Osteonecrosis Avascular Necrosis

Slide 1 · Osteonecrosis

(Avascular Necrosis)

Etiology • Morphology • Clinicopathologic consequences

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning objectives

Define bone infarction and identify its two principal anatomic patterns.

Explain the routes from ischemia to cell death, repair, collapse, and arthritis.

Correlate morphology with pain, imaging, staging, and management decisions.

Slide 3 · Osteonecrosis is infarction of bone and marrow

Bone infarction = death of bone and marrow after loss of perfusion

Vascular insufficiency causes ischemic necrosis of osseous tissue and its marrow.

The lesion may occupy trabecular marrow spaces or lie directly beneath a joint surface.

The anatomic location determines much of the clinical course.

Slide 4 · Why a bone infarct is mechanically important

Ischemia

Cell death

Weakened repair–load balance

Structural failure

Conceptual causal pathway

Viability and structural integrity are different properties of bone.

Slide 5 · Two osteonecrosis patterns

Feature

Medullary infarct

Subchondral infarct

Site

Trabecular bone and marrow

Immediately beneath articular cartilage

Typical structural outcome

Cortex spared

Risk of surface collapse

Clinical tendency

Often silent

Often painful

Slide 6 · Anatomic framework of the femoral head

Articular cartilage

Subchondral trabeculae

Cancellous marrow

Slide 7 · Perfusion and collateral protection differ by compartment

Cortical shell

Collateral periosteal circulation

Trabecular marrow

Local intraosseous vascular supply

Ischemic territory

Marrow necrosis with cortex spared

Compartment schematic

Slide 8 · Cartilage can survive while subchondral bone dies

Cartilage remains nourished

Bone below may be necrotic

Subchondral support is vulnerable

Slide 9 · Risk factors converge on impaired bone perfusion

LOCAL VASCULAR

Trauma / fracture

Vasculitis

DRUGS / THERAPY

Corticosteroids

Radiation

SYSTEMIC

Sickle cell crisis

Vascular compromise

UNASSIGNED

No known cause

Idiopathic group

Slide 10 · Trauma: Mechanical interruption of vessels

Fracture / disruption

Vessel interruption

Ischemia

Bone infarct

Conceptual causal pathway

A fracture can directly disrupt osseous vessels.

Slide 11 · Vasculitis: Vascular injury without a fracture

Vascular inflammation

Flow disturbance

Ischemia

Osteonecrosis

Conceptual causal pathway

Inflammatory damage can compromise the lumen or vessel wall.

Slide 12 · Sickle cell disease: A systemic ischemic setting

Sickle cell crisis

Microvascular obstruction

Bone ischemia

Infarction

Conceptual causal pathway

Sickle cell crises are recognized predisposing conditions.

Slide 13 · Corticosteroids: An important nontraumatic association

Corticosteroid exposure is included among drug-related risk factors.

A clear fracture history is not required for an ischemic lesion.

The mechanism of glucocorticoid-associated osteonecrosis is not fully established.

Slide 14 · Radiation: Therapy-associated vascular vulnerability

Radiation is listed among conditions predisposing to bone ischemia.

Prior irradiation should be considered in the exposure history.

The morphologic endpoint can resemble infarcts arising from other causes.

Slide 15 · Idiopathic osteonecrosis

No identified cause ≠ no ischemic mechanism

Some infarcts have no recognized predisposing cause.

The textbook estimates that approximately one quarter are designated idiopathic.

“Idiopathic” describes the limits of etiologic attribution—not a different morphology.

Slide 16 · Osteonecrosis of the jaw: Separate clinical context

The Robbins section notes a rare jaw complication of prolonged bisphosphonate treatment.

Medication-related jaw osteonecrosis should not be equated automatically with classic femoral-head infarction.

Its diagnostic framework is outside the present bone-infarct morphology sequence.

