Bone infarction

Last revised by Dr Henry Knipe on 07 Jul 2022

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 recognized microscopically by alterations in the cytoplasm (becomes eosinophilic) and in the nucleus (swelling, pyknosis, karyorrhexis, karyolysis). Bone infarction is a result of ischemia, 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.

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.

Whilst serpiginous sclerosis is a classic feature, radiographic findings can vary. In cases where radiographic findings are inconclusive, MRI is usually definitive 11

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 hyperemic ischemic zone. With time collagen granulation tissue becomes layered around the necrotic core. The demarcation between the normal surrounding marrow, the ischemic 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 vascularization, convex articular surfaces are affected the most. Impairment of blood flow may be caused by vascular compression, trauma, vessel occlusion by nitrogen bubbles (caisson disease) or rigid sickle cells (sickle cell anemia). The mechanism of ischemia and necrosis in other non-traumatic osteonecroses is not yet fully understood 1.

Rarely, bone infarcts can undergo cystic degeneration or liquefaction as bone marrow necroses 4.

General causes of osteonecrosis include:

The above list applies to both bone infarct and subchondral avascular necrosis. Some conditions are more likely to lead to one over the other: sickle cell disease and Gaucher disease very commonly cause bone infarcts and less commonly cause subchondral avascular necrosis.

General features include:

  • location
    • medullary
    • metaphyseal
  • serpiginous border
  • often symmetrical and/or multiple

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

CT features are similar to those seen on plain film. Again, onset of the infarct frequently precedes radiographic features by several months 12. The typical appearance is regions of patchy or serpiginous sclerosis surrounding a central metadiaphyseal lucency.

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 a 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 a double-line sign does not exclude bone infarct
    • central signal usually that of marrow
  • gradient echo
    • will also show double-line
    • edema obscured by susceptibility
  • bone scan
    • no uptake (cold spot/photopenia) where blood supply absent
    • mildly increased uptake at periphery during the acute phase

General imaging considerations include:

ADVERTISEMENT: Supporters see fewer/no ads

Cases and figures

  • Case 1: Gaucher disease
    Drag here to reorder.
  • Case 2: ALL on corticosteroids
    Drag here to reorder.
  • Case 3
    Drag here to reorder.
  • Case 4
    Drag here to reorder.
  • Case 5
    Drag here to reorder.
  • Case 6
    Drag here to reorder.
  • Case 7: bilateral bone infarctions around knees
    Drag here to reorder.
  • Case 8: bone infarct of humerus
    Drag here to reorder.
  • Case 9
    Drag here to reorder.
  • Case 10
    Drag here to reorder.
  • Case 11: multifocal bone infarcts
    Drag here to reorder.
  • Case 12: multifocal bone infarcts
    Drag here to reorder.
  • Case 13: Freiberg disease with distal tibial and navicular bone infarcts
    Drag here to reorder.
  • Case 14: alcoholism
    Drag here to reorder.
  • Updating… Please wait.

     Unable to process the form. Check for errors and try again.

     Thank you for updating your details.