Osteonecrosis of Femoral Head

Osteonecrosis of femoral HEAD (Chandler’s disease)

Aetiology

Atraumatic

– High-dose corticosteroid use

– Alcohol abuse: >8 ml of alcohol per day is associated with increased risk

– Smoking

– Thrombophilias and hypofibrinolsysis

– Renal osteodystrophy

– Solid organ transplantation

– Hemoglobinopathies

– HIV infection: mainly due to antiretrovirus therapy

– Gaucher’s disease

– Hyperlipidemia

– Pancreatitis

– Chemotherapy

– Radiation therapy

– Liver disease

– Gout

– Systemic lupus erythematosus

– Caisson disease

– Idiopathic (most common)

– Pregnancy

– Genetic: collagen type II gene mutation

– Genetic polymorphism such as alcohol metabolizing enzymes and the drug transport protein P-glycoprotein and eNOS polymorphisms

Traumatic

1. Displaced femoral neck fractures

2. Fracture dislocation Hip

3. Iatrogenic injury secondary to anterograde medullary nailing (rare)

The treatment of Post- traumatic Osteonecrosis is not included in this review.

Theories of Pathogenesis:

1. Direct cellular toxicity: radiation, chemotherapy, or thermal injuries can cause injury to

and death of marrow cells and osteocytes

2. Extraosseous arterial: fracture of the femoral neck. Hip dislocations, post surgery,

abnormalities in major vessels about the hip, including the retinacular arteries

3. Extraosseous venous

4. Intraosseous extravascular:

· Hemorrhage: presence of intramedullary hemorrhage in the osteonecrotic lesion of core biopsy specimens is a supporting evidence

· Elevated Bone Marrow Pressure: This theory proposes that the bone acts like a Starling resistor in which thin-walled vessels traverse the space within a rigid outer cortex. Any increase in the pressure within this compartment causes the vessel walls to collapse, thus leading to decreased blood flow

· Cellular Hypertrophy and Marrow Infiltration: examples are (a) corticosteroid therapy, (b) Gaucher's disease, (c) leukemia, or (d) caisson disease or dysbarism.

10 to 30% of nontraumatic osteonecrosis is caused by Cortisone administration. Corticostroids may direct bone marrow stromal cells in to the adipocytic pathway as opposed to osteoblastic pathway.

Dosages typically considered being associated with the disease are >2 g of

Prednisone, or its equivalent, within a period of two to three months.(Griffith et al..)

· Bone Marrow Edema

5. Intraosseous intravascular: examples to support this hypothesis are sickle cell disease, lipid emboli, thrombophilias

6. Hypersensitivity reactions: immune complex deposition may lead to vascular damage

7. Multifactorial

Current evidence suggests that intravascular coagulation and microcirculatory thrombotic occlusion likely provide a final common pathway for nontraumatic osteonecrosis

Pathogenesis:

· The resultant hypoxia® increased cell membrane permeability® fluid and electrolytes enter the cell, and the cell swells. Intracellular lysosomal enzymes are released, resulting in autodigestion or coagulation, necrosis and cell rupture® Vascular injury ® tissue edema and Hemorrhage®inflammatory response, characterised by the appearance of neutrophils and macrophage

· The hematopoietic elements are the first to undergo anoxic death (in from 6 to 12 hours), followed by bone cells (osteocytes, osteoclasts, and osteoblasts) (in 12 to 48 hours) and, subsequently, marrow fat cells (48 hours to 5 days)

· Infarcts can be subdivided into four zones: a central zone of cell death surrounded by successive zones of ischemic injury(transition zone, active hyperemia, and finally normal tissue

· In the periphery of the necrotic area where vascularity is present (called ‘transition zone’) an active process of repair occurs.

· If the lesion is small in the non-weight bearing area it may undergo revascularization and be completely replaced with viable bone or it may form a sequestrum surrounded by a wall of new bone. This usually does not collapse.

