Osteonecrosis Imaging

Anatomy

The bone is a complex organ composed of cortical and trabecular bone structures. Osteonecrosis involves the trabecular and subcortical bone. The pathophysiology of osteonecrosis is characterized by cell death due to lack of blood supply, followed by a complex process of bone resorption and formation in an attempt to heal. The healing process includes walling off the dead bone by forming a fibrotic rim at the margin between the living and dead bone. At this interface, granulation tissue develops with osteoblasts encapsulating the dead trabeculae and osteoclasts that partially reabsorb the dead bone. In the subchondral trabeculae, the bone resorption rate exceeds the bone formation rate, leading to a net removal of bone and loss of structural integrity.[3] This area is then predisposed to increased compressive forces and subsequent subchondral collapse. 

These histological changes can be observed on radiographs as serpentine areas of sclerosis and lucency. The lucent areas represent bone resorption, whereas the sclerotic areas represent mixed areas of living and dead bone trabeculae.[1][3] These changes are most prominently observed in the diaphysis and metaphysis of long bones. Osteonecrosis affecting the diaphysis and metaphysis is less clinically important because dead bone in long bones is not subject to the same compressive forces, and it is considered just as strong as living bone without the ability to remodel.[1] In these locations, it often goes underdiagnosed as it is typically asymptomatic and often incidentally found. 

Osteonecrosis affecting small bones commonly has a history of antecedent trauma. This condition affects many bones of the hands and feet, the most commonly involved being the scaphoid bone, lunate, and talus. On plain film, it often appears as an increased area of sclerosis requiring MRI for further evaluation. 

Most osteonecrosis sites are associated with a specific eponym (see Table 1. Common Osteonecrosis Eponyms).

Table 1. Common Osteonecrosis Eponyms

The etiologies of osteonecrosis are diverse. Trauma is a frequent cause of symptomatic osteonecrosis of the femoral head, scaphoid, and talus due to disruption of the end arterial supply. The most common nontraumatic causes of osteonecrosis include chronic corticosteroid use, excessive alcohol consumption, and idiopathic factors. Sickle cell disease is an important consideration of nontraumatic causes due to the precipitation of hemoglobin S in low-oxygen environments, leading to vasocclusion and bone ischemia.[2] Drug therapy with bisphosphonates has a well-known association with osteonecrosis of the jaw due to inhibition of bone turnover.[4] In the renal transplant population, there is also a high prevalence of this condition due to chronic high-dose steroid use and chronic immunosuppression. Nontraumatic causes are often bilateral and have multiple affected sites. A detailed clinical history, including the patient's predisposing risk factors, is crucial when interpreting diagnostic imaging studies, particularly for plain radiographs, to improve sensitivity in detecting subtle areas of osteonecrosis, particularly in the epiphysis. 

Some of the more common causes of osteonecrosis include the following:

• Trauma
• Chronic high-dose corticosteroid use 
• Alcohol use disorder
• Sickle cell disease or hemoglobinopathies
• Systemic lupus erythematosus
• Antiphospholipid antibody syndrome
• Gaucher disease 
• Metabolic diseases such as hyperlipidemia
• Renal transplantation
• HIV
• Prior radiation therapy
• Chemotherapy
• Decompression sickness 
• Bisphosphonate use

Plain Films

Plain films or radiographs are good initial imaging exams to begin the evaluation. Although not as sensitive for detecting early changes in osteonecrosis, plain radiographs are readily accessible, inexpensive, and can exclude other underlying causes of bone pain. Radiographs have imaging characteristics that may limit the need for additional imaging evaluations.[1]

Early findings may show minor osteopenia compared to the contralateral bone. In small bones, osteonecrosis appears as areas of increased sclerosis compared to adjacent bones. In long bones, early to chronic characteristic imaging findings show patchy areas of lucency with a serpentine rim of sclerosis. The serpentine sclerotic rim is most conspicuous in meta-diaphyseal zones (see Image. Metaphyseal Osteonecrosis).

