Osteonecrosis (AVN)

Definition

• In situ death of a segment of bone due to ischaemia

Locations

• Femoral Head
• Femoral Condyles
• Humeral Head
• Capitellum
• Lunate
• Scaphoid
• Talus
• ie. Convex bones or small cuboidal bones
• Following surgery
  • eg. Head of first metatarsal

Aetiology

• Trauma
• Fractures
• Dislocations
• Non-Traumatic
• Alcohol abuse
• Corticosteroid usage
• Caissons Disease
• Sickle cell disease
• Thalassaemia
• Gauchers disease
• Infection
• Congenital
  • medial (multiple epiphyseal dysplasia)
• Developmental
  • Perthes disease
  • SUFCE
• Idiopathic (most common)

Pathogenesis

• Due to ischaemia of bone
• Numerous theories
• Four mechanisms that are mutual rather than exclusive
• Interruption arterial supply
  • Capillary occlusion
  • Intraosseous capillary tamponade
  • Injury to vessel wall
• 1. Arterial insufficiency
  • Fractures & dislocations most often seen
  • SUFCE & Perthes related
  • NOF
    • poor associated collateral blood supply
  • DDH
    • following treatment
• 2. Intravascular Capillary Occlusion
  • Due to vascular sludging
  • Caissons Disease
    • nitrogen bubbles
  • Corticosteroids
    • fat emboli
  • Alcohol
    • fat emboli
  • Sickle Cell disease » abnormal RBC
• 3. Intraosseous Capillary Tamponade (intraosseous HTN)
  • Osteonecrosis as a compartment syndrome
  • Commonest cause of AVN
  • Corticosteroids
    • enlarged marrow fat cells
  • Alcohol
    • enlarged marrow fat cells
  • Post-infection
    • inflammatory response
    • also related to activation of intravascular DIC
  • Gauchers Disease
    • glycocerebroside in bloated macrophages
• 4. Vessel Wall Damage
  • DXRT
    • radiation-induced vessel disease
  • SLE
    • vasculitis
• Can also add…
  • Venous Occlusion (Chandler’s disease)
  • Venular pressure > Arteriolar pressure
  • Must be very extensive to produce vascular stasis
  • Capsular tamponade from effusion, trauma etc
  • Perthes disease
  • Infection

Pathogenesis

• Stages of disease process
• 1. Death
  • Ischaemic event
  • Segmental bone death
    • opaque yellow marrow
  • Marrow cells die in 6-12 hours
  • Osteocytes die in 24-48 hours
• 2. Inflammation/ Revascularisation
  • Capillaries & mesenchymal cells advance from adjacent live marrow
  • Grow into dead marrow spaces
  • Cuff of vascular granulation tissue
  • Mesenchymal cells differentiate
  • Pluripotential cells within femoral head
• 3. Repair
  • Macrophages remove the dead fat & cellular debris
  • Dead bone resorbed by the osteoclasts
  • Creeping Substitution
  • New bone laid down on the dead trabeculae by osteoblasts
  • Sclerosis on XR
  • If healing incomplete
  • Dead bone replaced by fibrous tissue & granulation tissue
  • Cystic areas appear within lesion due to osteoclastic resorption
  • Surrounding bone becomes sclerotic
  • At this stage fracture/ collapse can occur due to
  • Stress fracture of dead bone
  • Stress riser at edge of creeping substitution
  • Weakness of repair front trabeculae due osteoclastic activity
  • Dead bone may fracture without superior articular surface collapse
  • Due to strength of the subchondral bone
• 4. Remodelling
  • Dead trabeculae removed
  • Woven bone turned into lamella
• 5. Osteoarthritis
  • Secondary to collapse
  • Altered force transmission due to subchondral collapse

Traumatic AVN

• Overlying superficial cartilage to tideline that receives nutrition from joint fluid not involved
• Cartilage below tideline dies due to disruption of blood supply
• The bone below this area also necrotic
• Influx of inflammatory cells & macrophages to remove infarcted marrow
• Then see ingrowth of fibrovascular tissue that differentiates into osteoblasts & deposits new bone on dead trabeculae
• Then replacement of the central necrotic bone – Creeping substitution
• If fibrovascular tissue fails to reach infarct then necrotic marrow undergoes ectopic calcification – MUCH more common in non-traumatic infarcts

