Bone infarct refers to ischemic death of the cellular elements of the bone and marrow. A considerable lack of uniformity exists in the use of terminology for bone infarct. At present, the term osteonecrosis is accepted and used widely. In general, bone infarct refers to lesions occurring in the metaphysis and diaphysis of bone. Lesions in the epiphysis are called avascular necrosis (AVN). [1, 2, 3, 4]
Osteonecrosis can be idiopathic or secondary to a number of conditions that reduce blood supply to the bone; such conditions include an intraluminal abnormality, an extrinsic compression, or a combination of both. CT scans, MRIs, and bone scans play a significant role in diagnosing the disease at an early stage and thereby reducing the number and/or severity of complications and morbidity associated with the disease. See the images below.
Plain radiography is not sensitive in the detection of bone infarction. However, plain radiography has a role in the differential diagnosis. Radionuclide imaging and MRI are much more sensitive than plain radiography and may show changes caused by altered hemodynamics early in the course of disease. CT scanning is complementary to the other techniques, but it is not as sensitive as radionuclide imaging or MRI. CT scans may demonstrate subtle trabecular irregularity with bone necrosis when plain radiographic findings are normal. [2, 5, 6, 7, 3, 4] Ultrasonography may be useful in differentiating bone infarction from osteomyelitis in patients with sickle cell disease. [8, 9, 10, 11, 12, 13, 14]
For osteonecrosis of the femoral head, MRI has become the imaging modality of choice because of its high sensitivity and specificity. Radionuclide bone scans are less sensitive and specific than MRI but can be used to detect inflammatory activity if MRI is contraindicated. [4, 6, 15, 16, 17, 7] In patients with spontaneous osteonecrosis of the knee, diagnosis can be difficult because of the time before typical changes appear. MRI may provide an earlier diagnosis than other modalities. [15, 16, 17]
The American College of Radiology has published Appropriateness Criteria for osteonecrosis of the hip (Legg-Calve-Perthes disease), including the following  :
The initial imaging evaluation of suspected hip osteonecrosis is done using radiography.
MRI is the most sensitive and specific imaging modality for diagnosis of osteonecrosis of the hip.
The clinical significance of hip osteonecrosis is dependent on its potential for articular collapse.
The likelihood of articular collapse is significantly increased with involvement of greater than 30-50% of the femoral head area, which is optimally evaluated by MRI, often in the sagittal plane.
Contrast-enhanced MRI may be needed to detect early osteonecrosis of the hip in pediatric patients, revealing hypoperfusion.
In patients with a contraindication for MRI, use of either CT or bone scintigraphy with SPECT (single-photon emission CT) are alternative radiologic methods of assessment.
Imaging helps guide treatment, which may include core decompression, osteotomy, and, ultimately, need for joint replacement.
Limitations of techniques
No radiologic findings are specific for bone infarction. A variety of pathologies may mimic bone infarction, including stress fractures, infections, inflammations, and metabolic and neoplastic processes. A bone infarct may mimic a bone tumor on imaging. The limitations apply to all imaging modalities, including plain radiography, radionuclide studies, CT, and MRI. However, when the global picture is considered, including the history, clinical findings, and course of events, the diagnosis can be achieved with the help of imaging in most patients. 
Stage 0: normal findings are demonstrated.
Stage I: the appearance may vary from normal to subtle trabecular mottling, but an isotopic bone scan or MRI shows abnormal bone.
Stage II: stage IIa - focal radiopacity is associated with osteopenia; stage IIb - radiopacity is associated with osteoporosis and an early crescent sign.
Stage III: stage IIIa - an established crescent sign is associated with cyst formation; stage IIIb - mild alteration in the configuration of the femoral head is caused by a subchondral fracture, but the joint space is maintained.
Stage IV: marked collapse of the femoral head is demonstrated with an associated acetabular abnormality.
Stage V: joint space narrowing is demonstrated with changes of secondary osteoarthrosis.
