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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 the 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.
Bone infarct accounts for one of the 'I's in the popular mnemonic for lucent bone lesions FEGNOMASHIC.
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 osteonecrosis (previously termed "avascular necrosis") 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:
corticosteroid excess (both endogenous and exogenous)
The above list applies to both bone infarct and subchondral osteonecrosis. 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 osteonecrosis.
General features include:
often symmetrical and/or multiple
There is a significant delay between the infarct onset and development of radiographic signs. The 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, the 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.
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
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
will also show double-line
edema obscured by susceptibility
no uptake (cold spot/photopenia) where blood supply absent
mildly increased uptake at periphery during the acute phase
Treatment and prognosis
Bone infarcts may occasionally dedifferentiate to a tumor such as 5-7:
General imaging considerations include:
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