Atraumatic AVN

• The differences are related to the fact that the original fibrovascular tissue from first infarct prevents further new ingrowth of mesenchymal tissue after this & so it becomes calcified with repeated infarction
• The area of subchondral bone beneath viable cartilage resorbed & so stress fracture common in this area
• Interior of infarct remains unrepaired
• Subchondral/ Juxta-articular AVN
• Most commonly affects
• Anterosuperolateral portion of femoral head
• Central dome of humeral head
• Infarction of medullary bone & cortex
• Loss of medullary & cortical architecture
• Painful & progressive
• If subchondral collapse
• Crescent Sign
• Secondary Osteoarthritis
• Wrinkle appears at dead margin
• Then fissures appear
• Escape of bony detritus through crack into joint leads to synovitis
• Cartilage may lift off
• Fibrocartilage may form on sequestrum
• Stage 1
• Joint unaltered & external examination of joint shows no abnormalities
• Cut section of necrotic zone shows wedge shaped region with dull-yellow & chalky marrow in subarticular area
• Surrounding marrow separated by thin red hyperaemic border
• Microscopically the articular cartilage is viable down to calcified zone (tidemark)
• The subchondral bone has replaced marrow elements with eosinophilic granular material containing ghosts of fat cells
• Extensive calcification maybe present due to repeated AVN episodes
• At margin of infarct is proliferation of osteoblasts & fibroblasts/ capillaries moving into medullary space
• Radiologically not detectable
• Stage 2
• The overall shape of bone intact & articular surface radiologically intact
• However see Sclerotic Rim at the boundary between necrotic zone & unaffected marrow
• Central region of necrosis unchanged but the hyperaemic zone thicker
• Microscopically advancing front of granulation tissue, lipid laden macrophages, fibroblasts & capillaries at periphery & extending into necrotic zone
• A second front at a distance has dead bone being resorbed by osteoclasts – Creeping Substitution (Phemister) » removal of necrotic tissue whilst maintaining structural integrity
• Accounts for ↑ uptake on radionuclide scanning
• Stage 3
• Alteration in bone shape becomes radiologically identifiable
• Collapse in necrotic area occurs
• On gross inspection the trabecular bone is fractured below the bony end plate
• Subchondral fracture follows – Crescent Sign » the cartilage above springs back & lucent line produced
• Trabecular fracture due to
• – Cumulation of fatigue-induced microfractures
• – Weakness of trabecular bone in reparative front due to osteoclastic
• activity
• – Stress risers at the junction of necrotic bone & the reparative front
• Microscopically appears as bony & cartilaginous debris
• Overlying cartilage may still look viable
• Appearance of unstable non-united fractures elsewhere
• Deep trabecular fracture may produce no overlying changes although can see articular depression
• Stage 4
• Morphological changes of degenerative arthritis
• Medullary Osteonecrosis
• Infarction of medullary bone
• Usually caused by medical conditions
• Dysbarism
• Haemoglobinopathies
• Gauchers disese
• Most commonly affects
  • Lower femur
  • Upper tibia
  • Upper humerus
• Variable extent
• Asymptomatic usually
• Silent & non-progressive
• Similar pathology
• Collagen Calcium
• “Coil of Smoke” sign
• Pathology
• Dead marrow yellow & opaque
• Surrounded by dense collagen layer that maybe calcified
• Cortical width ↑ if close

