Hip

Stage

ARCO 1

ARCO 2

ARCO 3

ARCO 4

Radiograph

Normal

Sclerosis and osteolysis in necrotic segment, sclerotic margin

Fracture (crescent sign), flattening of femoral dome

Osteoarthritis

MRI

Demarcated necrotic segment

Necrosis with reactive margin, double-line sign

Fracture

Osteoarthritis

Normal

Sclerosis and osteolysis in necrotic segment, sclerotic margin

Fracture, deterioration of spherical head shape

Osteoarthritis

Scintigraphy

Diffuse or cold spot

Cold in hot pattern

Hot in hot pattern

Hot spot

Imaging findings reflect the histopathologic features of AVN described above and have a great impact on treatment decisions. Radiographs are negative in ARCO stage 1, but might show the sclerotic zone of the reactive interface in stage 2, a subchondral fracture (“crescent sign”) and collapse in stage 3 (Fig. 1), and secondary osteoarthritis (OA) of the hip joint in stage 4. Similar findings can be seen on CT with a higher sensitivity for the detection of subchondral fractures. As soon as fracture has occurred, preservation of the femoral head is usually futile and arthroplasty has to be performed in the majority of cases [1, 3].

Fig. 1

AVN of the femoral head (ARCO stage 3). Frog-leg lateral view shows sclerotic line (black arrowheads) of reactive interface between necrotic segment and normal bone. The curved subchondral radiolucent line (white arrows) indicates fracture of the femoral head (“crescent sign”)

On MR imaging (Fig. 2), ARCO stage 1 is characterized by the presence of a subchondral area of signal loss (“band lesion”), which in stage 2 is separated from normal bone marrow by an interface consisting of two parallel lines (“double-line sign”). This sign can be seen on images with T2 contrast and on gadolinium-enhanced T1-weighted images and describes the presence of an inner hyperintense line (fibrovascular tissue) and an outer hypointense line (osteosclerosis) bordering the avascular bone segment. In stage 3, a fracture line might become visible within the area of necrosis which typically runs parallel to the surface of the femoral head. Similar to radiographs and CT, femoral head collapse and OA are features indicative of stages 3 and 4 [1, 3, 6, 7]. Bone marrow edema can be associated with AVN of the femoral head but does not occur before the demarcation of necrosis and thus, does not represent an early sign of ischemia as previously believed [2, 3, 7]. In patients with AVN, bone marrow edema has been shown to be associated with pain, femoral head collapse and a poor prognosis [8–10]. A recent study demonstrated that bone marrow edema adjacent to the demarcated necrotic fragment represents a secondary sign of subchondral fracture and therefore indicates ARCO stage 3, even if the fracture line is not visible on MR imaging [3].

Fig. 2

a–c AVN of the femoral head: progression from ARCO stage 2 to stage 3. (a) Coronal T1-weighted TSE image and (b) corresponding intermediate weighted TSE image with fat suppression show hypointense subchondral segment of osteonecrosis demarcated by a reactive interface (arrowheads). Note absence of femoral head collapse and bone marrow edema (ARCO stage 2). (c) Coronal intermediate weighted TSE image with fat suppression obtained five months later demonstrates hyperintense subchondral fracture line (arrows) within necrotic segment as well as bone marrow edema (asterisk) extending to the femoral neck and intertrochanteric area (ARCO stage 3)

The most important tasks of imaging in patient with suspected AVN of the femoral head are the verification of the diagnosis and the differentiation of AVN from other causes of hip pain, such as transient bone marrow edema syndrome (TBMES) and subchondral insufficiency fracture (SIF), and, if AVN is diagnosed, the distinction between ARCO stage 2 and 3.

Transient Bone Marrow Edema Syndrome

Transient bone marrow edema syndrome of the hip is a self-limited condition, which before the advent of MR imaging was referred to as transient osteoporosis (TO). It is almost exclusively observed in healthy middle-aged men and women in the third trimester of pregnancy or immediately postpartum. Unilateral, bilateral and migratory forms have been reported. The disease is characterized by the acute onset of hip pain and limited range of motion without previous trauma. Complete restitution can be expected after a period of 6–8 months. TBMES is nowadays regarded as a distinct clinical entity separate from avascular necrosis (AVN). Although different etiological mechanisms have been discussed, there is some evidence that the basic pathomechanism is venous congestion with an increase of intraosseous pressure. Histologic examinations have shown increased vascularity, interstitial edema, and signs of an abnormal bone turnover [1, 11, 12].

Radiographs are usually normal at the initial onset of symptoms and show reversible osteopenia over the ensuing few months. Bone scintigraphy reveals increased perfusion as well as abnormal tracer uptake in the femoral head and neck [1]. On MR imaging (Fig. 3), bone marrow edema is seen extending from the femoral head and neck to the intertrochanteric region in the absence of segmental or linear subchondral changes. Edema might spare the subchondral bone marrow particularly at the medial aspect of the femoral head. Accompanying joint effusion and synovitis are the rule [1, 6, 11, 12]. Perfusion studies typically show an increased contrast accumulation with a prolonged plateau phase in the femoral head supporting the theory of venous congestion [7]. As a sequel of demineralization, insufficiency fractures can occur during the course of the disease, in particular if unloading is inadequate or terminated following core decompression with relief of symptoms. On MR images, fractures are typically seen as linear areas of low signal intensity within the subchondral bone marrow [6, 11, 12]. On the basis of imaging findings, it is virtually impossible to distinguish TBMES with secondary insufficiency fracture from primary SIF. Patient age, sex and clinical history help to differentiate between the two entities.

