Osteonecrosis is the death of bone tissue due to a lack of blood supply. It can be caused by trauma or other events that disrupt blood flow, such as fractures or dislocations. Imaging like x-rays and MRIs are used to stage osteonecrosis and monitor for signs of bone death and structural damage over time. The femoral head, humeral head, and scaphoid bone are particularly susceptible to osteonecrosis due to their vascular anatomy. Long term complications can include bone collapse and osteoarthritis. Prevention focuses on minimizing corticosteroid use and maintaining circulation for patients with conditions like sickle cell disease.

1. OSTEONECROSIS
Dr.PONNILAVAN

2. • Death of bony tissue from causes other than infection
• Usually adjacent to a joint surface
• Caused by loss of blood supply as a result of trauma or another
event (e.g.,SCFE)
Idiopathic osteonecrosis of the femoral head & Legg-Calvé-Perthes
disease may occur in pts with coagulation abn’l.
• antithrombin factors , protein C & S
• lipoprotein (a)

3. Non
Traumatic
causes
Causes are
Traumatic and
Non Traumatic
Coagulation disorders
• Familial thrombophilia
• Hypofibrinolysis
• Hypolipoproteinaemia
• Thrombocytopenic
purpura
Infections
• Osteomyelitis
• Septic arthritis
Haemoglobinopathy
• Sickle cell disease
Storage disorders
• Gaucher’s disease
Caisson disease
• Dysbaric osteonecrosis

4. At the turn of 12th
century, Adolph Lorenz
demonstrated his
vigororous techniques of
closed reduction of the
hip, however because
his reductions were so
forceful, he has been
called the “father of
avascular necrosis”

5. Femoral head circulation -
3 sources:
1. Intraosseous cervical vessels
2. Artery of ligamentum teres
3. Retinacular vessels (main
supply)
AVN –
Commonly affects the hip
joint
• Leads to collapse &
flattening of femoral head,
most frequently the
anterolateral region
Profunda
femoris
79%

6. The most important retinacular
vessels arise from the deep branch
of the medial femoral circumflex
artery. These vessels supply the
main weight-bearing area of the
femoral head.
At the junction of the articular
surface of the head with the
femoral neck there is a second ring
anastomosis termed the
subsynovial intra-articular ring.

7. If damage to these vessels during d/l , or
during reduction & also due to delay in
diagnosis & Rx AVN femoral head &
later to degenerative arthritis.
Avascular necrosis OA as a
long-term complication.
Incidence of osteoarthrosis is 75% in
long-term follow-up.

8. Osteonecrosis
• One of the common causes of painful hip in older children and adults in
regions where sickle cell disease is common.
• Onset being just before epiphyseal plate closure & involving only a part of
the epiphysis.
• Common presenting complaints - painful hip with restriction of movements
depending on the stage of disease.
• Late stage - gross deformity, shortening & painful hip.
• Frequently B/L
• Progress of the disease is slower when humeral head is involved as
shoulder is a non-weightbearing joint. AVN of smaller bones presents as a
painful wrist or foot depending on the site.

9. Pathogenesis
The medullary
cavity of bone is virtually a
closed compartment containing
myeloid tissue, marrow fat and
capillary blood vessels. Any
increase in fat cell volume will
reduce capillary circulation
and may result in bone
ischaemia.

10. Sickle-cell disease
Dysbaric ischaemia
Thrombocytopenia
Fat embolism
Arteriolar
occlusion
Marrow
oedema
Sinusoidal
compression
Vascular
stasis
Gaucher’s disease
Tuberculosis
Cortisone/alcohol
Dysbaric ischaemia

11. • AVN INCIDENCE - femoral head following operative Rx of acetabular
fractures - 3 to 9%
• majority of the cases identified b/w 3 & 18 months of Sx.
Increased risk in injuries asso. with a posterior fracture-dislocation,
suggesting that the fate of femoral head is determined at the time of
the initial injury.
Once patient develops AVN, THR remains Rx of choice.
AVN – occurs in 15% of the dislocations usually within a year. But it
can occur up to 3 years.