Plain radiographic findings in established osteonecrosis may be characteristic of the disease. In the epiphyseal region, an arclike, subchondral, lucent lesion may be associated with areas of patchy loss of bone opacity intermingled with sclerotic areas and bone collapse. In the diametaphyseal region, a sheetlike lucency of varying size is usually surrounded by shell-like sclerosis and/or calcification and periostitis. In flat or complex bones, patchy lucencies and sclerosis are often associated with bone collapse or fractures (see the images below).
Posttraumatic osteonecrosis usually follows a fracture; most cases occur in areas with vulnerable blood supply, such as the femoral head, humeral head, talus, or scaphoid bone (see the image below).
Infarcted bone appears opaque as a result of compression. The femoral head is the most common site of osteonecrosis, which is a well-known complication of femoral head fractures and dislocations. Additionally, subchondral fracture of the femoral head has been associated with osteonecrosis, transient osteoporosis of the hip, and Pastel disease (ie, rapidly progressing osteoarthritis of the hip).
Radiographs obtained several months after the onset of symptoms may show a radiolucent crescent parallel to the articular surface secondary to subchondral collapse of the necrotic bone. Often, flattening of the articular surface is demonstrated, but the joint space tends to be preserved. The opacity of the infarcted femoral head is increased.
Radiographic changes in traumatic osteonecrosis of the talus are delayed (by 1-3 mo) and become apparent with osteoporosis of the surrounding bones, which creates relatively increased opacity in the body of the talus. The increase in radiopacity may be associated with a collapse of the articular surface.
Occasionally, a subchondral radiolucent band is demonstrated in the proximal talus; this finding is related to bone resorption. This Hawkins impingement sign usually indicates the presence of viable bone with an intact blood supply (see the image below).
Osteonecrosis of the humeral head is usually a complication of a fracture of the anatomic neck or severe fracture dislocation. Radiographic findings are delayed; they include flattening, sclerosis, and irregularity of part of the articular surface of the humeral head.
In the scaphoid bone, 10-15% of the fractures are complicated by osteonecrosis in the proximal pole of the scaphoid bone. Plain radiographic findings include relatively increased opacity in the infarcted pole of the scaphoid bone. This appearance may be delayed for 4-8 weeks, a period possibly associated with delayed union or nonunion of the fracture; collapse of the infarcted part of the bone; and, eventually, changes related to secondary osteoarthrosis.
Osteonecrosis of the capitate may occur after accidental or occupational trauma. The proximal part of the capitate is the site of AVN. After trauma or prolonged stress, AVN also may affect the lunate; the other carpal bones; the tarsal navicular bone; the mandibular condyle; the patella; the glenoid region of the scapula; and, occasionally, the metatarsal bones.
Osteonecrosis of the vertebral body (ie, Kümmell disease) usually occurs weeks to years after acute trauma. It usually causes vertebral collapse in middle-aged or elderly men or women. Generally, the lower dorsal or upper lumbar vertebrae are involved. Gas may be apparent in the vertebral body and may extend into the psoas muscles. These changes are depicted more elegantly on CT scans than on other images.
Spontaneous infarction of the femoral head is uncommon and affects men more often than women, in the group aged 40-70 years. Infarction may be unilateral or bilateral. The radiographic appearance depends on the severity of the disease. A minor form of femoral head infarction is recognized; this form affects a superficial area of the femoral head in a segmental distribution. The disease is nonprogressive. Radiographs may show a lobulated or segmental subcortical lucency, which may be surrounded by a sclerotic margin. The latter is better demonstrated on CT scans.
Spontaneous osteonecrosis around the adult knee (ie, Ahlbäck disease) is a distinct clinical entity that affects women more often than men. It commonly affects the medial femoral condyle and less commonly affects the medial or lateral tibial condyle. Initial radiographic findings are usually normal. Weeks or months later, subtle flattening and sclerosis of the weight-bearing femoral or tibial condyle may be seen. If untreated, further depression, sclerosis, and joint space narrowing occur. If the affected area is small, spontaneous recovery may ensue if weight-bearing is avoided.
