Bone infarction

Dr Owen Kang and Dr Andrew Dixon et al.

Bone infarction is a term used to refer to osteonecrosis within the metaphysis or diaphysis of a bone. Necrosis is a type of cell death due to irreversible cell injury, which can be recognised microscopically by alterations in the cytoplasm (becomes eosinophilic) and in the nucleus (swelling, pyknosis, karyorrhexis, karyolysis). Bone infarction is a result ischaemia, which can lead to destruction of bony architecture, pain and loss of function 1. Bone infarctions have numerous causes and have fairly distinctive imaging features on conventional radiography, CT and MRI. 

Terminology

Medullary infarct is a fairly equivalent term to bone infarct but is less frequently used. The term may also be applied to some cases involving the epiphysis, but should not be used to describe subchondral osteonecrosis, in which case avascular necrosis (AVN) is preferred. 

Pathology

Infarction begins when blood supply to a section of bone is interrupted. Once an infarct is established, a central necrotic core develops which is surrounded by a hyperaemic ischaemic zone. With time collagen granulation tissue becomes layered around the necrotic core. Demarcation between the normal surrounding marrow, the ischaemic zone and the necrotic core accounts for many of the radiographic appearances of bone infarcts.

Due to the smaller diameter of terminal vessels and the lack of collateral vascularisation, convex articular surfaces are affected the most. Impairment of blood flow may be caused by vascular compression, trauma, vessel occlusion by nitrogen bubbles (in Caisson disease) or rigid sickle cells ( in sickle cell anaemia). The mechanism of ischaemia and necrosis in other non-traumatic osteonecroses is not yet fully understood 1.

Aetiology

General causes of osteonecrosis include:

The above list applies to both bone infarct and subchondral avascular necrosis, however some conditions are more likely to lead to one over the other. Sickle cell disease and Gaucher disease for instance very commonly cause bone infarcts and less commonly cause subchondral AVN.

Radiographic features

General features include:

  • medullary lesion
  • serpiginous border
  • most common in metaphyses
  • often symmetrical and/or multiple infarcts
Plain radiography

There is significant delay between infarct onset and development of radiographic signs. Classic description is of medullary lesion of sheet-like central lucency surrounded by shell-like sclerosis with serpiginous border. Discrete calcification and periostitis may also be seen.

CT

Generally does not reveal much more than the plain film.

MRI

An important feature in differentiating bone infarct from other medullary lesions is that the central signal usually remains that of normal marrow. The marrow is not replaced.

  • T1
    • serpiginous peripheral low signal due to granulation tissue and to lesser extent sclerosis
    • peripheral rim may enhance post gadolinium
    • central signal usually that of marrow
  • T2
    • acute infarct may show ill-defined non-specific area of high signal
    • double-line sign: hyperintense inner ring of granulation tissue and a hypointense outer ring of sclerosis
    • absence of double-line sign does not exclude bone infarct
    • central signal usually that of marrow
  • GE (gradient echo)
    • will also show double-line
    • oedema obscured by susceptibility
Nuclear medicine
  • bone scan
    • no uptake (cold spot) where blood supply absent
    • mildly increased uptake at periphery during acute phase

Treatment and prognosis

Complications

Bone infarcts may occasionally dedifferentiate to a tumour such as 5-7

This most commonly occurs around the knee 8.

Differential diagnosis

General imaging considerations include:

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