· In the weight bearing area, the repair process is less effective. Bone resorption is more rapid than formation® cancellous bone collapses

· If the contour of the articular surface remains intact, ®development of fluid-filled space

beneath the cortical subchondral bone. This gives the appearance of a crescent sign in X-rays

Clinical Features:

· Common in young adults between 20 and 40 years

· Limp

· Hip pain or vague groin pain

· groin pain with ROM of the hip (internal rotation), which is not typically tender with direct palpation

· Bilateral in more than 50 %

· Positive Sectoral sign: The range of internal rotation is less in hip flexion compared to when in hip extension.

Investigations:

· The investigation of choice for this condition is MRI. It has been found to be 99% sensitive and 98% specific for this disease. The classic appearance of AVN on MRI is that of a focal lesion in the anterosuperior subchondral region of the femoral head . The lesions are non homogenous, segmental and well demarcated, with low SI on T1 and intermediate SI on T2. The T2 WI may show a so called double line sign, which is pathognomonic of AVN. This sign is thought to represent interface between viable and osteonecrotic bone, and it consists of concentric low and high signal intensity bands.

· Bone scan has been reported to be insenditive for the diagnosis of ON of femoral head.

Classification:

1. Association Research Circulation Osseous (ARCO): This is the Committee on Nomenclature and Staging of Osteonecrosis. The ARCO classification incorporates all the staging systems described below.

2. University of Pennsylvania staging system: 2^nd most commonly employed classification

3. Japanese classification (Ohzono et al.. CORR 1992)

4. Ficat and Arlet staging: Most commonly employed

§ The University of Pennsylvania staging is the first to use MRI as specific modality and the first to measure the lesion size and surface involvement

Extent of Necrosis:

§ Kerboul et al...(JBJS B1974): determined the extent of necrosis by measuring the arc of articular surface overlying the lesion on both AP and Lateral views. The combined necrotic angle is obtained by adding the angle in AP and lateral views.

>250° = large

>151°-<250°= medium

<150° = small

§ Koo and Kim et al. used MRI to determine the extent of necrosis(JBJS B 1995; 77)

§ The combined necrotic angle is a predictor of collapse after core decompression.

§ Combined necrotic angle of less than 190° suggests low risk of collapse, whereas if necrotic angle is more than 240° there is a high risk of collapse

§ Similarly, High fat content and bone marrow edema in the proximal femur appear to predict an increased risk of future collapse.

§ In the University of Pennsylvania staging the angles in AP and lateral are multiplied

§ The Japanese classification and the ARCO suggested the importance of location (anterior, medial, central etc). But this is not found to be important since most lesions are located in the anterosuperior area.

§ Similarly, Steinberg proposed volumetric measurements calculated from coronal and axial images in MRI. Lesions that occupy &<15% of the femoral head are defined as mild, 15% to 30% as moderate or medium, and &>30% of the femoral head as severe lesions.

Treatment of Nontraumatic Osteonecrosis of Femoral Head

Medical Management:

· Stanozolol: an anabolic steroid that alters lipoproteins and suppresses clotting factors

· Lovastatin: agent that lower circulating lipids( associated hypercholesterolemia or

hyperlipidemia)

· Long-term anticoagulation to treat coagulopathies using enoxaparin(for inherited

coagulation disorders)

· Alendronate: Agarwala et al found improvement in 100 hips after treatment with 10mg/day of alendronate.(4)

1. Published reports justify nonoperative treatment of small precollapse lesions (<10% Size)that are asymptomatic.

2. Extracorporeal shockwave therapy, pulsed electromagnetic fields, hyperbaric oxygen are not currently recommended.

Management Guidelines(Based on Ficat and Arlet staging)

Stage I and IIA:

Normal radiographs, positive MRI, Asymptomatic: Observation, pharmacologic treatment

Core decompression and bone grafting: for symptomatic precollapse lesion

• Decreases intraosseous pressure in the femoral head and may immediately relieve the associated pain
• Bone grafting allows for removal of weak necrotic bone, decompression of the femoral head, and stimulation of repair and remodeling of subchondral bone.
• Bone grafting also maintains articular congruity and prevents collapse
• Indicated for small- to medium-sized precollapse lesion.
• core decompression involves the use of an 8- to 10-mm trephine or cannula inserted under fluoroscopic guidance to penetrate the lesion
• Weight-bearing should be protected for 5 weeks after surgery to avoid fracture.
• Another technique for core decompression is drilling multiple times in to the lesion with a small 3.2 mm diameter pin.