Conventional tomography may show angular or wedge-shaped areas of patchy sclerotic bones and subtle collapse of the bone surface that is undetected on plain radiographs. The diagnosis of spontaneous osteonecrosis of the knee is being questioned. Current theories suggest that this entity is actually a subchondral stress fracture that most often occurs in the medial femoral condyle.
Spontaneous osteonecrosis of the tarsal navicular in adults (ie, Mueller-Weiss syndrome) may occur, especially in women. Plain radiographic features include medial or dorsal protrusion of a portion of the bone or the entire navicular bone.
These findings are often associated with a comma-shaped deformity caused by collapse of the lateral part of the bone. The disease may be bilateral or asymmetric and may be associated with pathologic fractures. The disease can be progressive at times, and it is associated with severe pain and disability. This syndrome is distinct from the osteochondrosis of the tarsal navicular bone that occurs in children (ie, Köhler disease).
Osteonecrosis secondary to Cushing disease
Osteonecrosis secondary to Cushing disease occurs as a result of excess levels of endogenous steroids. Most of the steroids are present in the vertebral bodies. Characteristic features are osteoporosis, osteosclerosis, subchondral radiolucent shadows, wedging and/or collapse, and bone fragmentation associated with a relatively normal articular space.
Osteonecrosis that affects the epiphysis and diaphysis is a known complication of Gaucher disease and is commonly associated with bone pain. In the long bones, bands of sclerosis and radiolucency alternate. These findings are associated with periostitis and a bone-within-bone appearance identical to that seen in sickle cell disease. 
Osteonecrosis may complicate hemophilia and is usually found in the femoral head and talus (see the image below). Bone infarction results from intraosseous hemorrhage with the subsequent collapse of bone or intracapsular hemorrhage and an elevation in intra-articular pressure that causes vascular compromise and eventual osteonecrosis. Radiographic features are similar to those of traumatic osteonecrosis. Ossification related to bleeding in the periarticular region may be apparent.
Caisson disease or dysbaric osteonecrosis
Two types of bone lesions that occur in patients with dysbaric osteonecrosis can be identified on plain radiographs: juxta-articular lesions, which are more common and mostly affect the head of the humerus and femur, and diaphyseal and metaphyseal lesions that occur at a distance from the joint.
Juxta-articular alterations are frequently encountered in the region of the head of the femur and humerus. They are depicted as radiopaque areas, spherical segmental radiopaque areas that may eventually produce a snow-capped appearance, radiolucent subcortical bands termed the crescent sign, and osseous collapse and fragmentation.
Diaphyseal and metaphyseal lesions are demonstrated as ill-defined radiopaque foci; irregular intraosseous areas of shell-like calcification; and, rarely, radiolucent defects. These changes may be unilateral or bilateral.
Osteonecrosis is a known complication of pancreatitis; it is usually associated with chronic or inactive forms of pancreatitis (see the image below).  Epiphyseal involvement is characterized by lucencies of mottled appearance or lucencies interspersed with sclerosis, subchondral radiolucent areas, and partial or complete collapse of the involved bone. Diaphyseal and metaphyseal involvement is associated with radiolucency, calcification, and periosteal new bone formation. The distal femur and the proximal tibia are the sites most commonly involved.
Osteonecrosis in pregnancy appears to be closely associated with childbirth. The femoral and humeral heads are the sites most commonly involved.
Systemic lupus erythematosus
The pathogenesis of osteonecrosis in patients with SLE is not clear, and the role of steroids is speculative. The overall radiographic appearances of bone infarcts are similar to those of infarcts in patients without SLE. The most commonly affected sites are the humeral head, femoral condyles, tibial plateaus, and talus. An unusual feature is the involvement of small bones of the wrist, hands, and feet; examples include the carpus, tarsus, and metatarsal and metacarpal heads.
Exposure to internal or external, accidental, or diagnostic and/or therapeutic radiation may produce diverse osseous changes, including disruption of growth, bone infarction, scoliosis, and benign and malignant neoplasms. Osseous changes are usually related to dose and age. Various parts of the skeleton respond differently upon exposure to radiation. Most osseous changes result from secondary radiation exposure during radiation therapy for soft tissue cancers. Common sites of involvement include the mandible, skull, shoulder, sternum, and shoulder. The threshold for osseous radiation injury is believed to be 3000 cGy, with cell death occurring at 5000 cGy.
