Bone infarction
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 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 affect 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 osteonecrosis is not yet fully understood 1.
Aetiology
General causes of osteonecrosis include:
- trauma
- Caisson disease
- haemoglobinopathies, e.g. sickle cell disease
12 - radiotherapy
- connective tissue disorders
- renal transplantaion
- corticosteroid excess (both endogenous and exogenous)
- pancreatitis
- gout
- Gaucher disease
- alcohol
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 4-65-7
-
malignant fibrous histiocytoma (most common
78) - osteogenic sarcoma
- fibrosarcoma of bone
- angiosarcoma of bone (extremely rare)
This most commonly occurs around the knee 78.
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/avascular-necrosis">osteonecrosis</a> within the <a href="/articles/metaphysis">metaphysis</a> or <a href="/articles/diaphysis">diaphysis</a> of a bone. 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/avascular-necrosis">avascular necrosis</a> (AVN) is preferred. </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. Demarcation between the normal surrounding marrow, the ischaemic zone and the necrotic core accounts for many of the radiographic appearances of bone infarcts.</p><h5>Aetiology</h5><p>General causes of osteonecrosis include:</p><ul>- +<p><strong>Bone infarction</strong> is a term used to refer to <a href="/articles/avascular-necrosis">osteonecrosis</a> within the <a href="/articles/metaphysis">metaphysis</a> or <a href="/articles/diaphysis">diaphysis</a> 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 <sup><span style="font-size:11px">1</span></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/avascular-necrosis">avascular necrosis</a> (AVN) is preferred. </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. 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 affect 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 osteonecrosis is not yet fully understood <sup>1</sup>.</p><h5>Aetiology</h5><p>General causes of osteonecrosis include:</p><ul>
-<li>haemoglobinopathies, e.g. <a href="/articles/sickle-cell-disease">sickle cell disease </a><sup>1</sup>- +<li>haemoglobinopathies, e.g. <a href="/articles/sickle-cell-disease">sickle cell disease </a><sup>2</sup>
-</li></ul><h4>Treatment and prognosis</h4><h5>Complications</h5><p>Bone infarcts may occasionally dedifferentiate to a tumour such as <sup>4-6</sup></p><ul>- +</li></ul><h4>Treatment and prognosis</h4><h5>Complications</h5><p>Bone infarcts may occasionally dedifferentiate to a tumour such as <sup>5-7</sup></p><ul>
-<a href="/articles/malignant-fibrous-histiocytoma">malignant fibrous histiocytoma</a> (most common <sup>7</sup>)</li>- +<a href="/articles/malignant-fibrous-histiocytoma">malignant fibrous histiocytoma</a> (most common <sup>8</sup>)</li>
-</ul><p>This most commonly occurs around the knee <sup>7</sup>.</p><h4>Differential diagnosis</h4><p>General imaging considerations include:</p><ul>- +</ul><p>This most commonly occurs around the knee <sup>8</sup>.</p><h4>Differential diagnosis</h4><p>General imaging considerations include:</p><ul>
References changed:
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- 8. Domson G, Shahlaee A, Reith J, Bush C, Gibbs C. Infarct-Associated Bone Sarcomas. Clin Orthop Relat Res. 2009;467(7):1820-5. <a href="https://doi.org/10.1007/s11999-009-0744-7">doi:10.1007/s11999-009-0744-7</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/19229663">Pubmed</a>
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- 4. Hermann G, Singson R, Bromley M, Klein M, Springfield D, Abdelwahab I. Cystic Degeneration of Medullary Bone Infarction Evaluated with Magnetic Resonance Imaging Correlated with Pathologic Examination. Can Assoc Radiol J. 2004;55(5):321-5. - <a href="https://www.ncbi.nlm.nih.gov/pubmed/15646462">Pubmed</a>
- 7. Torres F & Kyriakos M. Bone Infarct-Associated Osteosarcoma. Cancer. 1992;70(10):2418-30. <a href="https://doi.org/10.1002/1097-0142(19921115)70:10<2418::aid-cncr2820701007>3.0.co;2-e">doi:10.1002/1097-0142(19921115)70:10<2418::aid-cncr2820701007>3.0.co;2-e</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/1423172">Pubmed</a>
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- 1. Saito N, Nadgir RN, Flower EN et-al. Clinical and radiologic manifestations of sickle cell disease in the head and neck. Radiographics. 30 (4): 1021-34. <a href="http://dx.doi.org/10.1148/rg.304095171">doi:10.1148/rg.304095171</a> - <a href="http://www.ncbi.nlm.nih.gov/pubmed/20631366">Pubmed citation</a><div class="ref_v2"></div>
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- 5. Desai P, Perino G, Present D et-al. Sarcoma in association with bone infarcts. Report of five cases. Arch. Pathol. Lab. Med. 1996;120 (5): 482-9. - <a href="http://www.ncbi.nlm.nih.gov/pubmed/8639053">Pubmed citation</a><div class="ref_v2"></div>
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