Avascular Necrosis of Head of Femur, AVN, detailed, pathogenesis, histopathological staging, treatment options

1. Avascular Necrosis of
Femoral Head

2. Overview
• Introduction
• History
• Anatomy
• Epidemiology
• Etiology
• Pathogenesis
• Diagnosis and
staging
• Management
Source: sportsmedreview.com

3. Introduction
• Osteonecrosis, also referred to as avascular
necrosis (AVN), aseptic necrosis, and ischemic
necrosis, is not a specific disease but rather a
condition in which a circumscribed area of
bone becomes necrotic as a result of a loss of
its blood supply
• It is also known as CHANDLER’S DISEASES
[hip] and OSTEOCHONDRITIS DESSICANS

4. OSTEONECROSIS FEMUR HEAD
Osteonecrosis is death of living elements
of involved bone [cells including
marrow] with progressive destruction
and alteration of bone architecture as a
result of compromised vascularity.
The process is purely aseptic but may be
incited by loss of vascularity from
infarction.
Source: orthonorcal.com

5. History
• Osteonecrosis was first described by Hippocrates
circa 400BC
• First case of aseptic osteonecrosis was describe by
Paget in 1970
• Ficat (1985) stated this condition resulted from
blockage of osseous microcirculation with
intramedullary stasis and increased pressure

6. Blood Supply Of Femoral Head
Proximal end of femur is
supplied by three groups :
- Extracapsular arterial ring
- Ascending cervical branches of
retinacular arteries
- Arteries of ligamentum teres
Source: Orthobullets.com

7. Extracapsular arterial ring
• By medial femoral circumflex artery posteriorly and lateral circumflex
femoral artery anteriorly
• Minor contribution from superior and inferior gluteal arteries
Source: Researchgate.net

8. Ascending cervical branches
Ascending cervical branches of extracapsular arterial ring [also
known as epiphyseal arteries of Trueta of retinacular arteries
arises from ECA and ascend up the neck partly also supplying the
neck in due course .
• Divided into anterior, posterior, medial and lateral groups
• Lateral group is the most important group carrying the major
portion of blood supply to head and neck of femur

9. Concept of the Starling resistor as applied to
bone microcirculation.
a Raising the pressure in a rigid-walled
chamber can decrease fluid flow in a flexible-
walled tube passing through the chamber,
b In the case of bone, the intraosseous
extravascular compartment may function like
a rigid-walled chamber. Intraosseous
hypertension or space-occupying tissue may
sufficiently restrict microcirculatory blood
flow to produce ischemia
Intraosseous hypertension has been proposed
to develop from various inciting causes and is
considered the principal cause of ischemia in
non traumatic osteonecrosis.
Starling Resistor
Source: Europe PMC

10. Epidemiology
• Mean age of onset: 5th-6th decade
• M:W = 3:1 for non traumatic osteonecrosis
but the ratio is higher for traumatic
osteonecrosis as males seem to suffer high
velocity injuries more
• Atraumatic AVN is bilateral in 30-70%
but typically asymmetrical

11. Etiology
Source: Essential Orthopedics, principles and practice by Manish Kumar Varshney

12. Traumatic Osteonecrosis
• Dislocation of hip (10-25%) or
fracture neck of femur(15-50%)
• Prompt relocation helps in reducing
incidence of ONFH
• 52% hips dislocated for more than
12hrs developed ONFH compared
with 22% of those reduced within
12hrs

13. Dysbarism
• Also known as CAISSON Disease,
Decompression Sickness
• Tunnel workers and others associated
with deep sea diving (1-4%)
• Formation of nitrogen bubbles from
the dissolved saturated nitrogen of
the blood vessels due to sudden
decrease in the atmospheric pressure
precipitates infarction in the vascular
capillaries and eventually
osteonecrosis

14. Alcoholism
• 10-40% incidence
• There is increased risk of femoral head osteonecrosis in
individuals consuming greater than 400 ml of alcohol/
week
• Alcohol induces increase in serum triglyceride and
cholesterol levels along with liver and bone marrow fatty
infiltration.
• There is pyknosis in osteocytes due to triglyceride
deposition and ultimately death leading to an increased
percentage of empty osteocytes lacunae.
• Hyperlipidemic state – enhances thrombus

