Osteonecrosis

Karel Pavelka

MD, PhD

Associate Professor of Internal Medicine and Rheumatology; Director, Institute of Rheumatology;

Senior Lecturer, Charles University, Prague

Institute of Rheumatology, Na Slupi 4, 128 50 Prague 2, Czech Republic

Osteonecrosis (avascular necrosis, aseptic necrosis or subchondral avascular necrosis) is not a

speci®c disease entity but the ®nal common pathway of a number of conditions leading to bone

death. The main predisposing factors (trauma, glucocorticosteroids, alcoholism and connective

tissue disorders) should be carefully sought, but osteonecrosis can also be idiopathic in origin. Its

most common localization is to the femoral head, followed by the humeral head, the knee and

the small bones of the wrist and foot. New imaging techniques, especially magnetic resonance

imaging, have improved the early diagnosis of osteonecrosis as radiographs may be normal in

the initial stages. The outcome for the patient is in¯uenced by many factors, the size and

localization of the bone necrosis being of primary importance. Early intervention (both surgical

and non-surgical) has de®nitively improved the outcome, but still nearly 50% of cases of femoral

head osteonecrosis necessitate arthroplasty. In this chapter, we shall concentrate on patients at

high risk of osteonecrosis, on evidence-based diagnosis, especially in the early stages, and on

evidence-based treatment suited to the staging system of osteonecrosis.

Key words: osteonecrosis; avascular necrosis; osteochondritis dissecans; magnetic resonance

imaging.

Osteonecrosis (ON; avascular necrosis, aseptic necrosis or subchondral avascular

necrosis) is not a speci®c disease entity but the ®nal common pathway of a number of

conditions (

Table 1

) mostly leading to an impairment of the blood supply to the bone.

The aetiological factors are well known in some conditions (trauma, caisson disease and

sickle-cell disease) but less clear in others (systemic lupus erythematosus [SLE],

corticosteroid administration, pancreatitis and excessive alcohol intake); idiopathic

forms are also frequent. In addition ON can develop during pregnancy. This probably

has a multifactorial aetiology and may involve mechanical, hormonal and coagulation

factors.

1

Idiopathic ON of the hip in twins has been reported

2

, as has familial idiopathic

ON, probably caused by hypo®brinolysis.

3

EPIDEMIOLOGY

There are few data on the incidence or prevalence of ON. The number of new cases

detected annually in the USA is estimated to be 15 000.

4

In one Japanese study of non-

traumatic ON, 34.7% of the cases were caused by corticosteroid treatment and 21.8%

by alcohol abuse, 37.1% being considered idiopathic; other conditions mentioned were

less frequent.

5

A systematic review of the published literature estimated the incidence

1521±6942/00/020399+16 $35.00/00

*

c 2000 Harcourt Publishers Ltd

BaillieÁre's Clinical Rheumatology

Vol. 14, No. 2, pp. 399±414, 2000

doi:10.1053/berh.2000.0072, available online at http://www.idealibrary.com on

12

of ON of the hip in long-term steroid treatment after transplantation to be 8%.

6

In SLE

in long-term observation (so-called late lupus), ON has been shown to develop in

10%.

7

The incidence of ON in trauma with fracture of the femoral neck, especially in

the subcapital region, is estimated to be 30% in displaced fractures. In haemophilia, the

prevalence of reported ON is 2.8%.

8

The most commonly a€ected sites are the femoral

head

9

, the humeral head

10

, the knees (femoral condyles and proximal tibia

11

), the small

bones of the foot

12

, the small bones of the hand (including the scaphoid and lunate

bones

13

,

14

) and the vertebrae.

15

Many of these, especially from the group of idiopathic

ON occurring in childhood or adolescence, have historical names.

PATHOGENESIS

ON is the result of an interruption of the circulation, which leads to a disparity

between the oxygen need of the bone cell and the ability of the local circulation to

supply that need. This may be caused by vascular compression (external pressure),

trauma or occlusion of the vessels by nitrogen bubbles (in caisson disease) or rigid

sickle cells (in sickle-cell anaemia). The mechanism of ischaemia and necrosis in other

non-traumatic ON is not clear. Several possible mechanisms have been proposed to

explain ON

16

:

1. microfractures and osteoporosis;

2. primitive vascular problems (including vessel infarction, stenosing arteritis, arterio-

sclerotic disease, extraosseous arterial involvement or extraosseous venous

abnormality);

3. fat embolism;

4. venous intra-osseous factors;

5. the hypertrophy of fat cells;

6. compartment syndrome (compression of the bone microvasculature).