Early findings may show slight osteopenia in comparison to the opposite bone. In small bones, osteonecrosis will appear as areas with increased hardness compared to nearby bones. In long bones, characteristic imaging findings from early to chronic stages include scattered areas of hollowness surrounded by a winding rim of hardness. This winding hard rim is most noticeable in the areas between the metaphysis and diaphysis

Plain radiographs also show late findings and complications involving the epiphysis, such as articular collapse. Articular collapse occurs when there is epiphyseal osteonecrosis with areas extending to the junction of the articular surface and subchondral bone (see Image. Articular Collapse). When stress is maximally exerted at these sites, the underlying necrotic subchondral bone collapses, creating a linear crescentic subchondral lucency known as the crescent sign (see Image. Crescent Sign).[5] Eventually, the bone cortex collapses and fragments, leading to secondary progressive degenerative changes.

Computed Tomography

CT is useful in the advanced stages of osteonecrosis and for surgical planning once the diagnosis of osteonecrosis is established. This technique is valuable in evaluating bony details to delineate the location and extent of articular collapse, particularly when there is epiphyseal involvement. CT scans typically share similar imaging characteristics as observed in plain radiographs, showing a serpentine sclerotic rim around the area of osteonecrosis and detecting subchondral fractures with the crescent sign (see Image. Crescent Sign on CT scan).

There is limited use of CT for early detection, and it should not be used as first-line imaging when clinically suspecting osteonecrosis.[6] Consideration should be given to the risk of radiation exposure, particularly in younger patients. However, preoperative CT before total hip arthroplasty has shown improved sensitivity for femoral head collapse, ultimately upstaging femoral head osteonecrosis in 20% of patients, according to the Association Research Circulation Osseous (ARCO) classification.[7] Thus, the advantages and disadvantages of CT imaging before surgery should be considered with the patient individually. 

Magnetic Resonance

MRI is the gold standard for imaging and characterizing osteonecrosis, with a high sensitivity and specificity of nearly 100%. MRI should be performed when there is clinical suspicion for osteonecrosis as the next line imaging study, after plain radiographs, if needed for further characterization. MRI allows for the evaluation of volume and associated inflammatory changes.[6] Imaging findings on MRI can manifest as early as 1 week from vascular injury.[1] The classic MRI pattern is a rim of low signal intensity on all pulse sequences followed by a second inner rim of high signal intensity observed on fluid-sensitive sequences, known as the double-line sign (see Image. MRI of Double-Line Sign with Subchondral Collapse).[5] The rim of low signal intensity observed on all sequences represents the outside rim of sclerosis, and the inner rim of the high signal represents the reactive interface or zone of creeping substitution.[1]

In small bones, a double-line sign may not be as apparent. Characteristic findings of osteonecrosis in small bones generally demonstrate low signal intensity on T1 sequences (compared to skeletal muscle) with variable T2 signal. Fluid-sensitive sequences show early increased signal in acute osteonecrosis and decreased signal in advanced stages of the disease. Other secondary signs may be observed, such as changes in morphology and malignment of, and relative to, the adjacent bones and the development of secondary osteoarthritis.[1]

Contrast is generally not necessary in evaluating osteonecrosis. Occasionally, contrast-enhanced MRI and dynamic contrast-enhanced studies may be used to distinguish between transient bone marrow edema syndrome and subchondral insufficiency fracture. Contrast-enhanced exams may demonstrate areas of reduced enhancement in osteonecrosis, thus confirming areas of devascularization.[8][9]

MRI is useful for assessing the volume and presence of bone marrow edema and joint effusions, which in turn help predict the risk of subchondral collapse. However, MRI has limitations in evaluating the extent of articular collapse required for surgical planning. In contrast, CT is better suited for assessing osseous details and visualizing fractures that extend to the cortex.[10] CT and MRI can be complementary to each other.