15. Source: Researchgate.net

16. Haemoglobinopathies
Mainly sickle cell disease(20-68%), hereditary
thrombophilia and antiphospholipid antibodies syndrome
can lead to sludging, thrombosis and eventual infarction
at capillary level

17. Drug Induced
• Steroids, phenytoin, indomethacin
• Steroid induced (10-30%): glucocorticoids are most
common cause of non traumatic osteonecrosis
• Mechanism :
Proposed hypothesis emphasis small vessel occlusion by fatty
emboli and increased impedance of sinusoidal blood flow
secondary to rise in intraosseous pressure [venous
obstruction]
• Patients receiving steroid therapy have an approximately
20 fold increase in their their likelihood of developing
osteonecrosis

18. Source: International journal of biological sciences

19. Collagen disease
• RA and systemic lupus erythematosus
• Inflammation of small peripheral blood vessels
promotes the formation of vascular thrombosis and
tissue infarction

20. Radiation
•The necrosis is primarily induced by vasculitis
caused by radiation that leads to thrombosis and
occlusion
•Capillaries are also damaged directly by
radiation and endothelial damage makes them
leaky which leads to development of bone edema
and further compromises vascular profusion
• A threshold dose of 3000 rads

21. Idiopathic
• Most common cause of osteonecrosis
• Factors rendering bone liable to infarction at its
articular edge
-small diameter of terminal vessels in subchondral
region
-lack of collateral circulation
-reduced blood flow in bone with high marrow fat
-in-expandable nature of bone tissue

22. Etiopathogenesis
• The bony compartment function essentially as closed
compartment within which one element can expand
only at expense of others
• Vascular occlusion and venous stasis leading to
osteocyte necrosis play a central role in pathogenesis
of AVN

23. Source: Essential Orthopedics, principles and practice by Manish Kumar Varshney

24. Pathogenesis
• Hypoxia
• Increased cell membrane permeability, which allows fluid
and electrolytes to enter the cell, causing it to swell.
• lysosomal enzymes are released
•Auto digestion or coagulation necrosis and cell rupture
• Vascular injury leads to tissue edema and haemorrhage

25. Inflammatory response ensues
Disappearance of osteocytes from
within their lacunae
Centre of the necrotic lesion
remains avascular and repair is not
possible
Repeated stresses
Dead trabeculae undergo micro
fractures that cannot be repaired
Source: Journal Laboratory Investigation

26. Transition zone at the periphery,
an active process of repair begins
Macrophages and osteoclasts
remove dead marrow elements
and bone
Granulation and fibrous tissue
are formed
Source: Journal Laboratory Investigation

27. Osteoblasts form new bone, laid
down directly on remnants of
dead trabeculae
The resulting trabeculae are much
thicker than normal
Responsible for the sclerotic
margin that surrounds the lesion
Source: Journal Laboratory Investigation

28. • Small lesion (not in a major weight-bearing region) -
Revascularization and completely replaced with
viable bone
• Larger lesions, particularly those in a region of major
weight bearing, have a poor prognosis - Gradual
collapse

29. If the contour of the
articular surface
remains intact, a fluid
filled space beneath
the cortical
subchondral bone
develops, which gives
the appearance of a
crescent sign on
radiograph

30. The mechanical stresses on the collapsed and irregular
articular surface Damage to and death of
chondrocytes
These abnormal stresses are transferred to the
otherwise normal cartilage of the acetabulum -
Secondary degenerative changes.

31. Joint space narrowing
Typical changes of degenerative joint disease appear
and include sclerosis, cyst formation, and marginal
osteophytes
End-stage arthritis of the hip eventually ensues

32. Histopathological staging
STAGE 1
Cut Section:
Necrotic wedge shaped (dull,
chalky, opaque and yellow),
sub articular lesion, well
demarcated
Micro :
Cartilage normal, subchondral
bone shows eosinophilic changes
lacking cellular elements, osteocytic
lacunae empty

33. • Margin of infarct : increased
osteoclastic activity with
infiltration of granulation tissue
(thin red rim)
• Beyond infarct and
hypervascular zone; bone and
marrow remain unchanged

