4. Definition
Cellular death of bone components secondary to interr
uption of blood supply
Consequent collapse of bone components
Pain, loss of function of joints
5. Areas commonly affected
• Femoral head
• Femoral condyles
• Head of humerus
• Capitulum of humerus
• Proximal part of scaphoid and talus
6. Predisposing factors
• Distance from vascular territory of bone
• Enclosed by cartilage limiting vascularity.
• Vascular sinusoids (type of capillaries which has open
pores which increases their permeability, and seen in b
one marrow, liver etc).
Are compressed by increased pressure and volume of
marrow tissue.
7. Pathophysiology
Interruption of blood flow to bone
Affect bones with single terminal blood supply:
Talus
Carpals, tarsals
Proximal humerus
Head of femur
Femoral condyles
Results in necrosis of Bone marrow, medullary cavity (
place where bone marrow resides) and cortical bone( t
ype of lamellar bone, with densely packed lamellae)
Final pathway from multiple causes
8. Pathways to necrosis
Bone necrosis after 12 – 48 hrs of anoxia
Reactive new bone formation around necrotic bone
Granulation tissue over necrosed bone – sclerosis
Structural failure in heavily stressed part of the necroti
c segment – linear fractures
9. Crack may break through the articular cartilage and at su
rgery necrotic part lifts off like cracked shell of hard boile
d egg.
Articular cartilage retains it's thickness but in final stages
deformity and destruction of joint surface is seen.
10.
11. The medullary cavity is the central cavity of bone shafts
where red bone marrow and/or yellow bone marrow
(adipose tissue) is stored. It has walls composed of
spongy bone (cancellous bone) and is lined with a thin,
vascular membrane (endosteum).
12. Traumatic causes
In fractures and dislocations of hip the retinacular vessels
supplying the femoral head are torn. If in addition, there is
damage to or thrombosis of the ligamentum Teres, osteone
crosis is inevitable.
In fractures of scaphoid, proximal part is more prone to n
ecrosis
13. • Fracture of talus, avascular necrosis is commonly seen. It is
because the anastomotic ring of blood vessels run postero-
laterally. Therefore blood supply is often cut off during neck
fractures.
14.
15. Non-Traumatic causes
• Intravascular thrombosis
• High dose of corticosteroids and alcohol abuse leads to
hyperlipidemia and fatty degeneration of liver.
• Hypercoaguable states- thrombophilia
• Systemic lupus erythrematosis - deficiency of anti-
phospholipid.
• Hematologic disorder- sickle cell anemia ( enhanced
coagulability)
16.
17. Extravascular marrow swelling
• High dosage of alcohol and corticosteroids leads to fat cell
swelling in the marrow.
• This leads to intra-osseous pressure increase and compression
of sinusoids as in femoral head.
Caisson disease and Dysbaric osteonecrosis
• Decompression disease seen in deep - sea divers and
compress air workers.
• Under increased pressure, the blood and other tissues (fat)
becomes super saturated with nitrogen.
18. • These gas bubbles leads to tissue damage and prolonged tissue
damage leads to swelling of marrow fat cells and decrease
blood supply due to toxicity.
Gaucher's disease
• Lack of enzyme glucocerebrocide in the macrophages of the
reticuloendothelial system.
• Affects spleen and bone marrow.
• Leads to sinusoidal compression in hip.
19. Radiation therapy
• Prolonged exposure to radiations leads to bone death.
• This is due to combined effects of damage to small blood
vessel, marrow cells and bone cells
Malignancy
• Corticosteroids
• Bisphosphonates (long term IV use leads to osteonecrosis of
jaw)
• Certain types of chemotherapy
• Radiotherapy
20. • Patients who are being treated for acute myeloid
leukaemia, acute lymphoblastic leukaemia, lymphomas,
testicular cancer, ovarian cancer, breast cancer, and
multiple myeloma have an increased risk of developing
AVN regardless of the treatment they receive
• Bone Marrow or Stem Cell Transplantation
21. Presentation - History
Trauma
Corticosteroid use
Alcohol intake
Medical conditions – malignancy, thrombophilia, SLE, SCD
22. Presentation - examination
Groin pain
Antalgic gait
Restricted ROM
Tenderness around bone
Muscle wasting
'Click' sound in the joints
Joint deformity
23. Imaging: X ray
Initially normal upto 3 months
Sclerosis
Flattening
Subchondral radiolucent lines (lines only seen in x-ray in b
one below the articular cartilage) (cresent sign)
Collapse of cortex
OA
24.
25. Imaging: CT scan
Used to assess extent of disease and calcification
Clearly shows articular deformity
Calcification and bone collapse
Central sclerosis in femoral head produces star shaped
structure (asterisk sign)
29. Radionuclide scan
Donut sign – central reduced uptake with surrounding
rim of increased uptake
More sensitive than plain films in early AVN
Less sensitive than MRI
Necrotic zone surrounded by reactive new bone forma
tion
30.
31. Histology
Definitive diagnosis
Usually a confirmatory during surgery for treatment
Occasionally biopsy of sclerotic lesion
Necrosis of cortical bone is followed by a regenerative
process in surrounding tissues.
32. Intramedullary pressures
Cannula into metaphysis
Measure at rest and after saline injection
Femoral head:
10 – 20 mmHg, increasing by 15 mmHg after saline
Markedly increased values in AVN (3 to 4 fold)
Less marked increase in OA
33. Ficat and the Steinberg Classification
Stage 1 • X-ray - no changes
• Diagnosis will be based on
intra-osseous pressure and
bone biopsy
Stage 2 Femoral head contour was
still normal but there were
early signs of Reactive
changes in the subchondral
bone
34. Stage 3 Clear evidence of
osteonecrosis and
structural damage and
distortion of bone
outline.
Stage 4 Collapse of articular
surface and signs of OA.
35.
36. Management principles
Early stages (I & II):
Bisphosphonates prevent collapse
Unloading osteotomies
Medullary decompression + bone grafting
Intermediate stage (III):
Realignment osteototmies, Decompression, Curettage
Arthrodesis
Late stage (IV):
Analgesia, activity modification
Arthrodesis
Total joint replacement
37. Management - conservative
Offloading affected joints with use of crutches
Immobilisation
Analgesia
Bisphosphonates delays bone break down in femur
Statins in patients on high dose corticosteroids – reduc
ed lipid deposition
38. Core decompression
8 – 10 mm anterolateral core of bone
Filled with bone graft (vascularised/non vascularised)
Decompresses medullary cavity, reduces pain
Vascularised graft may reverse necrosis
39.
40. Realignment osteotomy
Used to relocate necrotic area from weight bearing portion
of femoral head
Angular osteotomies more common
Multiple techniques for holding the fixation
41.
42. Arthroplasty
Main aim is pain reduction
Young patients will need revision
Higher failure rates than in OA
Hemi arthroplasty an option