Slide 17 · Etiologic classification: Known versus unknown

Pathway

Recognized factor

Shared endpoint

Local vascular

Fracture; Vasculitis

Reduced perfusion

Systemic / exposure

Steroids; Sickle cell; Radiation

Reduced perfusion

Unassigned

Idiopathic

Bone infarction

Slide 18 · Three routes to an ischemic infarct

Mechanical disruption

Vessel cut / disrupted

Thrombotic occlusion

Lumen obstructed

External compression

Flow impeded from outside

Tissue ischemia → bone and marrow necrosis

Slide 19 · Mechanical disruption: Loss of continuity

Vessel damage

Distal hypoperfusion

Osteocyte death

Marrow injury

Conceptual causal pathway

An injured vessel fails to deliver blood to downstream bone.

Slide 20 · Thrombotic occlusion: Loss of luminal patency

Obstructed lumen

Decreased blood flow

Bone / marrow infarct

Conceptual causal pathway

A vessel can remain anatomically intact yet become blocked.

Slide 21 · Extravascular compression: Impeded flow

Pressure outside vessel

Flow compromise

Ischemia

Necrosis

Conceptual causal pathway

External pressure can compromise perfusion through a vessel.

Slide 22 · Different causes, identical final tissue injury

Vascular insult

Bone and marrow death

Attempted repair

Fate depends on location

Conceptual causal pathway

Etiologic agents differ upstream of ischemia.

Slide 23 · The biological lesion and the mechanical lesion differ

Biologic event

Structural event

Clinical result

Loss of viability

Architecture may persist

May be occult

Slow repair

Compression microfractures

Pain with loading

Failure of support

Articular surface collapse

Secondary arthritis

Slide 24 · Medullary infarcts are geographic lesions

Regional marrow + trabecular infarct

Preserved cortical rim

Schematic cross-section

Slide 25 · Why the cortex survives a medullary infarct

Cortical shell

Collateral periosteal circulation

Trabecular marrow

Local intraosseous vascular supply

Ischemic territory

Marrow necrosis with cortex spared

Compartment schematic

Slide 26 · Subchondral infarcts have a wedge-like geometry

Articular cartilage

Wedge of subchondral necrosis

Broad base near joint surface

Slide 27 · The gross femoral-head lesion

Pale wedge-like infarct

Compression fracture line

Gross morphology schematic

Slide 28 · Microanatomy: Osteocyte lacunae become empty

Empty osteocyte lacunae

Loss of nuclei in dead bone

Trabecular mineral matrix persists

Schematic illustration — not a clinical/histologic specimen

Slide 29 · Marrow adipocytes also undergo necrosis

Adipocytes in marrow spaces

Cell membrane injury and death

Fatty acids → calcium soaps

Schematic illustration — not a clinical/histologic specimen

Slide 30 · Fat necrosis produces calcium soaps

Adipocyte death

Fatty acids released

Calcium binding

Insoluble soaps

Conceptual causal pathway

Fatty acids are released from necrotic marrow adipocytes.

Slide 31 · What remains after the cells die?

Persistent dead trabeculae

Empty osteocyte lacunae

New bone apposed on scaffold

Schematic illustration — not a clinical/histologic specimen

Slide 32 · Microscopic recognition: Paired tissue compartments

Tissue

Key observation

Meaning

Trabecular bone

Empty osteocyte lacunae

Death of osteocytes

Marrow fat

Necrotic adipocytes

Marrow injury

Infarct repair

New bone and resorption

Reaction to dead scaffolding

Slide 33 · Dead trabeculae form the initial repair scaffold

Dead bone scaffold

Osteoblast activity

New matrix apposition

Conceptual histologic repair — all elements editable

Slide 34 · Osteoblasts deposit new bone on old trabeculae

Dead bone scaffold

Osteoblast activity

New matrix apposition

Conceptual histologic repair — all elements editable

Slide 35 · Osteoclasts resorb necrotic trabeculae

Dead bone scaffold

Osteoclast activity

Resorbed trabecula

Conceptual histologic repair — all elements editable

Slide 36 · Repair is not equivalent to immediate load-bearing recovery

Necrotic trabecula

Slow remodeling

Continued loading

Compression fracture

Conceptual causal pathway

The remodeling process consumes time while the joint remains mechanically loaded.

Slide 37 · Why subchondral infarcts collapse

Subchondral compression fracture

Dead support under load

Slow remodeling

Slide 38 · The subchondral fracture is a biomechanical turning point

Infarction

Trabecular weakening

Subchondral fracture

Loss of congruity

Conceptual causal pathway

A fracture changes the lesion from cellular necrosis to structural failure.

