Bone infarction
- Philips Australia, Paid speaker at Philips Spectral CT events (ongoing)
Updates to Article Attributes
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 of 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.
Bone infarct accounts for one of the 'I's in the popular mnemonic for lucent bone lesions FEGNOMASHIC.
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.
Diagnosis
Whilst serpiginous sclerosis is a classic feature, radiographic findings can vary. In cases where radiographic findings are inconclusive, MRI is usually definitive 11.
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. The 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 (caisson disease) or rigid sickle cells (sickle cell anaemia). The mechanism of ischaemia 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.
Aetiology
General causes of osteonecrosis include:
corticosteroid excess (both endogenous and exogenous)
alcohol
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.
Radiographic features
General features include:
-
location
medullary
metaphyseal
serpiginous border
often symmetrical and/or multiple
Plain radiograph
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
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.
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 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
oedema obscured by susceptibility
Nuclear medicine
-
bone scan
no uptake (cold spot/photopenia) where blood supply absent
mildly increased uptake at periphery during the acute phase
Treatment and prognosis
Complications
-
Bone infarcts may occasionally dedifferentiate to a tumour such as 5-7:
malignant fibrous histiocytoma (most common 8)
-
angiosarcoma of bone (extremely rare)
this most commonly occurs around the knee 8
medullary infarcts may function as sequestra, predisposing patients to osteomyelitis and soft-tissue infection 10
Differential diagnosis
General imaging considerations include:
enchondroma: chondroid matrix, central marrow signal is absent
healing non-ossifying fibroma
normal red marrow: will not extend beyond physeal scar
marrow tumour: central marrow signal is absent
-<p><strong>Bone infarction</strong> is a term used to refer to <a href="/articles/osteonecrosis-2">osteonecrosis</a> within the <a href="/articles/metaphysis">metaphysis</a> or <a href="/articles/diaphysis">diaphysis</a> of a bone. <a href="/articles/necrosis-1">Necrosis</a> 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 of ischaemia, which can lead to destruction of bony architecture, pain, and loss of function <sup>1</sup>. Bone infarctions have numerous causes and have fairly distinctive imaging features on conventional radiography, CT and MRI.</p><h4>Terminology</h4><p><strong>Medullary infarct</strong> 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 <a href="/articles/osteonecrosis-2">avascular necrosis (AVN)</a> is preferred.</p><h4>Diagnosis</h4><p>Whilst serpiginous sclerosis is a classic feature, radiographic findings can vary. In cases where radiographic findings are inconclusive, MRI is usually definitive <sup>11</sup>. </p><h4>Pathology</h4><p>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. The demarcation between the normal surrounding marrow, the ischaemic zone, and the necrotic core accounts for many of the radiographic appearances of bone infarcts.</p><p>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 (<a href="/articles/decompression-sickness">caisson disease</a>) or rigid sickle cells (<a href="/articles/sickle-cell-disease">sickle cell anaemia</a>). The mechanism of ischaemia and necrosis in other non-traumatic osteonecroses is not yet fully understood <sup>1</sup>.</p><p>Rarely, bone infarcts can undergo cystic degeneration or liquefaction as bone marrow necroses <sup>4</sup>.