Table 1. Conditions associated with avascular necrosis of the femoral head.

Fracture of the femoral neck

Traumatic dislocation of the hip

Slipped capital femoral epiphysis

Reconstructive hip surgery, involving femoral head dislocation

Perthes disease

Caisson and diver's disease

Gaucher's disease

Sickle-cell disease and sickle-cell variants

Miscellaneous haemoglobinopathies and coagulopathies

Radiotherapy

High-dose corticosteroid treatment and Cushing's disease

Disturbances of lipid metabolism

Excessive alcohol intake

Pancreatitis and Weber±Christian disease

Gout

Arteriosclerosis and other occlusive vascular disorders

Osteomalacia and other metabolic bone diseases

Systemic lupus erythematosus and other connective tissue disorders

Pregnancy

HIV infection

Idiopathic

400 K. Pavelka

CLINICAL MANIFESTATIONS

The clinical features of ON are non-speci®c, being in¯uenced by localization, size,

associated conditions and the evolutive phase of the process. There appear to be

several di€erent variants of this condition. The severity ranges from asymptomatic to

severely disabling. The outcome can also range from healing to destruction of the joint

and a necessity for arthroplasty.

Pain is the most common presentation of ON. In ON of the femoral head, the pain

is most frequently located to the groin or anterior thigh, but it can also involve the

buttock or the knee. Many cases of ON are, however, asymptomatic.

17

In other

instances, the patient develops pain that persists for weeks before radiographs show

any changes. This is called the pre-radiological state, and the radiographic evidence of

ON may remain undetected until 6±10 weeks after the onset of the pain. The pain

usually occurs on weight-bearing, as in osteoarthritis, but is also very often present at

rest. Later on in the disease, patients may develop limping and a decrease of function.

The physical ®ndings are non-speci®c. They may be absent, or pain may be present

only in extreme rotation. The range of motion is usually limited after collapse of the

femoral head, when shortening of the limb can also develop.

The clinical picture of ON of the humeral head is also non-speci®c. There is usually

pain, often at rest, limitation of motion being a very late event as lack of movement at

the glenohumeral joint can be compensated for by motion at the scapulothoracic joint.

The onset of pain in ON of the knee is usually sudden and is often associated with

increased physical activity. Examination reveals tenderness over the involved area,

synovitis and joint e€usion may be present, so that it really mimics osteoarthritis of the

knee. There seem to be at least two distinct forms of this condition.

18

The ®rst one is

often related to corticosteroid treatment, sometimes being associated with ON of the

hip. This a€ects younger patients, is often bilateral and often a€ects both the tibial

plateaux and the femoral condyles. The second form of the condition a€ects an older

age group and is most often limited to a femoral condyle, most frequently on the

medial side, favoured by genu varum.

Avascular ON of the carpal bones follows corticosteroid therapy or trauma, may

remain asymptomatic but usually presents with wrist pain, limitation of motion and

tenderness in the anatomical snu€box.

ON of the tarsal navicular is characterized by pain, an antalgic gait and localized

tenderness and swelling over the navicular bone.

EVIDENCE-BASED DIAGNOSIS OF ON
The diagnosis of ON relies heavily on imaging methods, which include plain

radiography, conventional tomography, computed tomography (CT), scintigraphy and

magnetic resonance imaging (MRI). Invasive methods include bone marrow pressure

determinations and bone marrow biopsy. Although the appearance of ON on

conventional radiographs is well documented, these changes are often delayed.

Radionuclide bone scans o€er a unique possibility for the non-invasive detection of the

early stages of osteoarthritis. The method of ®rst choice today is MRI.

19

Radiographic changes
In the earliest stages of ON, plain radiographs are normal and pathological changes

must be detected by other techniques, for example MRI.

Osteonecrosis 401

Early radiographic changes in the femoral head include mottled radiodense areas

scattered in the anterosuperior region and a faint band of diminished density in the

anterosuperior subchondral bone (the crescent sign) (

Figure 1

), loss of sphericity, a

grossly triangular zone of sclerosis in the weight-bearing area, and initially subtle

¯attening of the femoral contour, best seen on pro®le views. Later on, there is

¯attening and often gross collapse of the femoral head (

Figure 2

). The joint space and

acetabulum are still normal. Later still, secondary osteoarthritis can develop, with joint

space narrowing and sclerotic and cystic changes in the acetabulum. A total

destruction of the femoral head can sometimes be observed (

Figure 3

).