Radiation osteitis is manifested by a mottled appearance with a mixture of osteoporosis, increased opacity, and coarse trabecular pattern demonstrated on plain radiographs. Different bones develop radiation-induced changes at varying times after the initial insult. Mandibular osteonecrosis commonly appears 1 year after radiation exposure; at other sites, the latent period is longer. Osteonecrosis is considerably more common in the mandible than in other bones owing to its compact bone structure and poor blood supply.
In addition, the mandible is exposed to a higher radiation dose because of its superficial location. Bone necrosis is usually mild and may be aseptic or associated with infection. Osteonecrosis appears as an ill-defined area of bone destruction without a sequestrum. An associated soft tissue mass is unusual with osteonecrosis; the presence of a soft tissue component suggests tumor recurrence.
Radiation necrosis of the skull usually occurs after a minimum radiation dose of 3500 cGy. The radiographic appearance is that of a mixed lytic and sclerotic area within the calvarium. If the osteonecrosis is associated with soft tissue necrosis, infection and/or osteomyelitis may ensue.
Osteonecrosis of the shoulder girdle may follow radiation therapy for breast carcinoma. Osteopenia is common after radiation therapy and is often associated with disorganized bone trabeculae that resemble findings in Paget disease. Pathologic rib fractures are common and often multiple. The edges of rib fractures show resorption, and the tips are often pointed or sclerotic. Clavicular and scapular fractures are often associated with these rib fractures.
Radiation necrosis of the humerus may develop as long as 7-10 years after radiation therapy. Changes include patchy bone resorption, fractures, and necrosis of the humeral head with a slipped proximal humeral head epiphysis.
Radiation necrosis of the sternum may follow treatment of breast cancer. Osseous changes may be mild and may be demonstrated as osteoporosis, abnormal trabecular patterns, localized lucencies, and sclerosis. More severe changes include abnormalities in alignment with localized pectus excavatum or complete necrosis of one or more segments of the sternum.
Unilateral or bilateral femoral neck fractures are reported in 2% of patients who are exposed to pelvic irradiation. These fractures are commonly subcapital. Often, sclerotic changes occur, and trabecular opacity increases in the femoral neck, preceding a fracture. Fractures usually heal normally with abundant callous formation. Protrusio acetabuli is also reported to occur after radiation therapy of the pelvis; this condition may be associated with peritoneal calcification. Changes indistinguishable from osteitis pubis may occur in the symphysis pubis.
Radionecrosis of the sacroiliac joints may cause widening and irregularity of the joint space. This condition is often associated with sclerosis, which is commonly symmetric and bilateral. Pathologic fractures of pelvic bones may occur after radiation therapy; these can involve the sacrum and may extend into one or both innominate bones.
Complications resulting from osteonecrosis
Complications from osteonecrosis usually are well depicted on plain radiographs. Cartilaginous abnormalities, such as fibrillation, erosions, and joint space narrowing, may affect joints. Changes of secondary osteoarthrosis may be apparent in cases involving significant collapse of an articular surface that occurs after an infarction. Loose bodies, either chondral or osteochondral, may be seen in a joint embedded within the depressed part of the bone or within the synovium.
Cystic degeneration in areas of bone infarction may occur, particularly in the diaphysis of tubular bones. Appearances are those of a well-marginated expanding osteolytic area eroding the cortex. The well-marginated cyst and the lack of cortical disruption help in differentiating the cyst from a malignant degeneration.
Malignant degeneration (eg, sarcoma) is a known complication of bone infarction irrespective of etiology.  Men are affected more often than women; patients are usually aged 40-70 years. Typically, the distal part of the femur or proximal tibia is involved, although other sites may be affected as well. The radiographic appearance is that of a soft tissue mass associated with bone destruction at a site of previous bone infarction.