</p><h5>Aetiology</h5><p>General causes of osteonecrosis include:</p><ul>-<li><a href="/articles/trauma">trauma</a></li>-<li><a href="/articles/caisson-disease">caisson disease</a></li>-<li>-<a href="/articles/haemoglobinopathies">haemoglobinopathies</a>, e.g. <a href="/articles/sickle-cell-disease">sickle cell disease </a><sup>2</sup>-</li>-<li><a href="/articles/radiotherapy-2">radiotherapy</a></li>-<li><a href="/articles/connective-tissue-disorders">connective tissue disorders</a></li>-<li><a href="/articles/renal-transplant-related-complications">renal transplantation</a></li>-<li>corticosteroid excess (both endogenous and exogenous)</li>-<li><a href="/articles/pancreatitis">pancreatitis </a></li>-<li><a href="/articles/gout">gout</a></li>-<li><a href="/articles/gaucher-disease">Gaucher disease</a></li>-<li>alcohol</li>-<li>-<a href="/articles/behcet-disease-2">Behçet disease</a> <sup>9</sup>-</li>- +<p><strong>Bone infarction</strong> is a term used to refer to <a href="/articles/osteonecrosis-2">osteonecrosis</a> within the <a href="/articles/metaphysis">metaphysis</a> or <a href="/articles/diaphysis">diaphysis</a> of a bone. <a href="/articles/necrosis-1">Necrosis</a> 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 of ischaemia, which can lead to destruction of bony architecture, pain, and loss of function <sup>1</sup>. Bone infarctions have numerous causes and have fairly distinctive imaging features on conventional radiography, CT and MRI.</p><p>Bone infarct accounts for one of the 'I's in the popular mnemonic for lucent bone lesions <a href="/articles/lucentlytic-bone-lesion-differential-diagnosis-mnemonic-1">FEGNOMASHIC</a>.</p><h4>Terminology</h4><p><strong>Medullary infarct</strong> 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 <a href="/articles/osteonecrosis-2">avascular necrosis (AVN)</a> is preferred.</p><h4>Diagnosis</h4><p>Whilst serpiginous sclerosis is a classic feature, radiographic findings can vary. In cases where radiographic findings are inconclusive, MRI is usually definitive <sup>11</sup>. </p><h4>Pathology</h4><p>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. The demarcation between the normal surrounding marrow, the ischaemic zone, and the necrotic core accounts for many of the radiographic appearances of bone infarcts.</p><p>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 (<a href="/articles/decompression-sickness">caisson disease</a>) or rigid sickle cells (<a href="/articles/sickle-cell-disease">sickle cell anaemia</a>). The mechanism of ischaemia and necrosis in other non-traumatic osteonecroses is not yet fully understood <sup>1</sup>.</p><p>Rarely, bone infarcts can undergo cystic degeneration or liquefaction as bone marrow necroses <sup>4</sup>.</p><h5>Aetiology</h5><p>General causes of osteonecrosis include:</p><ul>
- +<li><p><a href="/articles/trauma">trauma</a></p></li>
- +<li><p><a href="/articles/caisson-disease">caisson disease</a></p></li>
- +<li><p><a href="/articles/haemoglobinopathies">haemoglobinopathies</a>, e.g. <a href="/articles/sickle-cell-disease">sickle cell disease </a><sup>2</sup></p></li>
- +<li><p><a href="/articles/radiotherapy-2">radiotherapy</a></p></li>
- +<li><p><a href="/articles/connective-tissue-disorders">connective tissue disorders</a></p></li>
- +<li><p><a href="/articles/renal-transplant-related-complications">renal transplantation</a></p></li>
- +<li><p>corticosteroid excess (both endogenous and exogenous)</p></li>
- +<li><p><a href="/articles/pancreatitis">pancreatitis</a></p></li>
- +<li><p><a href="/articles/gout">gout</a></p></li>
- +<li><p><a href="/articles/gaucher-disease">Gaucher disease</a></p></li>
- +<li><p>alcohol</p></li>
- +<li><p><a href="/articles/behcet-disease-2">Behçet disease</a> <sup>9</sup></p></li>
-<li>location<ul>-<li>medullary</li>-<li>metaphyseal</li>- +<li>
- +<p>location</p>
- +<ul>
- +<li><p>medullary</p></li>
- +<li><p>metaphyseal</p></li>
-<li>serpiginous border</li>-<li>often symmetrical and/or multiple</li>- +<li><p>serpiginous border</p></li>
- +<li><p>often symmetrical and/or multiple</p></li>
-<strong>T1</strong><ul>-<li>serpiginous peripheral low signal due to granulation tissue and, to a lesser extent, sclerosis</li>-<li>peripheral rim may enhance post gadolinium</li>-<li>central signal usually that of marrow</li>- +<p><strong>T1</strong></p>
- +<ul>