Figure 1. Central area of radiolucency (the crescent sign), indicating a subchondral fracture.

Figure 2. Later changes include ¯attening and gross collapse of the femoral head.

402 K. Pavelka

Computed tomography
CT images display early sclerosis in the central part of the femoral head (the

asterisk sign) and joint e€usion. Some minimal anterior collapses can be detected by

CT scanning.

Scintigraphy
Bone scanning using methylene bisphosphonate labelled with technetium-99m has

been used in the investigation of ON. The technique is very useful in the early stages,

when radiographic pictures are normal, and to map the extent of the disease in

patients with multiple sites of ON. It has been documented that pre-treatment bone

scanning in slipped capital femoral epiphysis is a sensitive predictor of the development

of ON.

20

Bone scanning usually shows increased uptake either because of new bone

formation or as a result of metabolic activity around the necrotic area. Bone-scanning

might show cold areas at very early stages, when the necrotic bone is not taking up

isotope and new bone formation has not started yet. The technique is, however,

relatively insensitive in the early pre-collapse stages, when it gives a positive result in

only 70% of cases.

21

Bone scanning is also totally non-speci®c.

Magnetic resonance imaging
This technique has brought new quality into the diagnosis of ON, for several reasons.

MRI has been shown clearly to be more sensitive than plain radiography, CT or bone

scanning, especially in the early stages. MRI has been shown to have 97% sensitivity in

di€erentiating osteonecrosis from a normal hip, and 85% sensitivity in di€erentiating

ON of the femoral head from other hip disorders, giving an overall sensitivity of 91%.

22

Gadolinium-enhanced spin echo sequences and fat-suppressed images have further

improved speci®city (

Figure 4

). Many investigators have proved that MRI is accurate as

a method of detecting ON before clinical and radiographic changes become evident.

MRI has also been shown to be a better predictive test for subsequent femoral head

Figure 3. Total destruction of the femoral head.

Osteonecrosis 403

collapse (31%) than bone scanning.

23

MRI is indispensable in the accurate staging of ON

because it re¯ects the size of the lesion and the rough stage of the disease. MRI is today

the `gold standard' of non-invasive diagnostic methods in ON. Its sensitivity is 100% in

the post-collapse stages but only 80±100% in the pre-collapse stages. The speci®city of

MRI is 75±100%.

MRI images re¯ect histological changes. A central area of high signal intensity above

or within a low signal intensity ring corresponds to necrotic bone and marrow that has

not been reached by invading capillaries and mesenchymal tissue. The low signal

intensity band or ring represents the repair tissue interface of the mesenchymal and

®brous tissue, cellular debris and thickened trabecular bone adjacent to the necrotic

zone.

24

Most importantly, it can be followed from one corticle to the other on coronal

and saggital views, in contrast to the abnormalities caused by subchondral bone

fracture. Joint e€usion is also demonstrated by T2-weighted MRI images.

Based on the results of di€erent studies that compare histological and MRI ®ndings,

the following classi®cation system of MRI signal abnormalities may help to improve the

evaluation of ON:
. Type I. A band- or ring-like pattern with low signal intensity that surrounds a high

signal intensity central zone.

. Type II. A segmental pattern with a low signal intensity on T1-weighted images

(

Figure 5

) and an increase in signal intensity in the distal portions on T2-weighting.

. Type III. A segmental pattern with a low signal intensity on both T1- and

T2-weighted images (

Figure 6

). This classi®cation scheme may be extended to include

a di€use pattern of marrow abnormality with a low signal intensity on T1-weighting

and a high signal intensity on T2-weighting, which may indicate early ON in the

absence of radiographic ®ndings or focal subchondral MRI signal changes.

25

MRI may be employed prior to more costly interventional procedures used to detect

ON, such as core biopsy and decompression. MRI is also indicated in those patients in

whom the distinction between di€erent hip disorders is dicult using other techniques.

Figure 4. Large area of osteonecrosis of the knee on a T1-weighted frontal image. This shows stage III disease

in the femoral condyle.

404 K. Pavelka

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Osteonecrosis 405

Other investigations
Functional bone investigation can be carried out by the measurement of bone marrow

pressure, and intramedullary venography, demonstrating a decreased blood ¯ow with

increased bone marrow pressure, which is present in the early stages of all cases of

ON. Superselective angiography has now been replaced by MRI.