Degree of confidence
Radiographic features of bone infarction do not occur until several months after the onset of symptoms; therefore, plain radiography is not a sensitive technique in the detection of bone infarction. However, plain radiography has a role in the differential diagnosis.
Early radiographic features of a bone infarct, particularly in the metaphyseal region of long bones, lack specificity. Vague areas of radiolucencies may mimic infections and neoplastic processes. Osteochondritis dissecans may mimic spontaneous osteonecrosis around the knee.
Radiographic findings in dysbaric osteonecrosis are indistinguishable from those of osteonecrosis resulting from other causes. Virtually identical features may be seen with bone islands. Osteonecrosis of the vertebral body may be difficult to differentiate from an osteoporotic fracture and vertebral collapse secondary to malignancy.
Cyst formation that occurs after bone infarction is occasionally difficult to differentiate from a malignant degeneration, particularly in early stages when the cysts are poorly marginated. Mimics of malignant degeneration of bone infarcts include fibrosarcoma, malignant fibrous histiocytoma, chondrosarcoma, and, rarely, osteosarcoma.
Radiation-induced mandibular osteonecrosis may be difficult to differentiate from tumor recurrence. Other regions of radiation osteonecrosis may mimic osteomyelitis. Radionecrosis of the shoulder girdle may mimic Paget disease. Changes indistinguishable from osteitis pubis may occur in the symphysis pubis, with radionecrosis. Radionecrosis of the sacroiliac joints may mimic osteitis condensans ilii.
CT scans demonstrate central or peripheral areas of reduced attenuation. Reformatted sagittal and coronal images show subchondral fractures and collapse of the articular surface. CT findings may show subtle trabecular irregularity associated with bone necrosis when plain radiographic findings are normal. Collapse or buckling of articular surfaces indicates more advanced disease and influences the choice of treatment.
As with conventional radiography, CT is not sensitive in the detection of bone infarcts. However, CT scans can help in diagnosing bone infarction earlier than would be the case with plain radiographs. The sensitivity of CT in the diagnosis of bone infarction is lower than that of MRI and bone scintigraphy.
As with plain radiography, early CT features of a bone infarct lack specificity, particularly in the metaphyseal region of the long bones. Vague radiolucencies may mimic infections and neoplastic processes.
Magnetic Resonance Imaging
Ischemic bone changes become apparent in hematopoietic tissues on MRIs within 6-12 hours. Ischemia is detectable in osteophytes, osteoblasts, and osteoclasts within approximately 2 days. An inflammatory response surrounding the devascularized bone, resulting from increased vascularity and granulation tissue, is demonstrated well as an interface on MRIs. A risk of subsequent AVN is associated with the early conversion of active marrow to fatty marrow in the proximal femur and with prominent physeal scars that close off the femoral head (see the images below). [13, 14]
MRI characteristics of bone infarction are variable focal abnormalities and are commonly demonstrated as patchy areas of low signal intensity on T1-weighted spin-echo images. Diffuse abnormal signal intensity may be present in osteonecrosis of the femoral head; these changes are reflected on both T1- and T2-weighted images.
The most characteristic appearance is the double-line sign, which consists of a hyperintense inner ring and a hypointense outer ring, on T2-weighted MRIs. This finding reflects the reactive interface between ischemic and nonischemic bone. The absence of a double-line sign does not exclude osteonecrosis. On T1-weighted MRIs, the interface appears as a low-signal-intensity line, which reflects a combination of granulation tissue and, to a lesser extent, sclerotic bone. Gadolinium-enhanced short–inversion recovery images demonstrate diminished enhancement in early infarctions of the femoral head.
In sickle cell disease, acute bone infarcts are caused by sequestration of red blood cells in the bone marrow. Thus, non-enhanced T1-weighted fat-saturated sequences appear to be diagnostic of acute bone infarcts.  Contrast enhancement aids in the diagnosis of acute osteomyelitis. 
Gadolinium-based contrast agents have been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans. NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellows pots on the whites of the eyes; joint stiffness with trouble moving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness.
MRI is highly sensitive and specific for osteonecrosis of the femoral head. T1 images typically demonstrate a serpiginous band-like lesion with low signal intensity in the anterosuperior femoral head; a double-line sign is seen on T2 sequences. 