- +<li><p>serpiginous peripheral low signal due to granulation tissue and, to a lesser extent, sclerosis</p></li>
- +<li><p>peripheral rim may enhance post gadolinium</p></li>
- +<li><p>central signal usually that of marrow</p></li>
-<strong>T2</strong><ul>-<li>acute infarct may show ill-defined non-specific area of high signal</li>-<li>-<a href="/articles/double-line-sign">double-line sign</a>: hyperintense inner ring of granulation tissue and a hypointense outer ring of sclerosis</li>-<li>absence of a double-line sign does not exclude bone infarct</li>-<li>central signal usually that of marrow</li>- +<p><strong>T2</strong></p>
- +<ul>
- +<li><p>acute infarct may show ill-defined non-specific area of high signal</p></li>
- +<li><p><a href="/articles/double-line-sign">double-line sign</a>: hyperintense inner ring of granulation tissue and a hypointense outer ring of sclerosis</p></li>
- +<li><p>absence of a double-line sign does not exclude bone infarct</p></li>
- +<li><p>central signal usually that of marrow</p></li>
-<strong>gradient echo</strong><ul>-<li>will also show double-line</li>-<li>oedema obscured by susceptibility</li>- +<p><strong>gradient echo</strong></p>
- +<ul>
- +<li><p>will also show double-line</p></li>
- +<li><p>oedema obscured by susceptibility</p></li>
-<strong>bone scan</strong><ul>-<li>no uptake (cold spot/photopenia) where blood supply absent</li>-<li>mildly increased uptake at periphery during the acute phase</li>-</ul>-</li></ul><h4>Treatment and prognosis</h4><h5>Complications</h5><ul><li>Bone infarcts may occasionally dedifferentiate to a tumour such as <sup>5-7</sup>:<ul>-<li>-<a href="/articles/undifferentiated-pleomorphic-sarcoma-1">malignant fibrous histiocytoma</a> (most common <sup>8</sup>)</li>-<li><a href="/articles/osteogenic-sarcoma">osteogenic sarcoma</a></li>-<li><a href="/articles/fibrosarcoma-of-the-bone">fibrosarcoma of bone</a></li>- +<p><strong>bone scan</strong></p>
- +<ul>
- +<li><p>no uptake (cold spot/photopenia) where blood supply absent</p></li>
- +<li><p>mildly increased uptake at periphery during the acute phase</p></li>
- +</ul>
- +</li></ul><h4>Treatment and prognosis</h4><h5>Complications</h5><ul><li>
- +<p>Bone infarcts may occasionally dedifferentiate to a tumour such as <sup>5-7</sup>:</p>
- +<ul>
- +<li><p><a href="/articles/undifferentiated-pleomorphic-sarcoma-1">malignant fibrous histiocytoma</a> (most common <sup>8</sup>)</p></li>
- +<li><p><a href="/articles/osteogenic-sarcoma">osteogenic sarcoma</a></p></li>
- +<li><p><a href="/articles/fibrosarcoma-of-the-bone">fibrosarcoma of bone</a></p></li>
-<a href="/articles/angiosarcoma-bone-1">angiosarcoma of bone</a> (extremely rare)<ul><li>this most commonly occurs around the knee <sup>8</sup>-</li></ul>-</li>-<li>medullary infarcts may function as sequestra, predisposing patients to <a href="/articles/osteomyelitis">osteomyelitis</a> and soft-tissue infection <sup>10</sup>- +<p><a href="/articles/angiosarcoma-bone-1">angiosarcoma of bone</a> (extremely rare)</p>
- +<ul><li><p>this most commonly occurs around the knee <sup>8</sup></p></li></ul>
- +<li><p>medullary infarcts may function as sequestra, predisposing patients to <a href="/articles/osteomyelitis">osteomyelitis</a> and soft-tissue infection <sup>10</sup></p></li>
-<li>-<a href="/articles/enchondroma">enchondroma</a>: chondroid matrix, central marrow signal is absent</li>-<li>healing <a href="/articles/non-ossifying-fibroma-1">non-ossifying fibroma</a>-</li>-<li>normal <a href="/articles/bone-marrow">red marrow</a>: will not extend beyond physeal scar</li>-<li>marrow tumour: central marrow signal is absent</li>- +<li><p><a href="/articles/enchondroma">enchondroma</a>: chondroid matrix, central marrow signal is absent</p></li>
- +<li><p>healing <a href="/articles/non-ossifying-fibroma-1">non-ossifying fibroma</a></p></li>
- +<li><p>normal <a href="/articles/bone-marrow">red marrow</a>: will not extend beyond physeal scar</p></li>
- +<li><p>marrow tumour: central marrow signal is absent</p></li>
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