STAGING SYSTEMS FOR ON

The severity of ON has been categorized using several di€erent staging systems. For

example, Ficat and Arlet

26

proposed a system based on radiographic, haemodynamic

and symptomatic criteria, which had four stages: stages 1 and 2 were the early stages,

with reversible bone changes, stages 3 and 4 being described as end-stage disease with

irreversible destruction of the bone and joint structures. The nomenclature

subcommittee of ARCO (l'Association de Recherche en Circulation Osseuse) has

recently proposed a new internationally accepted system of classi®cation of the various

stages of ON (

Table 2

).

4

This system should help researchers carrying out comparative

epidemiological studies, as well as when comparing di€erent methods of treatment.

OSTEONECROSIS IN PATIENTS WITH SLE

Osteonecrosis has been recognized as an important cause of disability in lupus,

occurring in 10% of patients followed for a long period of time.

7

Up to two-thirds of

Figure 6. A T1-weighted saggital image shows marked hypointensity of the condyle and surface irregularity

of the patellar cartilage consistent with chondromalacia.

406 K. Pavelka

patients with SLE who develop ON are receiving high-dose steroids. They are usually

younger and have active disease with multiple organ involvement.

The hip is the most commonly involved joint, but other joints can also be a€ected.

We have reported young women who have developed seven sites of ON after 2 years

of SLE treated with high steroids.

27

The mechanism of the pathology of ON in SLE

patients is unclear. Vasculitis has been found in only a minority of histological samples

from osteonecrotic bones. Nagasawa et al have proposed abnormal haemostatic states

in these patients.

28

They detected abnormalities on MRI investigation of the hip in 35%

of patients with SLE with hip pain and a negative radiograph. The prevalence of ON in

SLE patients with anti-phospholipid antibodies is unknown.

ON IN PATIENTS TREATED WITH CORTICOSTEROIDS

Steroid-induced ON is a disease of modern medicine. The mechanism of ON in these

patients is not well known. Speculation has revolved around fat metabolism, with fat

embolization causing vascular occlusion.

16

Other biochemical factors may, however, be

involved, for example cellular cytotoxic factors. Pathology may result from a direct

metabolic e€ect on the osteogenic cells.

29

In a study of patients receiving gluco-

corticosteroid replacement therapy, the incidence of ON was 2.4%.

30

In renal trans-

plant patients on steroid therapy, the incidence is 5%.

30

Brinker et al

31

reported a high incidence of ON in patients treated for a short time

(6 weeks) with high-dose steroids (20 mg or more). Estimating the incidence of ON in

patients with rheumatoid arthritis and other connective tissue diseases is dicult

because of the possible in¯uence of underlying active disorder. It is generally accepted

that the risk of low-dose corticosteroids is relatively small and that even patients

treated for a long time will not develop ON.

Nevertheless, many questions regarding corticosteroid-induced ON have still to be

answered, for example concerning (a) the dose, route and duration of corticosteroid

Table 2. ARCO staging of osteonecrosis.

Stage

Findings

Diagnostic Techniques

0

All imaging methods are normal or

non-diagnostic; necrosis on biopsy

Biopsy and histology

1

Radiographs and CT scan normal

Positive result from at least one of the

techniques opposite

Radionuclide scan, MRI

Functional bone investigation

2

Radiographic abnormalities without

collapse (sclerosis, cysts, osteopenia)

Biopsy and histology

3

Crescent sign

Radiographs

4

Flattening or evident collapse

CT scan initially

5

As for stage 4, with narrowing of the

joint space

Radiographs only

6

As for stage 5, with destruction of

the joint

CT ˆ computed tomography; MRI ˆ magnetic resonance imaging.

Osteonecrosis 407

therapy necessary to induce ON, (b) the minimum and maximum time intervals

between corticosteroid usage and the onset of ON, and (c) host factors that modulate

these events.

OTHER FORMS OF ON

There are a number of other conditions of undetermined aetiology that represent

variants of avascular necrosis, some of which predominantly involve children.

These include Legg±Calve±Perthes disease, KoÈhler's disease, Freiberg disease, osteo-

chondritis dissecans and various other conditions. Di€erent areas of the body can be

a€ected, and the treatment and prognosis often vary considerably from those

described in the treatment of ON of the femoral head in the adult.

Congenital dislocation of the hip in infants
ON in congenital dislocation of the hip (CDH) may result from abduction splinting.

32

During the one-stage surgical treatment of CDH, it was shown to develop in 3 out of

33 hips.

33

The rate of ON was comparable to that developing when traction was used.

The application of Pavlik's harness is also associated with a high incidence of ON

(36%).