Slide 39 · Articular cartilage fails secondarily

Loss of articular support

Surface deformation

Secondary cartilage damage

Slide 40 · Secondary osteoarthritis is the late joint outcome

Distorted joint surface

Cartilage loss

Secondary osteoarthritis

Slide 41 · Morphologic sequence: Ischemia to arthritis

Ischemia

Bone/marrow necrosis

Incomplete repair

Fracture + collapse

Secondary OA

Sequence is conceptual; Durations vary by patient and lesion

Slide 42 · Medullary versus subchondral: Why outcomes diverge

Parameter

Medullary

Subchondral

Configuration

Geographic trabecular focus

Triangular subarticular focus

Cortex / cartilage

Cortex spared

Cartilage initially viable

Typical consequence

Usually silent

Collapse → osteoarthritis

Why different?

Less direct effect on joint surface

Load-bearing plate loses support

Slide 43 · Clinical expression depends on infarct location

Pattern

Anatomic condition

Expected presentation

Medullary

Away from articular support

Often silent

Subchondral

Beneath load-bearing cartilage

Pain; Risk of collapse

Collapsed

Irregular joint surface

Secondary OA phenotype

Slide 44 · Early subchondral pain is activity related

Load-dependent symptoms connect structure to function

Pain may initially appear with weight-bearing activity.

A vulnerable load-bearing segment is being mechanically stressed.

Early clinical severity does not establish the full extent of necrosis.

Slide 45 · Pain may become constant with progression

Load-related pain

Subchondral failure

Secondary changes

Persistent pain

Conceptual causal pathway

Fracture and secondary joint changes can make pain persistent.

Slide 46 · Medullary infarcts may remain undetected clinically

Regional marrow + trabecular infarct

Preserved cortical rim

Schematic cross-section

Slide 47 · Femoral-head osteonecrosis: Clinical integration

Loss of articular support

Surface deformation

Secondary cartilage damage

Slide 48 · A relevant history narrows the differential

Ask about fracture or dislocation, corticosteroid exposure, and systemic disorders.

Radiation and vascular inflammatory disease may be relevant.

Risk-factor absence does not exclude idiopathic osteonecrosis.

Slide 49 · Suspected femoral-head osteonecrosis: Imaging workflow

Suspect osteonecrosis

Radiography

If occult: MRI

Assess fracture / stage

Conceptual causal pathway

Slide 50 · Plain radiographs: Useful for structural change

Late changes can include a sclerotic margin or focal osseous abnormality.

A subchondral crescent sign reflects fracture.

Radiography may be normal before overt structural change appears.

Slide 51 · MRI: Detecting the pre-collapse lesion

Clinical suspicion

Radiograph normal

MRI demonstrates lesion

Pre-collapse assessment

Conceptual causal pathway

MRI can show an osteonecrotic area before radiographs become abnormal.

Slide 52 · 2019 revised ARCO classification: Four stages

I

X-ray normal

MRI positive

II

Bone changes

No fracture

III

Fracture

± depression

IV

Secondary

Osteoarthritis

2019 revised ARCO staging; For osteonecrosis of the femoral head

Slide 53 · ARCO stage I: Occult on the radiograph

Stage I: X-ray normal; MRI / bone scan positive

Plain radiographs do not yet show abnormalities.

MRI or bone scintigraphy identifies the lesion.

This is a pre-collapse imaging category.

Slide 54 · ARCO stage II: Abnormal bone but no fracture

Stage II: X-ray abnormal; No fracture or flattening

Radiographs show sclerotic, osteopenic, or cystic change.

Neither subchondral fracture nor femoral-head flattening is established.

Stage II remains within the pre-collapse spectrum.

Slide 55 · ARCO stage III: Fracture has developed

Stage III is defined by fracture; IIIA and IIIB use 2-mm depression

Radiography or CT demonstrates fracture in the subchondral or necrotic zone.

Stage IIIA: Femoral-head depression ≤ 2 mm.

Stage IIIB: Femoral-head depression > 2 mm.

Slide 56 · ARCO stage IV: Secondary osteoarthritis

Stage IV: Radiographic osteoarthritis

Radiographs demonstrate an osteoarthritic joint.