No consensus has been reached regarding the best MRI sequences or imaging planes to use, although sagittal images, particularly when combined with the application of surface coils and small fields of view, appear to be more helpful than other images. 
Degree of confidence
MRI is considered more sensitive than standard scintigraphy. MRI is sensitive in the detection of spontaneous infarction around the knee.
MRI is useful in assessing the response to therapy, particularly the response of the femoral head to core decompression in which ischemic areas may shrink and edema may resolve. However, more often, the MRI characteristics of the infarcted area change little over time.
Diffusely distributed abnormal MRI findings of osteonecrosis in the femoral head may mimic transient osteoporosis of the hip, infection, or neoplasia. For instance, diffuse abnormal signal intensity on both T1- and T2-weighted images may mimic findings in infective and neoplastic processes.
A combination of scintigraphy and ultrasonography has been used in the differentiation of osteomyelitis from bone infarction in patients with sickle cell disease. [8, 9] Scintigraphic studies are useful in locating all areas of suggested osteomyelitis. Ultrasonography has a role in confirming the presence of a subperiosteal fluid collection and in guiding aspiration, which can be performed to distinguish a hematoma from an abscess.
In one series of 23 patients in whom osteomyelitis was associated with sickle disease, 21 patients had a subperiosteal fluid collection that was more than 10 mm at its thickest point. By contrast, patients with sickle cell crises had fluid collections less than 10 mm. Aspiration of fluid under ultrasonographic guidance is useful in differentiating osteomyelitis from infarction. In patients with osteomyelitis, the identification of the organism guides antibiotic administration. Needle decompression can help to relieve pain in patients with osteomyelitis and sickle cell crises.
After acute osteonecrosis occurs, technetium-99m diphosphonate uptake can be absent after 72 hours. Subsequently, with revascularization and associated osteoblastic repair, intense activity is seen.
The clinical assessment of posttraumatic AVN of the femoral head is difficult, though the preoperative identification of AVN is important. The displacement at the fracture site and the degree of femoral head ischemia are significantly correlated, but plain-film radiology is not reliable in the prediction of ischemia.
The appearances on isotopic scans depend on the time elapsed since injury (see the images below). Initially, the area of infarction has a photon-deficient or doughnut-like appearance, with increased activity surrounding the photopenic area. Subsequently, the photopenic area shrinks; as healing progresses, activity becomes uniform and intense. These changes are reliable, with a predictive value of 92.5%. Further improvement may be achieved by using single-photon emission tomography (SPECT). The major role of SPECT is in demonstrating a persistent photopenic defect resulting from incomplete vascularization.
Because myeloid tissue death precedes death of osteophytes, it has been proposed that radiocolloid imaging is superior to imaging with99m Tc diphosphonate in determining the viability of the femoral head, although some success has been achieved by using99m Tc sulfur colloid or99m Tc antimony colloid. However, false-positive scanning results have been reported in inactive marrow, particularly in elderly patients.
The scaphoid bone is the most frequently fractured carpal bone. Approximately one quarter to one half of fractures are missed on radiographs. Isotopic bone scans are 100% sensitive in the diagnosis of scaphoid fractures. AVN of the proximal fragment of the scaphoid bone is often a concern. On scintigraphs, a photopenic area may be demonstrated in the proximal fragment.
In patients with sickle cell disease, bone infarcts are typically multiple during the course of a sickle cell crisis. Areas of infarction are demonstrated as photopenic foci within 72 hours after the crisis. Splenic infarcts are also known to take up99m Tc diphosphonate and are a useful hint to the presence of sickling (see the image below). 
Revascularization results from collateral vessels that are predominantly derived from the periosteal blood supply; revascularization can be observed on isotopic bone scans as peripheral stripes of enhanced activity that extend with the healing process. However, a true bone infarct seldom occurs in an epiphysis because the epiphysis usually has an adequate collateral blood supply.