34

Legg±Calve±Perthes disease.
Perthes disease usually a€ects children between 4 and 12 years of age. It can be uni- or

bilateral and is probably related to an alteration of the blood supply to the femoral

head.

35

There is usually no history of trauma.

Perthes disease has many variations. The prognosis varies with the size of the

a€ected segment and the age of the child. When disease appears early in life, the

processes of repair are most active. Sometimes large areas or even a whole necrotic

femoral head may be gradually replaced by viable bone. The remodelling process may

lead to a ¯attening and enlargement of the head and a broadening of the neck,

although in some patients the femoral head can be nearly normal. The more residual

distortion there is, the more likely the patient is later to develop secondary

osteoarthritis.

Figure 7

shows radiographs of a boy with Perthes disease, who was

operated on at the age of 15 (pelvic osteotomy) and again on his hips 10 years later, at

the age of 25.

The treatment of Perthes disease can be either surgical or non-surgical. Remodelling

of the femoral head is best if it can be contained within the acetabulum during the

healing process. The a€ected limb should therefore be maintained in a moderate

degree of abduction by the use of any one of a number of splinting or bracing devices.

In this position, full weight-bearing is often allowed. The surgical procedures, including

osteotomies of the pelvis and of the proximal femur, provide better coverage and

containment of the femoral head within the acetabulum, improving anatomical

relationships and eliminating the need for years of bracing in abduction.

17

Trauma
Intracapsular fractures or compressive fractures, as well dislocations, can compromise

the blood supply to the femoral head, which can lead to a higher incidence of ON. The

408 K. Pavelka

exact prevalence data are unknown. Trauma is also a common factor in ON of the

carpal (especially the semilunar and scaphoid) bones.

Osteochondritis dissecans
Osteochondritis dissecans is a speci®c condition in which a fragment composed of

articular cartilage and subchondral bone becomes demarcated and often separated

from the surrounding bone and cartilage. The aetiology of this condition is unknown;

local ischaemia and trauma have been implicated so it is similar to ON in this respect.

The most commonly a€ected site is the distal femur, but the talus, elbow and hips can

be a€ected as well. The clinical manifestations are usually knee pain, swelling, e€usion,

functional impairment and limping.

Radiographically, osteochondritis dissecans appears as a well-circumscribed sclerotic

lesion, which is separated from the surrounding bone by a radiolucent line.

36

The

osteochondral fragment may remain in situ or it may be separated from the subchondral

bone and displaced into the joint (

Figure 8

). When evaluating the extent of involvement,

other imaging methods (tomography and MRI) or arthroscopy can be employed.

Figure 7. Morbus Legg±Calve±Perthes, showing a smoothly ¯attened femoral head and acetabular margin

with a prominent greater trochanter. (The patient developed morbus Perthes in 1987 when he was 13, an

osteotomy being performed in 1989, result as shown in 1999.)

Osteonecrosis 409

The prognosis and treatment of osteochondritis dissecans depend on the joint

involved, the size of the lesion and the age of the patient. The chance of spontaneous

healing is better in the young, skeletally immature patient. Treatment is either

conservative (including immobilization) or surgical. Many of the surgical procedures are

performed arthroscopically. The replacement of necrotic cartilage by osteochondral

allograft is sometimes necessary, with acceptable results. Surgery should be considered

only when skeletal growth is over as some of the images are mere aberrant loci of

ossi®cation.

MANAGEMENT OF ON
Preventative measures must, whenever possible, be instigated. Hyperlipidaemia and

diabetes should be treated and alcohol intake minimized. All cases of new applications of

corticosteroids, especially if for longer than a month or if given in a higher dose, should

be carefully considered. Most decompression accidents can be avoided if all decom-

pressions follow the established rules (slow resurfacing with a staged decompression).

The principal decision at the beginning of the treatment is that of surgical versus

non-surgical management. This decision is highly in¯uenced by the potential reversi-

bility of the process, based on the staging of the ON. In Ficat's staging, the reversible

stages are stages I and II.

26

Figure 8. Osteochondritis dissecans. A frontal view showing subchondral ¯attening and a radiolucent

area along the medial femoral condyle. There is a transchondral fracture, the bone fragment having remained

in situ.

410 K. Pavelka

Conservative treatment
The discontinuation of weight-bearing for at least 4±8 weeks, using high crutches, is

necessary. This may be e€ective, especially in ON with involvement of the medial

aspect of the femoral head and an extent of less than one-quarter of the diameter of

the head.