12. TRAUMATIC OSTEONECROSIS
• In fractures and dislocations of the hip
the retinacular vessels supplying the femoral head are easily torn. If, in
addition, there is damage to or thrombosis of the ligamentum teres,
osteonecrosis is inevitable.
Over 20% of the displaced fractures of femoral head are complicated by
avascular necrosis
• fractures of the scaphoid and talus
proximal fragment always suffers as principal vessels enter the bones
near their distal ends and take an intraosseous course from distal to
proximal

13. Pathology
• Bone cells die after 12–48 hours of anoxia
• A characteristic feature of ischaemic segmental necrosis is the
tendency to bone repair, and within a few weeks one may see new
blood vessels and osteoblastic proliferation at the interface between
ischaemic and live bone.
• As the necrotic sector becomes demarcated, vascular granulation
tissue advances from the surviving trabeculae and new bone is laid
down upon the dead; it is this increase in mineral mass that later
produces the radiographic appearance of increased density or
‘sclerosis’.

14. • Earliest stage of bone death is asymptomatic
• By the time the patient presents, the lesion is usually well advanced.
• Pain is a common complaint.
• It is felt in or near a joint, and perhaps only with certain movements.
• Some complain of a ‘click’ in the joint, probably due to snapping or
catching of a loose articular fragment. In the later stages the joint
becomes stiff and deformed.

15. • Local tenderness may be present
• if a superficial bone is affected, there may be some swelling
Movements – or perhaps one particular movement – may be
restricted
• in advanced cases there may be fixed deformities.

16. Imaging
• X-ray
• The early signs of ischaemia are confined to the bone marrow and
cannot be detected by plain x-ray examination.
• they rarely appear before 3 months after the onset of ischaemia
• X-ray changes:
(a) reactive new bone formation at the boundary of the ischaemic area
and
(b) trabecular failure in the necrotic segment.

21. Avascular necrosis – x-ray (a) Earliest x-ray sign - thin radiolucent crescent just below convex articular
surface where load bearing is at its greatest. This represents an undisplaced subarticular fracture in the early necrotic
segment.
(b) At a later stage the avascular segment is defined by a band of increased density due to vital new bone formation.
At this stage the femoral head may still be spherical and (unlike osteoarthritis) the articular space is still
well-defined.
(c) In late cases there is obvious collapse and distortion of the articular surface.

22. The cardinal feature distinguishing primary
avascular necrosis from the sclerotic and
destructive forms of osteoarthritis is that the
‘joint space’ retains its normal width because
the articular cartilage is not destroyed until
very late.

23. Staging the lesion-Ficat and Arlet
Stage 1 showed no x-ray change and the diagnosis was based on
measurement of intraosseous pressure and histological features of
bone biopsy (or nowadays on MRI).
In Stage 2 the femoral head contour was still normal but there were
early signs of reactive change in the subchondral area.
Stage 3 was defined by clearcut x-ray signs of osteonecrosis with
evidence of structural damage and distortion of the bone outline.
In Stage 4 there were collapse of the articular surface and signs of
secondary OA.

24. ARCO staging of osteonecrosis
Stage 0 Patient asymptomatic and all clinical investigations
‘normal’
Biopsy shows osteonecrosis
Stage 1 X-rays normal. MRI or radionuclide scan shows
osteonecrosis
Stage 2 X-rays and/or MRI show early signs of osteonecrosis
but no distortion of bone shape or subchondral ‘crescent
sign’
Subclassification by area of articular surface involved:
A = less than 15 per cent
B = 15–30 per cent
C = more than 30 per cent

25. Stage 3 X-ray shows ‘crescent sign’ but femoral head still spherical
Subclassification by length of ‘crescent’/articular surface:
A = less than 15 per cent
B = 15–30 per cent
C = more than 30 per cent
Stage 5 Changes as above plus loss of
‘joint space’ (secondary
OA)
Stage 6 Changes as above plus marked
destruction of articular
surfaces
Stage 4 Signs of flattening or collapse of
femoral head
A = less than 15 per cent of articular surface
B = 15–30 per cent of articular surface
C = more than 30 per cent of articular
surface

26. BONE SCAN
• A classic cold area
surrounded by a
rim of increased
uptake - AVN

32. • AVN - common complication of NOF # in children.
• With union of the # usually revascularization takes place.
Therefore, avascular necrosis is treated nonoperatively
in children.

33. Prox. humerus
AVN

34. Avascular necrosis of
the humeral head
14% - 3-part # Rx with closed reduction
34%- 4-part # .
Shoulder Pain & stiffness & may ultimately
require total shoulder arthroplasty.
AVN incidence is directly
proportional to complexity of # & extent of
surgical dissection
Malunion & AVN humeral head
in 3- and 4-part # usually requires prosthetic
replacement.
Frequently,
posttraumatic arthritis is
present on the glenoid surface, & a glenoid
component also should be used.