34. STAGE 2
Articular surface remains
intact
Cut section : rim of bony
sclerosis at the boundary
between necrotic zone and
unaffected zone

35. Microscopy : advancing front of
granulation tissue following which
second front of osteoblasts
(creeping substitution)
- Increased vascularity with
osteoblastic activity and new
bone formation

36. STAGE 3
Alteration in shape of articular bone
Gross : buckling
Cut section : fracture just below
articular end plate or on the necrotic
side of advancing sclerosis in
reparative front
- Fracture occurs due to weakening
of trabeculae due to increased
osteoclastic activity

37. STAGE 4
Articular deformity
Cut section : residual
fragments of articular
cartilage and dense fibrous
connective tissue in the area
of infarction
- Articular surface dense
sclerotic eburnated
- OA changes

38. Clinical features
• Pain usual presenting symptom
• Intense and sudden in onset as in infarct or it can be
insidious and chronic
• Groin pain but radiating to anterior and anteromedial
thigh less common to buttocks
• Pain present at rest worsens with motion and weight
bearing
• O/E – Antalgic gait
Decreased ROM particularly flexion and IR

39. SECTORAL SIGN
The range of internal rotation is
less in hip flexion compared to
when hip in extension
Source: Jepomedicine.com

40. Imaging
RADIOGRAPHY
(AP view and frog leg lateral views)
• Initial Radiographs will be normal
Sequel:
•crescent sign
•Sclerosis
•Cystic changes
•Loss of spherical weightbearing dome
•Partial collapse of head
• Advanced cases : secondary OA

41. Kerboul Necrotic Angle
• Determined by measuring arc of the
articular surface overlying the lesion
on AP and lateral radiographs
• These two are added and referred
to as the combined necrotic angle
Source: Osteonecrosis by Babhulkar Sudhir

42. MR Imaging
• Abnormalities in femoral head on MRI can be made out as
early as 7 to10 days after the onset of symptoms
• Better precision
• Low intensity signal band on both T1 weighted and T2
weighted images – early abnormality
• In more advanced lesions – T1 images continue to show low
intensity signal but T2 images may exhibit signals of
alternating high and low intensity (double line sign)

43. MRI(T1)
MRI(T2)

44. Staging
Ficat and Arlet classification of osteonecrosis femoral head
Source: Jodt.org

45. Steinberg University Of Pennisilvenisa
Source:Researchgate.net

46. Source:THE JOURNAL OF BONE & JOINT SURGERY

47. CT Scan
• Can Visualize a small lesion not easily seen on routine
radiographs, and it may demonstrate small areas of articular
surface collapse that are not apparent on plain films
• It may also be used to help quantitate the extent of femoral
head involvement

49. Bone scan
• With technetium labelled phosphate analogue used for
early
detection of ON
• Not as sensitive as MRI
• During acute phase decreased uptake of bone
tracer associated with vascular compromise
• Increased accumulation in chronic venous stasis in
repair and revascularisation
• Can be useful, especially in assessing the status of
multiple joints

51. Goals of management
• Relief of pain
• Arrest the progression of disease
• Prevent the collapse of head
• Prevent secondary degenerative arthritis

52. Treatment Modalities
Non Operative/ Conservative Operative
Non weightbearing Core Decompression
Bisphosphonates Mesenchymal stem cell
implantation/ growth factor based
treatment
Anti-coagulants, statins,& other
vasodilators
Non-vascularized bone graft
Extracorporeal shock wave therapy Porous tantalum implant
Pulsed Electromagnet theory Vascularized bone graft
Hyperbaric oxygen Proximal femoral osteotomy
Arthroplasty

53. ALGORITHM OF OSTEONECROSIS FEMORAL HEAD MANAGEMENT
Source:Researchgate

54. Non operative Treatment
• Nonoperative management of Osteonecrosis femur
head includes restricted weight-bearing,
pharmacological agents and biophysical modalities of
treatment.
• The goal of drug treatment in the pre-collapsed stage
is to:
1. improve hip function
2. provide pain relief
3. prevent radiographic progression to subchondral
fracture and collapse
4. allow healing of the necrotic lesions.