37

,

38

Surgical treatment
Core decompression decreases intramedullary pressure within the femoral head and

neck, and improves circulation in the femoral head. Mont and Hungerford

37

have

reviewed 42 reports and found satisfactory clinical results in 63.5% after surgery

compared with only 22.7% after non-operative treatment. When considering only pre-

collapse hips, the results were good in 41.0% and 35.4% respectively. Decompression

can be accompanied by bone grafting using cortical or cancellous bone.

Di€erent osteotomies have been used in various planes. Belal and Reichelt

39

reviewed the results of trochanteric rotational osteotomies. The results tended to

deteriorate over time. Despite the overall unsatisfactory results at ®nal follow-up, the

procedure was valuable as it delayed the need for total hip arthroplasty. The mean

time to arthroplasty was nearly 7 years.

In the later stages, the method of choice is total hip replacement. The results of this

operation in ON are not as good as those in other diseases of the hip (such as

osteoarthritis). The outcome after arthroplasty is also related to the aetiology, better

results being obtained in idiopathic ON (92.3% good results) than in alcohol-induced

ON (87%), renal transplantation (78%) and SLE (62.5%).

31

The choice of surgical procedure must be made according to the stage of the

disease. It is extremely important to evaluate by proper methodology the integrity of

the subchondral plate. In the pre-collapse stages, core decompression may be

successful. In cases with the crescent sign or a little ¯attening of the femoral head,

osteotomy or bone grafting can be used. In cases of evident collapse, total hip

replacement is the most important method.

SUMMARY

Osteonecrosis is not a speci®c disease entity but the ®nal common pathway of a number

of conditions that lead to impairment of the blood supply to the bone. The reasons for

this can be traumatic or non-traumatic. Pathogenetic factors are well known in some

cases of non-traumatic ON but poorly understood in others. In serious studies of non-

traumatic ON, the majority of cases occurred in patients treated with corticosteroids, in

patients with systemic connective disease (such as SLE) and in alcoholics. The most

commonly a€ected sites are the femoral head, the humeral neck, the knees and the

small bones of the hands and feet. The clinical picture is non-speci®c, and depends on

localization, size, associated conditions and the evolutive phase. The evidence-based

diagnosis of ON initially relies heavily on imaging methods and eventually on bone

marrow pressure determinations and bone marrow biopsy. Because the early stages of

ON are radiographically silent, MRI is the gold standard of diagnosis at this stage.

Radiographic changes include di€use osteopenia and a central subchondral of

radiolucency (the crescent sign, indicating a subchondral fracture); later changes include

¯attening and gross collapse of the bone. The process terminates in severe secondary

osteoarthritis.

Osteonecrosis 411

For proper treatment and prognosis, many staging systems have been developed, of

which the ARCO system is now internationally accepted. Therapy can be conservative

or surgical. Conservative therapy involves a discontinuation of weight-bearing for

at least 8 weeks but is e€ective only in the earlier stages of ON. The alternatives in

surgical treatment are core decompression, various osteotomies and ®nally total joint

replacement.

Acknowledgement

The author would like to thank Dr Gatterova for help with radiographic documentation, and

Dr CharvaÂt for help with MRI documentation.

Practice points

When should one think about osteonecrosis?
The clinical symptoms of ON are absolutely non-speci®c, and the radiographic

picture is negative in the early stages of the disease. An early diagnosis can be made

by more sophisticated (and expensive) techniques, so the timing of these

investigations is of critical importance. When should we thus consider these

investigations?
. sudden, intensive pain of the hip, which persists, often present at rest, with

minimum signs of OA on a radiographic picture

. pain in other less frequent localizations of ON in at-risk patients, especially in

the shoulder, knee and small joints of the hands and feet

. any history of trauma with or without dislocation
. the special risk group who might have caisson or diver's disease
. related to the age of the patient: in young patients, think of Perthes disease

and other special forms of avascular necrosis; in old patients, think also of

tumours, arteriosclerosis and other occlusive vascular disorders, gout and

metabolic bone disease

. think of ON when facing any hip pain in patients with risk factors of ON

(SLE, corticosteroid therapy or alcohol abuse)

. MRI is the gold standard for diagnosis in the early stages

Research agenda

. the aetiopathogenesis of idiopathic and other forms of ON needs to be

investigated

. exact early diagnosis in the pre-collapse stage is necessary
. a study should be made of the therapeutic use of bone morphogenic proteins

and bone marrow stem cells

412 K. Pavelka

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