Joint-space narrowing and acetabular change may accompany destruction.

This category represents an advanced articular consequence.

Slide 57 · Staging records the major pathologic transition

Stage

Radiograph / CT

Major distinction

I

X-ray normal

MRI / scan positive

II

Bone changes, no fracture

Pre-collapse

III

Fracture ± depression

Subchondral failure

IV

Osteoarthritic joint changes

Secondary joint degeneration

Slide 58 · Management responds to structure, symptoms, and stage

Assess lesion and function

Pre-collapse options

Structural collapse

Arthroplasty if needed

Conceptual causal pathway

Slide 59 · Conservative strategies: Mechanical symptom control

Reducing weight-bearing can lessen stress on vulnerable trabeculae.

Immobilization or activity modification is included’s management spectrum.

These approaches do not guarantee reversal of established infarction.

Slide 60 · Hip-preserving surgery is stage dependent

Core decompression is a possible early-stage, pre-collapse procedure.

The procedure seeks to reduce intraosseous pressure and facilitate revascularization.

Outcomes depend on lesion characteristics and whether collapse has occurred.

Slide 61 · Advanced collapse may require joint replacement

Femoral-head deformation compromises load-bearing congruity.

Secondary osteoarthritis can create marked pain and loss of function.

Hip arthroplasty is among surgical options for advanced disease.

Slide 62 · Case: Pain after prolonged corticosteroid treatment

CLINICAL PROBLEM

• A 46-year-old develops gradually increasing groin pain without remembered trauma.

• The patient has received long-term systemic corticosteroids.

? Plain radiographs are unrevealing. What study best evaluates suspected early osteonecrosis?

Slide 63 · Case reasoning: Detect disease before collapse

Suspect osteonecrosis

Radiography

If occult: MRI

Assess fracture / stage

Conceptual causal pathway

Slide 64 · Case: Subchondral fracture and deformation

CLINICAL PROBLEM

• A patient with established femoral-head osteonecrosis develops persistent pain.

• CT shows fracture in the necrotic zone and 3-mm head depression.

? Which 2019 ARCO stage best describes these findings?

Slide 65 · Case reasoning: ARCO IIIB

I

X-ray normal

MRI positive

II

Bone changes

No fracture

III

Fracture

± depression

IV

Secondary

Osteoarthritis

2019 revised ARCO staging; For osteonecrosis of the femoral head

Slide 66 · Case: Incidental medullary bone infarction

CLINICAL PROBLEM

• An incidental geographic lesion involves trabecular marrow within a long bone.

• The cortical shell is preserved and there is no nearby articular collapse.

? What morphology-based clinical tendency is expected?

Slide 67 · Case reasoning: A medullary infarct may be silent

Regional marrow + trabecular infarct

Preserved cortical rim

Schematic cross-section

Slide 68 · Microscopic challenge: Identify necrotic bone

Empty osteocyte lacunae

Loss of nuclei in dead bone

Trabecular mineral matrix persists

Schematic illustration — not a clinical/histologic specimen

Slide 69 · Microscopic answer: Two compartments have died

Persistent dead trabeculae

Empty osteocyte lacunae

New bone apposed on scaffold

Schematic illustration — not a clinical/histologic specimen

Slide 70 · Osteonecrosis: Five clinicopathologic rules

Bone and marrow infarction is the defining lesion.

Vascular compromise has traumatic, thrombotic, and compressive routes.

Medullary lesions often spare cortex; Subchondral lesions threaten the joint.

Empty lacunae and marrow fat necrosis support morphology.

Slow repair plus loading can lead to collapse and secondary osteoarthritis.

Slide 71 · Source references and visual provenance

Robbins, Cotran & Kumar, Pathologic Basis of Disease, 11th ed. (2026): Chapter 26, pp. 1075–1077.

AAOS OrthoInfo: Osteonecrosis of the Hip; ACR Appropriateness Criteria: Osteonecrosis (2022).

Yoon et al. J Arthroplasty. 2020;35:933–940. DOI: 10.1016/j.arth.2019.11.029.

Anatomic and histologic drawings are original editable schematics—not diagnostic specimens.