55. Non- Weight Bearing
• Restricted weight-bearing using cane, crutches or a walker is effective in early-stages ON hip (Ficat and
Arlet Stage-I and II) when the osteonecrotic lesion is <15% and located far from the weight-bearing dome
(medial lesions)
• In 1/3rd of the patients with small or medium sized lesion [<50% of head involvement ] progress to symptoms
or collapse in spite of non weight bearing whereas large lesions have more chances of disease progression.
• Progression of the advanced stage depends largely on location, size of the lesion and aetiology
• Therefore non weight bearing modality of treatment cannot be accepted as a standard isolated modality of
treatment and maybe an additive treatment to medical or surgical management
• Decreases the degree of discomfort in patients who are symptomatic, they have not been shown to alter the
natural course of this disorder
• Following certain types of surgical procedures, such as core decompression, grafting, and osteotomies,
where it is used as an adjunct.
• Protects the weakened regions from fracture, and perhaps protects the femoral head as well, until the
healing processes have progressed satisfactorily

56. Bisphosphonate:
• Bisphosphonates promotes bone healing by inhibiting osteoclastic
activity in osteonecrotic lesion site
• It prevents collapse in early osteonecrotic hip or prevents onset of
subchondral fracture
• In advanced condition where collapse has already taken place, it
delays the need of total hip replacement surgery
• Therefore alendronate in osteonecrosis femoral head patients can be
used in a dose of 70 mg weekly for 3 years in stage I,II & III [
STEINBERG CLASSIFICATION]

57. Anticoagulants, Statins & other Vasodilators
• Thrombophilia and hypo fibrinolysis leads to venous stasis and reduce
arterial flow, thus increasing intra osseous pressure and hypoxic bone
death which has been postulated as a major and common etiological
factor for osteonecrosis.
• Systemic anticoagulation therapy started before irreversible segmental
collapse of the femur head may arrest or, speculatively, sometimes
reverse the process of ischemic osteonecrosis
• Lipid lowering agents are also helpful in steroid induced
osteonecrosis
• Steroid causes hyperlipidemia which increases the fat content and
also increases intracortical pressure, leading to sinusoidal collapse
and osteonecrosis

58. • Statins are lipid clearing agents that dramatically reduce lipid levels
and blood and tissues
• Adreno Corticotropic Hormone also shows some protection against
steroid induced osteonecrosis
• It enhances osteoblastic activity and stimulates vascular endothelial
growth factor that enhances neovascularization in femoral head

59. Extracorporeal Shock Wave
Therapy[ESWT]
• EWST enhances neovascularization by stimulating the
expression of angiogenic growth factors but the exact
mechanism is unclear
• It has been compared to core decompression and
found to improve function of hip to a greater extent
• It can be used as an adjunct with hyperbaric oxygen
therapy and bisphosphonates

60. Pulsed electromagnetic Therapy
• Pulsed electromagnetic therapy affects favorably in early
stage osteonecrosis through stimulation of osteogenesis and
angiogenesis similar to ESWT
• It can be used as an adjunct to core decompression

61. Hyperbaric Oxygen
• Mechanism:
1. Improves oxygenation
2. Reduces edema by
vasoconstriction
3. Induces angiogenesis
4. Reduces intraosseous pressure
and improves microcirculation
• Procedure:
100% oxygen at 2-2.4
atmospheric pressure for 90
minutes by mask for about 100
days to the patient of early stage
osteonecrosis.

62. Bone marrow infiltration
• The small no. of progenitor cells in the proximal
extremity of the femur with ONFH causes insufficient
creeping substitution after osteonecrosis
• Red bone marrow graft contains osteogenic
precursors, which help in the reparative process
• Used in adjunct to Core Decompression

63. Operative treatment
Surgical treatment for pre-collapsed stage ONFH involves hip
preserving procedures (CD, non-vascularized bone-graft, vascularized
bone-graft) whereas prosthetic hip surgery is reserved for advanced-
stage of collapse and arthritic hip.

64. Core decompression
• Core decompression is the most commonly performed surgical
procedure for treatment of early osteonecrosis femur head.
• Mechanism:
1. Decreases interosseous pressure
2. Increases blood flow to necrotic areas
3. Augmentation of new bone formation
• Core decompression is currently the gold standard management of
stage I & II osteonecrosis [ARCO system, i.e. precollapse]
• It has been cost effective surgical procedure for osteonecrosis femur
head
• Success of the treatment is largely dependent on the etiology, lesion
size, location or collapse of the lesion.