Nuclear Medicine

When MRI is inconclusive or when there are contraindications to MRI, bone scans are often used as an alternative route to image early changes of osteonecrosis and determine the risk of impeding bone collapse.[11] The most common bone scan is technetium-99m methylene diphosphonate (99mTc-MDP). This scan is often performed as a single delayed phase or in 3 phases—flow, blood pool, and delayed phase. MDP is a phosphate analog taken up by osteoblasts through chemisorption, binding to crystalline hydroxyapatite in the osseous matrix.

Osteonecrosis is a progressive condition, and its appearance in bone scans often depends on the stage of the disease. Osteonecrosis can be visualized on bone scans as soon as 7 to 10 days from an event, typically appearing as normal or as a general area of photopenia on delayed images due to a lack of radioisotope uptake in avascular bone.[5] Increased radiotracer activity is observed after 1 to 3 weeks due to increased osteoblastic activity at the reactive interface around the necrotic component as the tissue attempts to heal. On imaging, this gives the classic donut sign or ring sign with a hot area of increased activity around a central cold photopenic defect. Overall sensitivity in diagnosing osteonecrosis of the femoral head ranges from 78% to 91%, depending on the healing phase. However, it remains relatively nonspecific as many bone pathologies may present similarly. MDP bone scans are limited by spatial resolution; however, combining them with single-photon emission computed tomography/CT has improved accuracy at 3-dimensional localization.[11]

Positron emission tomography (PET) imaging using F18 glucose is a diagnostic imaging technique used to detect metabolic abnormalities. Although it is not ideal for examining the bone in isolation, it can detect areas of increased bone metabolism. Thus, it is useful for identifying osteoblastic activity and bone turnover. Studies on femoral head osteonecrosis have shown that F18 PET/CT has improved sensitivity and accuracy compared to MRI.[12] Evidence suggests that the metabolic information obtained may predict the risk of impeding femoral head collapse before changes become apparent on plain film.[13] Metabolic activity is quantified through maximum standardized uptake value (SUVmax) and increases with stage progression. Kubota et al concluded that SUVmax >6.45 leads to femoral head collapse within 12 months. When combined with plain radiographs or MRI for type classification, PET imaging has shown increased specificity for predicting femoral head collapse.[13] Thus, PET can be used as an adjunct in early clinical management for joint preservation but should not be used as first-line screening due to its excessive cost and radiation exposure.

Clinical Significance

Patients with osteonecrosis in epiphyseal locations in the femoral head and small bones, such as the lunate, are at an increased risk of subchondral collapse. Early diagnosis and treatment are crucial for joint preservation. The goal of imaging should be to identify osteonecrosis before it undergoes irreversible change. The care of patients with osteonecrosis necessitates a collaborative approach among healthcare professionals to ensure patient-centered care and improved overall outcomes. Radiograph and MRI classification systems have been developed in conjunction with clinical findings to help accurately describe the progression of osteonecrosis for further risk stratification. Below is a summary of commonly used classification systems in clinical practice for femoral head and lunate osteonecrosis. 

Osteonecrosis affecting long bone metaphysis and diaphysis is often clinically occult and may go underdiagnosed. A rare complication of osteonecrosis that clinicians should be made aware of when new clinical findings arise is described. 

Staging of Femoral Head Osteonecrosis 

The most common site for osteonecrosis is the femoral head, with an increased prevalence observed among younger adults aged 20 to 40, accounting for 10% of annual total hip arthroplasties in the United States.[14] There are a few staging systems developed for adult femoral head osteonecrosis, the 3 main ones being—Ficat and Arlet (see Table 2. Ficat and Arlet Staging of Osteonecrosis of the Hip), Steinberg (see Table 3. Steinberg Staging System of Osteonecrosis of the Hip), and the Association Research Circulation Osseous (ARCO) classification (see Table 4. ARCO 2019 Revised Staging System). These systems are designed to stage osteonecrosis from clinically occult disease to positive imaging findings to subchondral collapse and the late findings of secondary osteoarthritis. These classifications are clinically significant for epiphyseal osteonecrosis as they predict the likelihood of articular collapse. Successful treatment depends on accurate staging. There is no consensus on the best classification system, as all have demonstrated interobserver and intraobserver reliability.[15]