Ischemia may stimulate only osteoblastic activity, which results in increased isotope uptake without a photopenic stage. This feature poses problems in differentiating a bone infarct from osteomyelitis in the setting of sickle cell disease. Scanning with gallium-67 citrate may be required because its uptake is decreased or absent in acute infarction and is normal or increased in healing infarcts.67 Ga citrate is useful in differentiating septic infarction from fulminant photon-deficient osteomyelitis.
Similar changes occur in patients with Gaucher disease. In these patients, vascular compromise is caused by the accumulation of lipid-filled enlarged histiocytes within the medulla. The radioactivity is reduced, with a subsequent increase in isotopic uptake in the healing phase.67 Ga citrate is invaluable in differentiating photo-deficient osteomyelitis from a bone infarction.
Radiation necrosis is dose dependent and most probably is related to alteration in the microvasculature rather than direct bone damage. In most instances, affected bone is incidentally irradiated during the course of therapy in an adjacent organ. The isotopic uptake in radiation necrosis is variable. Changes indistinguishable from radiation necrosis may occur as a result of frostbite.
Bone scintigraphy reveals a focal increase in activity in spontaneous osteonecrosis around the knee, which can be identified long before radiographic changes become apparent. Similar findings apply to AVN of the talus that occurs after trauma.
Steroid-induced AVN causes a variety of changes, a fact that probably reflects its multifactorial etiology. A large photopenic area may be seen, similar to changes associated with major vascular compromise; however, more often, intense activity is noted at the site of infarction. These changes are less common than findings of patchy areas of increased accumulation of the radionuclide, sometimes with a streaky pattern of increase in the uptake. On occasion, multiple small areas of uptake are seen in the infarcted area.
Caisson disease is characterized by large areas of increased activity, which mostly is juxta-articular. The role of radionuclide scans is proposed to lie in predicting the development of necrosis in the lesions and thereby predicting the risk of the later development of osteoarthrosis.
Degree of confidence
Radionuclide uptake can be absent after 72 hours in viable osteocytes, whereas MRI findings are not altered for as long as 6 weeks. MRI findings in a series of 8 patients were negative, whereas radionuclide studies showed decreased isotope uptake in early osteonecrosis in patients at risk for AVN. This observation is not surprising because MRI depicts osteonecrosis by demonstrating bone marrow edema.
However, studies have revealed that fat cells are resistant to ischemia, dying 5 days after the initial insult. Though MRI findings may be negative, findings from isotopic scans may become positive during this period.
Many investigators have found that the series of changes in femoral neck fractures are reliable in ascertaining the viability of the femoral head. The accuracy in the prediction of such viability is 92.5%.
Bone scanning appears to be more sensitive than MRI in the detection of AVN of the scaphoid bone, but it is less specific. In scaphoid fractures, demonstration of a focal area of hyperemia and increased uptake provide reassurance in indicating revascularization.
Scintigraphic changes in steroid-induced osteonecrosis are detectable months before any abnormal findings are discernible on radiographs. Radionuclide scans have a sensitivity of 89% in detecting ischemic necrosis; by contrast, radiologic methods have a sensitivity of 41%.
Imaging characteristics of a bone infarct per se are nonspecific, and increased activity can be caused by a variety of conditions such as fractures, infections, inflammations, and metabolic and neoplastic processes. Photon-deficient bone lesions may occur with early osteomyelitis, plasmacytoma, histiocytosis X, bone metastases, and sickle cell crises.
Intramedullary phlebography has been used in the diagnosis of bone infarction in the femoral head. The technique involves traversing the trochanteric bone with a bone needle, such as the Jamshidi needle, and injecting radiographic iodinated contrast material through it. Normal venographic findings thus obtained are usually characterized by painlessness on injection and by the demonstration of draining veins without diaphyseal reflux or stasis. When necrosis of the femoral head is present, the injection is painful and is usually followed by reflux into the diaphysis and stasis of the contrast agent for as long as 15 minutes.
The exact sensitivity of intramedullary phlebography is not known. The technique is invasive, and because there are so many other techniques now available, phlebography is seldom indicated. The technique must be performed by a radiologist with expertise in this area.