Radiology

• Main change is calcification
• Wavy line of ↑ density – Coil of Smoke Sign
• Endosteal cortex thickened
• Difficult to distinguish from
• Bone island
• Calcified enchondroma
• Investigations
• Blood Tests
• Resistance to activated protein C
• Lipoprotein Lp(a)
• Protein C & S
• Tissue plasminogen activator & inhibitor
• Antiphospholipid antibodies
• Plain radiographs
• Mottling
• Sclerotic line at junction of dead bone
• Later
• Crescent sign with joint collapse (best seen in frog leg lateral of femoral head)
• Segmental collapse
• End-stage changes of Osteoarthritis
• Until Osteoarthritis joint space is maintained
• Dead bone appears dense due to
• Compression of dead trabeculae
• Subchondral fracture
• Calcium of dead marrow (saponification)
• Onlay of new bone on dead trabeculae
• Relative osteosclerosis with surrounding osteopenia
• Bone Scan
• Initially ↓ uptake
• Doesn’t absolutely predict AVN as revascularization may occur without necrosis
• Later ↑ uptake due to repair
• Hot later doesn’t necessarily predict good outcome as revascularization may be inadequate
• Non-specific
• Cold areas may be metastases
• Hot areas may have numerous causes
• Most useful to detect avascularity
• After acute femoral neck fracture or hip dislocation
• CT Scan
• Not useful in early stages
• Best to differentiate precollapse stage 2 from structural collapse of stage 3
• Good to detect
• Extent of subchondral fracture
• Flattening & collapse of articular surface
• MRI
• Gold standard in early detection
• Most sensitive & specific
• Femoral head most extensively studied
• Normal marrow rich in fat » High signal intensity on T1
• Dead marrow » Decrease in signal intensity on T1
• T1 see low signal line
• Earliest
• Avascular-Vascular bone interface
• T2 see double-line
• Outer low signal line is thickened trabeculae
• Inner high signal line is granulation tissue
• Advantages are
• Early detection » pre-radiological
• Accurate localisation & extent of area involved
• Change in signal early related to ↑ water content
• Functional Exploration
• 3-phase invasive investigations – Ficat
• Intraosseous pressure
• Abnormal > 30mmHg
• Intramedullary Venogram
• Biopsy
• No longer used
• Non-Traumatic Osteonecrosis of Femoral Head
• Epidemiology
• Most common in middle aged men
• M:F is 4:1
• Peak incidence is 30-60 years
• Bilateral in 50% of idiopathic & 80% of the corticosteroid-related
• Aetiology
• Exposure to alcohol & steroids make up 90% of cases where aetiology established
• Alcohol
• Most common presentation
• 15-75% of patients
• 5-30% of alcoholics develop AVN
• 50% bilateral
• Studies suggest as little as 400ml/ week is enough
• Most idiopathics likely to be alcohol-related
• Steroids
• Risk related to the length of treatment & size of dose
• Overall risk is 3-25%
• Interval from use to time of onset varies from 6 months to 3 years
• Often multiple sites involved
• Often bilateral (80%)
• Usually progresses to joint failure
• Conditions
• Post-Transplantation
• 20% initially
• Now 2% due to use of Cyclosporin instead
• Usually onset within 1 year but can be up to 6 years
• Involves the
• Femoral head
• Humeral head
• Femoral condyle
• In decreasing order of frequency
• Leukaemia/ Lymphoma
• Rheumatoid
• Asthma
• Differences from traumatic AVN are
• Anterolateral position of lesion in femoral head
• Repetitive nature of lesions compared with single event in traumatic form
• Clinical Features
• Aching pain in groin & thigh
• Radiates to knee & buttocks
• Gradual onset
• Occasionally sudden
• Initially mechanical
• ROM reduced due to pain particularly Internal rotation & Abduction
• Click
• Staging
• Ficat & Arlet (1980)
• Stage 1
• Onset of ischaemia
• Clinically evident
• XR normal
• MRI ± bone scan changes only
• Stage 2
• Pain
• Early XR changes
• Cystic/ Sclerotic areas appear
• Stage 3
• Structural changes
• Classical XR changes
• See Crescent Sign & Flattening
• Stage 4
• Degenerative changes
• Modifications
• Hungerford & Lennox
• Added Stage 0 to Ficat & Arlet
• Preclinical
• XR normal
• Bone scan cold
• MRI double line on T2
• Steinberg – Stages 0-6
• Stage 3 divided into those with & those without collapse
• Also quantified the extent of subchondral fracture
• A – Mild < 15%
• B – Moderate 15-30%
• C – Severe > 30%
• Japanese Investigation Committee
• Radiographic location
• Medial – A
• Central – B
• Lateral – C
• Florida Classification – Enneking
• Treatment
• NON-Operative
• Observation & Protected Weight-Bearing
• Stage 1 & 2 left untreated will collapse in 85% at 2 years
• Metanalysis of 21 studies & 819 hips at 3 years
• – 74% had radiological progression
• – 76% required arthroplasty
