Osteonecrosis

Under the guidance of

Dr. Sanjay singh sir

Dr. C.D. Sahu sirDr. Amit Kumar sir Presented by

RAVISH KUMAR

Avascular necrosis Also known as

osteonecrosis ,aseptic necrosis, bone infarction

Implies that a segment has lost its blood supply so that cellular elements within it die.

Anatomic predisposition for osteonecrosis

Femoral head, Humeral head, Distal femur

Clinical presentation

Usually non-specific and depend on the cause and location.

Early phase symptoms are variable and often absent or relatively minor. This clinical latent period may range from a few weeks up to 1 year in duration

Evident, particularly when the articular surface collapses, altering joint function.. As progressive collapse of the joint surface occurs, greater pain and debility are to be expected.

localized and referred pain, antalgia, reduced and painful ranges of motion,and adjacent muscle atrophy.

Metaphyseal and diaphyseal infarcts -completely asymptomatic to acutely symptomatic.

Etiology Unilateral

Bilateral Common Spontaneous (idiopathic)

Alcoholism Surgery

Corticosteroid therapy

Trauma (fracture, dislocation) Spontaneous

(idiopathic) Uncommon Gout

Arteriosclerosis Hemophilia Caisson’s

disease Infection Cushing’s

disease

Gaucher’s disease

Hemoglobinopathy Lupus

erythematosus

Pancreatitis

Pheochromocytoma

pathology Ischemia results to death of all component of bone

cellRevascularization is seen at the live marrow and

dead marrow interface.Necrotic zone is invade by capillaries , fibroblasts

and macrophagesFibrous tissue replace dead marrow and may calcify.New osteoblast lay down fresh woven bone on

devitalise trabeculaeNeovascularisation and ossification-creeping

substitution(Phemister)Bone ends and cartilage recieves nutrition from

synovial fluid.

Osteonecrosis- femoral head

VASCULAR SUPPLY: FEMORAL HEAD. There are two sources of blood supply: profunda femoris (1)and ligamentum teres (2). From the profunda femoris the circumflex vessels (3 and 4) provide the medial andlateral epiphyseal arteries (5 and 6). It is probable that the site of precipitating occlusion is at the lateral epiphyseal vessels.

Radiological featuresAnterosuperior locationCortical collapse (step defect)Cystic radiolucenciesDegenerative joint diseaseFragmentationPeriosteal bone appositionSclerosis (snowcap sign)Subchondral fracture (crescent, rim sign)Trabecular alterationWedged or semilunar shape (bite sign)

EPIPHYSEAL INFARCTION: GENERAL FEATURES.

FA. Collapsed Articular Cortex. Observe the sharp, angular deformity (arrow) in the weight-bearing cortex (step defect). Sclerosis of the femoral head is also evident. B. Epiphyseal Fragmentation. Note that multiple cystic and linear lucencies produce a mottled, fragmented appearance to the femoral head. This is owing to a combination of fractures, subchondral cysts, and localized repair response. C. Subchondral Fracture. Note the thin curvilinear radiolucency (arrow) just beneath the weight-bearing articular cortex (crescent sign).

HIP AVASCULAR NECROSIS: PROGRESSIVE ARTICULAR COLLAPSE

. A. Initial Film. Note the two sharp, angular deformities (step defects) at the weight-bearing superior articular cortex (arrows). A slight increase in density is visible in the femoral head. B. 12-Month Follow-Up. Note that greater collapse is evident.Degenerative changes have also intervened, with loss of joint space and osteophyte formation. C. 18-MonthFollow-Up. Note that severe collapse and fragmentation have occurred, with considerable lateral displacement of the femur.

Pathologic-Radiologic Correlation in Epiphyseal Ischemic Necrosis

Pathologic Feature Radiologic Feature

Avascular Phase Loss of blood supply Small

epiphysis Bone death Normal

bone density

Cartilage growth Increased joint

space Low-grade synovitis

Increased joint space

Capsular swelling

Disuse, hyperemia Metaphyseal osteoporosis

Widened growth plate

Revascularization PhaseNeovascularization Periphery Peripheral sclerotic

rim Center Homogeneous

sclerosis (snowcap) Subchondral fracture Crescent sign Fibrous and granulation tissue Clefts and

fragmentation Woven bone Flattening of surface Altered biomechanical stress Widened

metaphysis

RepairBone deposition- Reconstitution of epiphysisRegression of osteoclasis - Disappearance of

cleftsDeformity bone - Deformed, articular surface

Metaphyseal diphyseal infarctionCortical or medullaryDistal femur, proximal tibia and proximal

humerus CorticalThe periosteum is often activated to produce a

fine layer of new boneLocalise rarefactionMedullaryCentral location Metaphyseal-diaphyseal

locationElongated lesion Sclerotic, serpiginous contourFocal internal calcification Unaffected adjacent cortex

METAPHYSEAL-DIAPHYSEAL INFARCTS

Observe the characteristic central location, undulating serpiginous contour, and dense calcific margin.