65. • Types:
1. Convention core decompression
2. Recent procedure
Convention core decompression:
• It is performed using 8-10mm cannula or trephine
• Disadvantage: potential risk of subtrochanteric fracture and hip joint
penetration.
Recent Procedure:
• This procedure is done by multiple small drilling [3mm diameter]
which has shown better results than the conventional core
decompression.
• The small diameter drill can more easily reach the anterior portion of
femoral head that is commonly involved with osteonecrosis.
• There is less risk of fracture, small incision and minimal morbidity
• The risk of bone weakening and articular surface penetration is
considerably reduced.
Post operatively patients are kept on protected weight bearing for about
6 weeks following conventional core decompression and about 3 weeks
when drilled with smaller drill holes

66. A
B
A: Conventional core
decompression
B: multiple small diameter core
decompression

67. Mesenchymal Stem-cell Implantation
• It augments osseous regeneration
in the necrotic lesion site.
• There is application of osteogenic
or angiogenic precursor cells with
or without growth factor
• Mesenchymal stem cells derived
from adult tissue represents a
highly promising option for the
treatment of osteonecrosis femoral
head in the pre-collapse stage.
• MSCs implantation has capability
to differentiate into multiple cell
lineages including the osteoblast,
chondrocytes and adipocytes.
• MSCs implantation can be used as
an adjunct to core decompression

68. Bone grafting
• Various authors have claimed success rate of 50 –
80% after CD with structural BG
• Non vascularised BG – Ficat 1 and 2
• Accurate placement of the graft within the lesion
and under the subchondral bone
• Standard core technique, Lightbulb technique,
Trap door technique

69. Non Vascularized Bone Graft
• Tibial autograft or fibular autograft or allograft are used to support
subchondral bone and articular cartilage after removal of the necrotic lesion
from the femoral head.
• The osteoconductive and osteoinductive properties of the bone graft help
inhaling of the osteonecrotic lesion.
• This modality of treatment is indicated in pre-collapse and early post collapse
[< 2mm collapse] osteonecrosis of femoral head where articular cartilage is
relatively undamaged [Ficat Stage I & II].
• Techniques:
1. Phemister technique [ grafting through core decompression track]
2. Trap Door [ grafting through a window created in femoral head]
3. Light Bulb Procedure [ grafting through a window created in femoral neck
or neck head junction]
• Rarely used as an isolated procedure, is usually combined with growth factors
and various bone graft substitutes.

70. Source: Europe PMC

71. Porous Tantalum Implant
• These implants provide structural support similar to that of bone graft.
• The porosity of this rod allows secure and rapid bone growth.
• Efficacy of porous tantalum rod can be further improved by addition
of bone marrow, growth factor or bisphosphonates.
• Avoids the risk of infectious complication and donors site morbidity
as seen with the use of allograft and autograft respectively

72. Vascularized Bone Graft
• Vascularized bone grafting is recommended modality of treatment
for early osteonecrosis femoral head [Ficat Stage I,II,III]
• The graft provides a viable structural support and prevents joint
collapse.
• Vascularized bone graft has osteogenic potential which augments
bone healing in the necrotic lesion site.
• Example:
1. Vascularized iliac crest graft
2. Vascularized fibular graft
3. Muscle pedicle bone graft

73. Muscle Pedicle Bone Graft
• Meyers first reported application of muscle pedicle bone graft for
treatment of osteonecrotic femoral head.
• Technique: After incorporating cancellous bone graft over the necrotic
lesion, quadratus femoris muscle with bone in its insertion is
elevated and placed over the necrotic lesion and fixed with cortical
screws .