• – The incidence of radiological progression was related to stage
• time to failure was not related to degree of NWB
• The very small lesions < 15% may heal & not progress with non op treatment
• OPERATIVE
• Core Decompression (Forage)
• Ficat & Arlet 1964
• Rationale
• – Reduction of Intramedullary pressure
• – Stimulate angiogenic & osteoblastic responses (enhances creeping substitution)
• – Pain relief
• – Tissue for diagnosis
• Procedure
• – Fracture table & II
• – Lateral trochanteric approach
• – Hollow biopsy trephine – 8-10mm
• – The anterolateral part of head within 5mm of the articular surface
• – 3mm drill used to penetrate the necrotic segment to subchondral bone
• Results
• Divergence of opinion
• Metanalysis of 24 studies involving 1206 hips at 3 years
• 37% did not progress radiologically
• 33% required arthroplasty
• Success related to stage
• – Stage 1 – 84%
• – Stage 2 – 65%
• – Stage 3 – 47%
• Two studies compared core decompression with non-op treatment
• No collapse in 61% vs 39%
• No arthroplasty in 75% vs 29%
• Complications
• Uncommon
• Include
• – Subtrochanteric fracture
• – Infection
• Indications
• Stage 1 & 2 disease
• Stage 3 where not suitable for more extensive procedure
• Non Vascularised Bone Grafting
• Cortical bone graft into defect produced with core decompression
• Rationale
• Provides mechanical support for articular surface during healing
• Procedure
• Cortical strut graft from the
• – Ilium
• – Fibula
• – Tibia
• Inserted into core track
• Protected weight bearing for 3-6 months until radiographic evidence of healing
• Results
• Conflicting reports
• Success rates of 60-80% with short term follow up
• Some long term reports have 30% successful outcome
• Disadvantages
• Prolonged restricted weight bearing
• Indications
• Early stage 3 lesions ?
• Unsuccessful core decompression
• Vascularised Bone Grafting (Urbaniak 1987)
• Rationale
• To enhance revascularisation so that progression of necrosis altered
• Vascularised grafts undergo more rapid & complete incorporation
• Procedure
• Considerable variability
• Donor site
• – Ilium
• – Fibula
• – GT
• Muscle pedicle artery & vein used
• – Inferior gluteal
• – Profunda femoris
• – Circumflex
• Results
• Most studies have short term follow up in small numbers
• Most comprehensive is Yoo – 81 hips at 5 years
• Vascularised fibula to profunda femoris
• 91% of Stage 2 & 3 had Good-Excellent results
• 89% had no radiological progression
• However the rate of conversion to THR is identical to core decompression at 20%
• Indications
• Stage 2 or early Stage 3 lesion
• Young patient
• Large lesion
• Osteotomy
• Rationale
• Transfer load from necrotic area to undamaged part
• Transection of bone may afford decompression
• Procedure
• Maybe flexion/ extension/ valgus/ varus or rotational
• If superolateral then need
• Flexion
• Valgus
• If central then
• Varus
• Flexion
• Sugioka
• Transtrochanteric rotational osteotomy
• Technically demanding
• Can rotate through 90°
• Poor results if not intertrochanteric with damage to blood supply of the head
• Results
• Sugioka osteotomy in 52 hips Stage 3
• 56-69% at average of 5 years successful
• If > 50% involved then results poor
• Deterioration with time – only 40% of hips surviving 7-10 years
• Cumulative necrotic sector angle (Kerboul)
• Angle from centre of femoral head to edges of necrotic sector measured on AP & lateral films & added together – if < 200° then a favorable outcome after femoral osteotomy may be expected
• Disadvantages
• Make subsequent THR difficult
• Indications
• Stage 3 disease
• Small lesion
• No ongoing cause for AVN
• Hemiarthroplasty
• Poor results – 50% revision rate
• Loosening & Protrusio biggest problem
• Study showed almost universal acetabular cartilage disease at time of arthroplasty
• Total Hip Replacement
• Better results – preferred treatment?
• Failure rate higher than for other diagnoses
• Related to poorer bone stock
• 30-50% revision rates at 10 years
• In < 50 yo with AVN cemented THR (metal on poly) has 50% failure rates at 10 years (Dorr) – apparently no other study gives better results than this
• Arthrodesis
• Usually contraindicated
• As the disease is bilateral in 50-80%
• Reasonable option in young, active, heavy man with unilateral disease
• Electrical Stimulation
• Not proven technique
• May be adjunct to other surgery
• AVN of Humeral Head
• 2nd most common site
• Smoking ↑ risk 4x
• Primary vascular supply
• Anterior circumflex humeral artery
• Arcuate artery once in bone
• 26-75% rate AVN after 4-part fracture
• Avoid activities above shoulder height
• » Greatest joint reaction force
• Benefit of core decompression ambiguous
• 94% relief of pain with prosthesis