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.
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.
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.
General causes of osteonecrosis include:
- Caisson disease
- haemoglobinopathies, e.g. sickle cell disease 2
- connective tissue disorders
- renal transplantation
- corticosteroid excess (both endogenous and exogenous)
- Gaucher disease
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.
General features include:
- medullary lesion
- serpiginous border
- most common in metaphyses
- often symmetrical and/or multiple infarcts
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.
Generally does not reveal much more than the plain film.
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 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 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
- no uptake (cold spot) where blood supply absent
- mildly increased uptake at periphery during acute phase
Treatment and prognosis
Bone infarcts may occasionally dedifferentiate to a tumour such as 5-7
- malignant fibrous histiocytoma (most common 8)
- osteogenic sarcoma
- fibrosarcoma of bone
- angiosarcoma of bone (extremely rare)
This most commonly occurs around the knee 8.
General imaging considerations include:
- 1.Fondi C, Franchi A. Definition of bone necrosis by the pathologist. Clinical cases in Mineral and Bone metabolism. 2007 Jan; 4(1): 21-6. Available at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2781178/#R11.
- 2. 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. doi:10.1148/rg.304095171 - Pubmed citation
- 3. Stoller DW, Tirman PF, Bredella MA. Diagnostic imaging, Orthopaedics. Amirsys Inc. (2004) ISBN:0721629202. Read it at Google Books - Find it at Amazon
- 4. Hermann G, Singson R, Bromley M et-al. Cystic degeneration of medullary bone infarction evaluated with magnetic resonance imaging correlated with pathologic examination. Can Assoc Radiol J. 2004;55 (5): 321-5. - Pubmed citation
- 5. Abdelwahab IF, Klein MJ, Hermann G et-al. Angiosarcomas associated with bone infarcts. Skeletal Radiol. 1998;27 (10): 546-51. - Pubmed citation
- 6. 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. - Pubmed citation
- 7. Torres FX, Kyriakos M. Bone infarct-associated osteosarcoma. Cancer. 1992;70 (10): 2418-30. - Pubmed citation
- 8. Domson GF, Shahlaee A, Reith JD et-al. Infarct-associated bone sarcomas. Clin. Orthop. Relat. Res. 2009;467 (7): 1820-5. doi:10.1007/s11999-009-0744-7 - Free text at pubmed - Pubmed citation