Table 2. Ficat and Arlet Staging of Osteonecrosis of the Hip

Reference for the table.[16]

Table 3. Steinberg Staging System of Osteonecrosis of the Hip (the University of Philadephia System)

* Stages 1 through 6 are further categorized into 3 subsets—mild (<15% articular surface), moderate (15% to 30%), and severe (>30%).[17][18]

Table 4. ARCO 2019 Revised Staging System

References for the table.[19][20]

When osteonecrosis occurs in the epiphyses of the femoral head and other long bones, the report should include specific items to communicate prognostic findings to the clinician as follows:

• Location of osteonecrosis
• Estimated volume of the femoral head and the percentage of weight-bearing surface 
• Presence of coexisting degenerative changes
• Presence of joint effusion 
• Presence of unstable osteochondral fragments or subchondral fracture [5]

The extent of the femoral head involved in osteonecrosis is a crucial factor in predicting femoral head collapse and is best evaluated using an MRI in the sagittal plane.[21] Osteonecrosis affecting >50% of the femoral head is much more likely to progress to articular collapse. Osteonecrosis affecting <30% of the femoral head is unlikely to lead to articular collapse. Additional factors associated with an increased risk of femoral head collapse include an increased thickness of the relative zone, joint effusion, surrounding edema, older age, and increased body mass index.[22] 

Kienbock Disease 

Osteonecrosis affecting the lunate is referred to as Kienbock disease or lunatomalacia. Although its etiology is often unknown, most patients have an antecedent history of trauma that disrupts the blood supply and ligaments surrounding the lunate.[23] Due to its variable blood supply, the lunate bone is at an increased risk of osteonecrosis. Radiographs are the initial imaging modality used to diagnose Kienbock disease, which often demonstrates an area of increased sclerosis or flattening with negative ulnar variance (see Image. Plain Film of Kienbock Disease). On MRI, the condition is diagnosed with near certainty when there is a diffuse T1 dark signal in the lunate, particularly in the setting of ulnar variance and normal appearing surrounding bones with variable T2 signal (see Image. MRI findings of Kienbock Disease). 

Delayed diagnosis can lead to lunate collapse and subsequent alternation of the surrounding capital architecture. Once recognized, surgery is often required to prevent wrist degenerative changes.

A reproducible osseous classification system called the Lichtman classification combines radiologic and clinical findings to help surgeons make the appropriate treatment decision preoperatively to prevent resulting carpal pathology (see Table 5. Lichtman Classification).[24] When radiographic findings are inconclusive, MRI can aid in identifying radiographically occult disease. 

Table 5. Lichtman Osseous Classification

 References for the table.[24][25]

Malignant Transformation 

Another important but rare complication of osteonecrosis is the malignant degeneration of extensive bone infarcts into secondary osteosarcoma, also known as bone infarct-associated sarcoma. This entity is extremely rare, however well documented, and important to recognize and consider in patients with osteonecrosis affecting metadiaphyseal locations of long bones.

This condition is believed to arise from the reactive interface at the periphery of a lesion where excessive proliferative activity occurs.[26] Ostenecrosis-associated sarcoma occurs in the fifth to sixth decade of life and typically has a poor prognosis.[27] 

Radiographs demonstrate previous characteristics of osteonecrosis with new focally aggressive osteolytic lesions extending through the cortex and involving the reactive interface of cancellous bone (see Image. Osteolytic Lesion). MRI shows a new mass-like replacement of the bone marrow in the area of osteonecrosis with associated cortical destruction and new soft tissue components (see Image. MRI of Malignant Transformation). Lesions are hypermetabolic on PET/CT and markedly hot on bone scintigraphy.[28] New bone pain in patients with known osteonecrosis affecting the metaphysis of long bones should be vigilantly monitored.