Bone grafting may involve any of the three techniques:

1. Cortical strut grafting through a core track in the femoral head and neck. Vascularised fibular graft is superior to nonvascualrised grafts.Vascularised fibular grafts are a reasonable option for patients younger than 50 years without collapse of the femoral head.

2. Bone grafting through the articular cartilage (the trapdoor procedure), was popularised by d’Aubigne. An arthrotomy is performed to dislocate the hip anteriorly, the necrotic segment of the head is curetted out, and iliac crest bone graft is packed inside. This is
done through a cartilage window of the femoral head.

3. Bone grafting through the femoral neck or femoral head neck junction (light bulb procedure).

· The Ioannina technique uses serial computed tomography (CT) scans of the proximal femur to identify the configuration of the femur, and the size, location, and configuration of the lesion. This has been developed for accurate graft placement(8)

· Recent research has focused on development of biologically based therapies that can enhance core decompression with either osteoinductive (BMPs) or osteogenic (mesenchymal cells) agents that have the clinical potential to provide better results for larger lesions(7)

· The role of use of tantalum rods is being debated and long term outcome studies are not available

Stages II B and above:

1. Angular intertrochanteric (varus and valgus) and rotational transtrochanteric (Sugioka):

• For Stage IIB and Stage III with less than 30 % head involvement and necrotic angle is less than 90°
• The Sugioka osteotomy is a posterior rotational osteotomy such that the necrotic lesion is shifted posteriorly into the non weight bearing area
• Good results are obtained in stage II Ficat compared to stage III
• Good fixation devices like the nail plate device should be used
• Results are best with patients aged 45 years or younger, with unilateral disease

3. Resurfacing arthroplasty: Hemiresurfacing : should be considered for 1) Ficat stage III disease 2) combined necrotic angle of >200 degrees or >30% involvement 3) femoral head collapse of > 2mm 4) no evidence of damage to acetabular cartilage.

Conversion to Total Hip arthroplasty maybe required in the presence of persistent groin pain after hemiresurfacing.

Total hip resurfacing can be performed in Ficat stage IV disease without significant deformity or cystic changes in the femoral head.

3. Bipolar hemiarthroplasty: Bipolar hemiarthroplasty has a high failure and complication rate and is associated with a high prevalenece of polythylene wear, so it is not recommended for treatment of osteonecrosis.

4. Total hip replacement:

• Indicated for patients with femoral head collapse and acetabular involvement.
• The presence of AVN in the proximal femoral canal may reduce the remodelling capacity of bone at the bone–cement interface and impair the establishment of osseointegration and therefore adequate long-term fixation of the prosthesis.
• Nevertheless, excellent long term results have been obtained using cementless fixation
• In the context of radiation induced osteonecrosis, reinforcement rings or highly porous metal socket is recommended
• The risk of prosthetic joint infection is higher if the underlying aetiological factor is related to immunosupression.
• Use of corticosteroids, ethanol abuse, systemic lupus erythematosus, or organ transplants negatively affect the prosthetic durability.