35. PREISER D/S
• Proximal 3RD scaphoid - intra-articular, except for
its attachment to lunate.
It is completely covered by hyaline cartilage, with a
single ligamentous attachment (the deep
radioscapholunate ligament) & negligible or
nonexistent independent blood supply.
Hence, the proximal third of the scaphoid is prone
to osteonecrosis. This also explains the high
incidence of nonunion & AVN proximal third
scaphoid.
# in this location take an average of 6 to 11 weeks
longer to heal than those in the middle 3rd , & have
an incidence of AVN of 14 to 39%.

36. AVN - 13 to 40% of all scaphoid #
# middle one-third of scaphoid bone are at a higher risk, with AVN of the proximal
pole being reported up to 30%. Nearly 100%of proximal pole injuries result in
avascular necrosis.
Independent of the fracture’s location, avascular necrosis has been reported to
occur in up to 50% of displaced.
AVN is suspected when the proximal pole remains radiodense & does not
participate in the disuse osteoporosis of the distal pole.
MRI may be useful in diagnosing avascular necrosis.

37. SCAPHOID
• K-wires are easier to insert and remove, do not require a radial
styloidectomy or extended approaches to facilitate exposure, and
provide satisfactory stability.
• They can be used in the presence of the avascular necrosis of the
proximal fragment when the screws are not advisable

38. Kienbock’s disease
- an isolated disorder of the lunate --from
vascular compromise to bone.
- Lunate # are relatively uncommon.
-often unrecognized until they progress to
Osteochondrosis of the lunate, at which time
they become symptomatic & are diagnosed as
Kienbock’s d/s.
Exact etiology and Rx of choice remain
controversial.
Other names (lunatomalacia,
aseptic necrosis, osteochondritis, traumatic
osteoporosis, osteitis and avascular necrosis of
lunate) reflect thecontroversy in etiology. This
condition produces significant disability in young
individuals.

39. • Reasons for early neglect are that the injury may be
ignored as a sprain, initial radiographs may be negative,
superimposition of radius, ulna and other carpal bones
on the lunate in the lateral view may confuse the picture
and osteonecrosis shows no radiographic evidence until
sclerosis and osteochondral collapse are seen.
• Hence, the diagnosis of Kienbock’s disease should be considered in
any patient presenting with wrist pain of uncertain origin.
• Classically, the patient is 20 to 40 years of age and
complains of wrist pain and stiffness of insidious onset
usually following trauma.

40. TALUS AVN
• Malunited neck of talus should
not be corrected by osteotomy
because it may cause
nonunion or avascular necrosis
of the body of the talus.
• If the body has developed
avascular necrosis. Blair's
procedure or calcaneotibial
arthrodesis may be indicated.

41. Sites vulnerable to ischaemic necrosis
• femoral head
• femoral condyles
• the head of the humerus
• the capitulum
• Proximal parts of the scaphoid and talus

42. Eponymous names for specific sites of
avascular necrosis
Ahlback disease: medial femoral condyle, i.e. SONK
Brailsford disease: head of radius
Buchman disease: iliac crest
Burns disease: distal ulna
Caffey disease: entire carpus or intercondylar spines of tibia
Dias disease: trochlea of the talus
Dietrich disease: head of metacarpals
Freiberg infraction: head of the second metatarsal
Friedrich disease: medial clavicle
Hass disease: humeral head Source –
www.radiopaedia.com

43. Iselin disease: base of
5th metatarsal
Kienbock disease: lunate
Kohler disease: patella or
navicular (children)
Kümmell disease: vertebral body
Legg-Calvé-Perthes
disease: femoral head
Liffert-Arkin disease: distal tibia
Mandl disease: greater trochanter
Mauclaire disease: metacarpal
heads
Milch disease: ischial apophysis
Mueller-Weiss disease: navicular
(adult)
Panner disease: capitellum of
humerus
Pierson disease: symphysis pubis
Preiser disease: scaphoid
Sever disease: calcaneal epiphysis
Thiemann disease: base of
phalanges
Van Neck-Odelberg
disease: ischiopubic synchondrosis

44. CONCLUSION
Prevention-
• Corticosteroids should be used only when essential and in minimal
effective dosage
• Anoxia must be prevented in patients with haemoglobinopathies.
• Decompression procedures for divers and compressed-air workers
should be rigorously applied.

45. THANK U
• SOURCE –MILLER REVIEW OF ORTHOPAEDICS
• HANDBOOK OF FRACTURES KENNETH J. KOVAL ( 3rd edition,
- Mercer’s textbook of orthopaedics & trauma ( 10th
edition)
- KULKANI
- APLEY ‘S