Pathologic-Radiologic Correlation in Epiphyseal
Ischemic Necrosis
 Pathologic Feature Radiologic Feature
 Avascular Phase
 Loss of blood supply Small epiphysis
 Bone death Normal bone
density
 Cartilage growth Increased joint
space
 Low-grade synovitis Increased joint
space
Capsular swelling
 Disuse, hyperemia Metaphyseal
osteoporosis
 Widened growth
plate

12.  Revascularization Phase
 Neovascularization
 Periphery Peripheral sclerotic rim
 Center Homogeneous sclerosis
(snowcap)
 Subchondral fracture Crescent sign
 Fibrous and granulation tissue Clefts and fragmentation
 Woven bone Flattening of surface
 Altered biomechanical stress Widened metaphysis

13.  Repair
 Bone deposition- Reconstitution of epiphysis
 Regression of osteoclasis - Disappearance of clefts
 Deformity
 bone - Deformed, articular surface

14. Metaphyseal diphyseal
infarction
 Cortical or medullary
 Distal femur, proximal tibia and proximal
humerus
Cortical
 The periosteum is often activated to produce
a fine layer of new bone
 Localise rarefaction
Medullary
 Central location Metaphyseal-diaphyseal
location
 Elongated lesion Sclerotic, serpiginous
contour
 Focal internal calcification Unaffected adjacent

15. METAPHYSEAL-DIAPHYSEAL INFARCTS
Observe the characteristic central location, undulating
serpiginous contour, and dense calcific margin.

16. METAPHYSEAL-DIAPHYSEAL INFARCTS.
Plain Film. Note that two mature infarcts are present, one within
the metaphysis (arrow), the other within the proximal humeral
diaphysis (arrowheads).

17. Ficat staging
 Stage 1- No changes visible
 Stage 2-Disuse osteoporosis except devitalise
avascular bone which appears sclerosed.
 Stage 3-subcortical zone of transradiancy and
trabecular loss beneath thin sclerotic cortex leading to
microfractures followed by collapse and trabecular
compression.
 Stage 4-flattened articular surface with increase
subarticular density
 Stage 5- Osteoarthritis with joint space narrowing

18. MRI features of osteonecrosis
 Highly sensitive and specific for AVN
 Useful in equivocal radigraphs and contralateral normal
hip on radiographs
 Assist for decision to perform operative procedures
 T1W characteristic serpiginous area of altered signal
intensity of anterosuperior part of femoral head.
 T2WI double line sign(pathognomonic)
Outer low intensity rim and inner high intensity
band
bright band sign

19. T1 images

20. T2 images

21. Mitchell classification
 Based on appearace of center region
signal,bounded by low signal rim on T1 and T2W
images
 Class A –fat like signal characteristic
early stages of disease
Class B-subacute blood like
high signal on both T1 and T2
Class C-Fluid like signal intensity
Class D- fibrous tissue like changes

22. Mitchell class images
A and B: Mitchell class A and D AVN: T1W coronal (A), STIR coronal
image of both hips (B)—shows area of altered signal in both femoral heads
with fat intensity signal on T1W and STIR on the right side-class A
and hypointense signal on the left side-class D

23. Mitchell class C and D AVN. T1W coronal image (A), T2W fat
suppressed coronal image of both hips (B), shows bilateral areas of
altered signal in femoral head showing hypointensity on T1W and mixed
hypo- and hyperintensity on T2WI

24. Secondary findings-
 fatty marrow of intertrochantric region
 Increase amount of synovial fluid
 Bone marrow oedema

25. Secondary findings AVN
Fatty marrow infilteration
T1W coronal (A) and STIR coronal images of both hips (B), showing
increase in intertrochanteric fatty marrow on the right side with marrow
edema on the left side with bilateral AVN

26. STIR coronal image of both hips showing
joint effusion on the left side with bilateral AVN

27. Gadolinium enhanced
imaging
Bilateral AVN. T1W coronal (A) and T1W axial (B) fat suppressed,
postgadolinium image of both hips showing necrotic nonenhancing areas
with enhancing viable interface and viable fragments

28. Dynamic contrast study
detect early femoral ischemia
delayed peak enhancement is noted
ADC value are higher in hip AVN ,but
staging is not possible
MR spectroscopy can detect early
changes in lipid/water spectra

29. Prognostic indicators on MRI
 Percentage of weight bearing surface that is involved by
AVN lesion is most reliable factor.
 In coronal image if less than 25%femoral head is
involved ,there is less likelihood of lesion to develop
collapse
 If more than 2/3rd weight bearing surface is involved -
74%chance of collapse of head
 On saggital if reactive interface cross the 12 oclock-
82% chance of collapse
 High risk marker early conversion from hematopoietic to
fatty marrow and dense intact physeal scar

30. Pitfalls in Diagnosis
 Fatty conversion does not occur occasionally
 Synovial herniation pit
 Subchondral bone cysts
 Fovea centralis

31. Pitfall images
A and B: X-ray pelvis and both hips—AP view (A) shows decreased
joint space on the left with subchondral cystic changes and osteophytes
and T1W coronal image of both hips (B) depicting subchondral
cyst with osteophytes—degenerative changes

32. Study choice and workup
 Radiograph-AP and Frog leg lateral
projection
 Radionuclide imaging- Tc 99MDP or
Tc99S
In early phase-cold photopenic zone
pathognomonic for AVN
Late stage reactive hyperemia and
reparative response may result in
doughnut sign
 CT scan- adjunctive role, in pt. with MR
contraindication

33. prognosis
 Rate of progression is unpredictable
 If disease dicovered prior to articular
collapse-core decompression and
rotational osteotomy
 Hip arthroplasty done in patients with
interactable pain and femoral head
collapse