Ficat and Arlet Staging

Stage	Symptoms	X-rays	Bone scan	Pathology	Biopsy
0	None	Normal	Decreased Uptake?
1	None	Mild/Normal	Cold spot	Infarction of weight bearing portion of head	Abundant dead marrow cells, osteoblasts, osteogenic cells
2	Mild	Density change in femoral head	Increased uptake		New bone deposited between necrotic trabeculae
2A		Sclerosis or cysts, normal joint line, normal head contour	Increased uptake
2B		Flattening (crescent sign)
3	Mild to moderate	Loss of sphericity, collapse	Increased uptake	Subchondral fracture, collapse, compaction and fragmentation of necrotic segment	Dead bone trabeculae and marrow cells on both sides of fracture line
4	Moderate to severe	Joint space narrowing, acetabular changes	Increased uptake	Osteoarthritic changes	acetabular cartilage degeneration

University of Pennsylvania Staging:

Stage 0: Normal or non-diagnostic X Ray, Bone scan or MRI

Stage I: Normal X Ray, Abnormal bone scan or MRI. A: < 15% of head involved (mild) B: 15- 30 % head involved (moderate) C: >30 % of head involved (Severe)

Stage II: Cystic and sclerotic changes in femoral head A:<15% of head involved (mild) B: 15- 30 % head involved (moderate) C: .30 % of head involved (Severe)

Stage III: Subchondral collapse without flattening (Crescent sign) A: <15% of articular surface (mild) B: 15- 30 % of articular surface (moderate) C: >30 % of articular surface (Severe)

Stage IV: Flattening of femoral head A: <15% of articular surface and <2mm depression (mild) B: 15- 30 of articular surface and 2-4 mm depression (moderate) C: >30 % of articular surface and >4 mm depression (Severe)

Stage V: Joint space narrowing and acetabular changes A: Mild Average of femoral head involved as in stage IV B: Moderate and acetabular involvement C: Severe

Stage VI: Advanced degenerative changes

Treatment Recommendation According to the University of Pennsylvania System of Classification and Staging (Lieberman et al. JBJS 2002; 84-A)

I and II (Asymptomatic) Observation, pharmacologic treatment, possible core decompression ± bone grafting

IA, IB, IC, IIA, IIB, and IIC (Symptomatic) Core decompression ± bone grafting, vascularised graft

IC, IIC, IIIA, IIIB, IIIC, and IVA (Symptomatic) Bone grafting (vascularised or nonvascularised), osteotomy, limited femoral head resurfacing, total hip arthroplasty

IVB and IVC (Symptomatic) Limited femoral head resurfacing, total hip arthroplasty

V and VI( Symptomatic) Total hip arthroplasty

.

Ref:

1. Steinberg ME, Hayken GD, Steinberg DR. A quantitative system for staging avascular necrosis. J Bone Joint Surg 1995;77B:34-41

2. Mont MA, Jones LC, Hungerford DS. Nontraumatic osteonecrosis of the femoral head: ten years later. J Bone Joint Surg 2006;88A: 1117-1132

3. Lieberman JR, Berry DJ, Mont MA, et al. Osteonecrosis of the hip: management in the 21st century. Instr Course Lect 2003;52: 337-355

4. Lai KA, Shen WJ, Yang CY, et al. The use of alendronate to prevent early collapse of the femoral head in patients with nontraumatic osteonecrosis. A randomized clinical study. J Bone Joint Surg 2005;87A:2155-2159

5. Urbaniak JR, Harvey EJ. Revascularization of the femoral head in osteonecrosis. J Am Acad Orthop Surg 1998;6:44-54.

6. Adili A, Trousdale RT. Femoral head resurfacing for the treatment of osteonecrosis in the young patient. Clin Orthop Relat Res 2003;417: 93-101

7. Gangji V, Hauzeur JP, Matos C, De Maertelaer V, Toungouz M, Lambermont M. Treatment of osteonecrosis of the femoral head with implantation of autologous bone-marrow cells. A pilot study. J Bone Joint Surg Am. 2004;86:1153–1160.

8. Beris AE, Soucacos PN. Optimizing free fi bular grafting in femoral head osteonecrosis: the Ioannina aiming device. Clin Orthop Relat Res. 2001; (386):64-70.