Bone infarction

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.

Terminology

Medullary infarct is a fairly equivalent term to bone infarct ¹³ 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.

Diagnosis

Whilst serpiginous sclerosis is a classic feature, radiographic findings can vary ¹³. In cases where radiographic findings are inconclusive, MRI is usually definitive ¹¹. 

Clinical presentation

Bone infarcts are mostly incidental findings with <50% of patients symptomatic ¹³. When symptomatic, patients may present with pain and/or decreased function ¹³.

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 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.

Etiology

General causes of osteonecrosis include:

• Gaucher disease ¹³

• alcohol ¹³

• caisson disease ¹³

• hemoglobinopathies, e.g. sickle cell disease ^2,13

• corticosteroid excess (both endogenous and exogenous) ¹³

• trauma

• radiation therapy

• connective tissue disorders

• renal transplantation

• pancreatitis

• gout

• Behçet disease ⁹

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.

Radiographic features

General features include:

• location: medullary cavity in the diaphysis or metaphysis ¹³

• irregular well-defined sclerotic border ¹³

• multiple in ~50% of cases ¹³

• often symmetrical ^ref

Plain radiograph

There is a significant delay between the infarct onset and development of radiographic signs, which can be variable ¹³.

The classic description is of medullary lesion of sheet-like central lucency surrounded by shell-like sclerosis with an irregular but well-defined border, although they may also appear as ill-defined lucencies ¹³.

Infarcts that have undergone cystic degeneration can be expansile lucenies with endosteal scalloping ⁴.

Discrete calcifications ¹³ and periostitis ^ref may also be seen.

CT

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.

MRI

An important feature in differentiating bone infarct from other medullary lesions is that the central signal usually remains that of normal bone marrow ¹³ except in rare cases of cystic degeneration ⁴. 

Signal characteristics

• T1

  • acute infarcts: intermediate-to-low signal ¹³

  • chronic infarcts: serpiginous peripheral low signal due to granulation tissue and, to a lesser extent, sclerosis ¹³

  • central T1 signal usually that of bone marrow although may be high in rare cases of cystic degeneration ⁴

• T2

  • acute infarct: ill-defined high signal ¹³

  • chronic infarct: low signal "geographic" rim with central fat-intensity signal or less commonly central low signal from marrow fibrosis/sclerosis ¹³

  • 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 ^ref

  • central T2 signal usually that of bone marrow ^ref although may be high in rare cases of cystic degeneration ⁴

• GRE

  • will also show the double-line sign

  • edema obscured by susceptibility

• T1 C+ FS (Gd): peripheral rim may enhance post gadolinium

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 tumor 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

• medullary infarcts may function as sequestra, predisposing patients to osteomyelitis and soft-tissue infection ¹⁰

Differential diagnosis

General imaging considerations include ^ref:

• enchondroma: chondroid matrix, central marrow signal is absent

• healing non-ossifying fibroma

• normal red marrow: will not extend beyond physeal scar

• bone marrow tumor: normal bone marrow signal is replaced

• bone reinforcement lines

• growth arrest lines