74. Vascularised fibular graft
• Rationale :
- Decompression of femoral head
- Excision of the sequestrum
- Filling the defect with osteoinductive cancellous graft and
viable cortical strut
• Longer recovery period and less uniform and less
complete relief of pain
• Success rate 80-91% for younger symptomatic patients
without collapse

76. Proximal Femoral Osteotomy
Principal:
• Mobilization of the necrotic bone of femur head away from the load
bearing area, replacing it with the uninvolved healthy portion of the head.
• It reduces the intra osseous venous pressure and improves vascularity
Types:
• Trans trochanteric rotational osteotomy
• Intertrochanteric varus or valgus osteotomy (combined with flexion or
extension)

77. McMurray’s Osteotomy
• Thomas Porter McMurry became
famous for introducing an osteotomy
for treatment of nonunion of fracture
neck of femur but later on also
advocated for fresh femur neck
fractures and osteoarthritis of hip.
Technique:
• It is an intertrochanteric, oblique
osteotomy of the hip, where the distal
osteotomized femoral shaft is
displaced medially under the neck and
femoral head
• This osteotomy starts from lateral
femoral cortex just below the level of
lesser trochanter and proceeding
obliquely to finish medially just
proximal to lesser trochanter
• The inward pull of psoas major muscle
helps in maintaining medial
displacement of the distal femur under
the femoral neck and head.

78. • Valgus/Flexion osteotomy – anterolateral lesion
• Varus/Extension - Central or superomedial lesion

79. Source:Campbell, John J Callaghan

80. Arthroplasty
• Arthroplasty is the final treatment when all other modalities of
treatment have failed, or joint is arthritic secondary to advanced
collapse ( >2mm)
• AVN of head of femur forms one of the major indication for total hip
replacement
• Between 5-12% of total hip replacement are performed in the patients
having AVN of femoral head
Indications:
1. Patients with advanced osteonecrosis hip (> Stage III ARCO) any age
(Patients <30 years of age may still be considered for alternative
procedures)
2. Older patients (>50 years of age ) with stage III or more disease
3. Combined necrotic angle of >240 degree where the failure rate of
other procedure is significantly high
4. All cases of failed pervious surgery.

81. Contraindications:
1. Not to be used in the all those patients who can be reasonably managed with
joint preservation procedures for early stage disease.
2. Very young patient < 30 years of age
• Cementless Total Hip Arthroplasty has reassuring results in patients < 60
years of age with no other associative hip pathology
• Whereas patients with > 60 years of age achieve better results with cemented
total hip arthroplasty

82. There are different designs and materials in hip replacement
• Consist of 2 basic component: Ball and socket components
• Ball component: highly polished metal, ceramic material
• Socket component: high molecular weight polyethylene, ceramic,
metal
• Total hip replacement could be cemented and uncemented
• Decision is based on factors like age, quality and strength of bone
and affordability of the patient.
Source:Orthobullrts.com

83. Metal-on-polyethylene
metal (cobalt-chrome) femoral head on polyethylene acetabular liner
Benefits:
• longest track record of bearing surfaces
• lowest cost
• most modularity
Disadvantages:
higher wear and osteolysis rates compared to metal-on-metal and ceramics
smaller head (compared to metal-on-metal) leads to higher risk of impingement

84. •Metal-on-metal
Benefits:
•better wear properties than metal-on-polyethylene
•lower linear wear rate
•debris particles much smaller (but more numerous) than those of metal-on-poly
•overall smaller volume of particles
•larger head allows for increased ROM before impingement
Disadvantages:
•more expensive than metal-on-polyethylene
•increased metal ions in serum and urine (5-10x normal)
•serum metal ion concentration highest at 12-24 months
•correlates with the initial "wear in" or "run-in" phase of increased particle generation,
but then followed by a "steady state" phase of decreased particle generation
•may form pseudotumors
•hypersensitivity (Type IV delayed type hypersensitvity)
•mediated by T-cells

85. Ceramic on Ceramic
Benefits:
• best wear properties of all bearing surfaces
• lowest coefficient of friction of all bearing surfaces
• inert particles
• no concern for cancer risk
Disadvantages:
• more expensive than metal-on-polyethylene
• worst mechanical properties (alumina is brittle, low fracture toughness)
• small 28mm heads only exist in zirconia because of alumina's inferior mechanical
properties
• squeaking
• impingement and acetabular malposition
• third-body wear
• loss of fluid film lubrication
• thin, flexible (titanium) stems
• less modularity with fewer neck length options
• stripe wear, caused by contact between the femoral head and rim of the cup during
partial subluxation
• results in a crescent shaped line on the femoral head