METAPHYSEAL-DIAPHYSEAL INFARCTS.

Plain Film. Note that two mature infarcts are present, one within the metaphysis (arrow), the other within the proximal humeral diaphysis (arrowheads).

Ficat staging Stage 1- No changes visible

Stage 2-Disuse osteoporosis except devitalise avascular bone which appears sclerosed.

Stage 3-subcortical zone of transradiancy and trabecular loss beneath thin sclerotic cortex leading to microfractures followed by collapse and trabecular compression.

Stage 4-flattened articular surface with increase subarticular density

Stage 5- Osteoarthritis with joint space narrowing

MRI features of osteonecrosis Highly sensitive and specific for AVN

Useful in equivocal radigraphs and contralateral normal hip on radiographs

Assist for decision to perform operative procedures

T1W characteristic serpiginous area of altered signal intensity of anterosuperior part of femoral head.

T2WI double line sign(pathognomonic) Outer low intensity rim and inner high intensity

band bright band sign

T1 images

T2 images

Mitchell classificationBased on appearace of center region

signal,bounded by low signal rim on T1 and T2W images

Class A –fat like signal characteristic early stages of disease Class B-subacute blood like high signal on both T1 and

T2 Class C-Fluid like signal intensityClass D- fibrous tissue like changes

Mitchell class images

A and B: Mitchell class A and D AVN: T1W coronal (A), STIR coronal image of both hips (B)—shows area of altered signal in both femoral heads with fat intensity signal on T1W and STIR on the right side-class Aand hypointense signal on the left side-class D

Mitchell class C and D AVN. T1W coronal image (A), T2W fat suppressed coronal image of both hips (B), shows bilateral areas of altered signal in femoral head showing hypointensity on T1W and mixed hypo- and hyperintensity on T2WI

Secondary findings-fatty marrow of intertrochantric

regionIncrease amount of synovial fluidBone marrow oedema

Secondary findings AVNFatty marrow infilteration

T1W coronal (A) and STIR coronal images of both hips (B), showing increase in intertrochanteric fatty marrow on the right side with marrow edema on the left side with bilateral AVN

STIR coronal image of both hips showingjoint effusion on the left side with bilateral AVN

Gadolinium enhanced imaging

Bilateral AVN. T1W coronal (A) and T1W axial (B) fat suppressed, postgadolinium image of both hips showing necrotic nonenhancing areas with enhancing viable interface and viable fragments

Dynamic contrast study detect early femoral ischemia delayed peak enhancement is noted

ADC value are higher in hip AVN ,but staging is not possible

MR spectroscopy can detect early changes in lipid/water spectra

Prognostic indicators on MRI Percentage of weight bearing surface that is involved by

AVN lesion is most reliable factor.

In coronal image if less than 25%femoral head is involved ,there is less likelihood of lesion to develop collapse

If more than 2/3rd weight bearing surface is involved -74%chance of collapse of head

On saggital if reactive interface cross the 12 oclock-82% chance of collapse

High risk marker early conversion from hematopoietic to fatty marrow and dense intact physeal scar

Pitfalls in DiagnosisFatty conversion does not occur occasionallySynovial herniation pit Subchondral bone cysts Fovea centralis

Pitfall images

A and B: X-ray pelvis and both hips—AP view (A) shows decreased joint space on the left with subchondral cystic changes and osteophytes and T1W coronal image of both hips (B) depicting subchondralcyst with osteophytes—degenerative changes

Study choice and workupRadiograph-AP and Frog leg lateral projection

Radionuclide imaging- Tc 99MDP or Tc99S In early phase-cold photopenic zone

pathognomonic for AVN Late stage reactive hyperemia and

reparative response may result in doughnut sign

CT scan- adjunctive role, in pt. with MR contraindication

prognosisRate of progression is

unpredictable

If disease dicovered prior to articular collapse-core decompression and rotational osteotomy

Hip arthroplasty done in patients with interactable pain and femoral head collapse