Fig. 3

(a, b) Transient bone marrow edema syndrome of the hip. (a) Coronal T1-weighted TSE image and (b) corresponding STIR TSE image show extensive bone marrow edema (asterisk) of the proximal femur in the absence of segmental or linear abnormalities of subchondral bone. Note reactive synovitis and joint effusion (arrowheads)

Stress Injuries

Subchondral Insufficiency Fracture

Subchondral insufficiency fracture of the femoral head is most often observed in elderly females and renal transplant recipients with osteopenic bone. Patients report a sudden onset of hip pain which is typically worse with weight-bearing. Biomechanical failure occurs in the statically over-loaded areas of the femoral head. Histologic examinations show a subchondral fracture with intraosseous callus formation and reactive hypervacularization of surrounding bone marrow. The natural course of the disease is either healing or collapse of the femoral head with consequent joint destruction. It is estimated that SIF of the femoral head accounts for 5–6% of all total hip replacements. The condition is likely to represent the underlying pathology in so-called “rapidly destructive osteoarthritis of the hip” [13–16].

MR imaging shows a hypointense subchondral fracture line as well as bone marrow edema in the femoral head and neck (Fig. 4). In the majority of cases the fracture is located in the anterior segment of the femoral head and runs parallel to the joint surface. In contrast to AVN, the bone marrow between the fracture and the articular cartilage enhances after intravenous contrast application. Cartilage defects, synovitis and joint effusion are typical associated findings [13, 14, 17]. With collapse of subchondral bone progressive loss of signal intensity, entrance of fluid and cyst formation might be seen.

Fig. 4

(a, b) Subchondral insufficiency fracture (SIF) of the femoral head. Coronal (a) T1-weighted TSE image, (b) intermediate weighted TSE image with fat suppression and (c) contrast-enhanced T1-weighted TSE image with fat suppression show a hypointense subchondral fracture line (arrow) oriented parallel to the surface of the femoral head with associated bone marrow edema (asterisk). Note contrast enhancement of the bone segment proximal to the fracture

Initial findings indicating a poor clinical prognosis include lateral location, non-parallel course and great extent of the fracture, large cartilage defects, bone marrow edema on both sides of the joint, and high patient age [13–15, 17].

Fatigue Fracture

Fatigue fractures of the femoral head and neck typically occur in runners and military recruits with the femoral neck representing the most common location at the hip. In runners, stress injuries of the femoral neck are usually the sequel of a changed regimen or an increased frequency or intensity of training. Patients complain about groin or anterior hip pain with loading rather than at rest. The clinical symptoms are however unspecific and may mimic a labral tear or a muscle injury. Whereas fatigue fractures at the inferomedial (basicervical) aspect of the femoral neck due to compression forces usually have an uncomplicated course and can be treated conservatively, superolateral (subcapital) fractures represent distraction injuries that bear a higher risk for dislocation and thus, might require surgery [18, 19].

Stress reactions are precursor lesions of fatigue fractures which are distinguished from the latter by the absence of a distinct fracture line.

Radiographs are not very sensitive in depicting stress injuries of bone. The first radiographic signs are the “grey cortex sign” (circumscribed cortical osteopenia) and a lamellar periosteal reaction, which might later transform into solid bone production. In the femoral neck, superficial new bone formation is however often minimal or absent. With a frank fatigue fracture a horizontal line of increased density might become visible. On MR imaging (Fig. 5), stress reactions of the proximal femur are characterized by bone marrow edema as well as increased T2-weighted signal intensity at the bone surface due to periosteal activation. A fatigue fracture should be diagnosed if a line of low signal intensity perpendicular to the cortex is seen in addition to the latter [18, 20]. In doubtful cases, CT might be helpful in depicting the fracture line or in differentiation of a stress injury from an osteoid osteoma. In the majority of patients with fatigue fractures of the femoral neck, abnormal signal intensity on MR imaging resolves within 6 months of the initial diagnosis. Residual sclerosis or fatty marrow conversion might remain at the former facture site [21].

Fig. 5

(a, b) Inferomedial fatigue fracture of the femoral neck. (a) Coronal T1-weighted TSE image and (b) corresponding STIR TSE image show a focal band of low signal intensity (arrowhead) perpendicular to the medial cortex surrounded by bone marrow edema

Articular Anatomy and Pathology

Hip Capsule

Stability of the hip results from its bony anatomy whereby the acetabular socket contains the majority of the femoral head, the labrum that further deepens the acetabular socket, and from the thick capsular ligaments that reinforce the hip capsule. The capsular ligaments of the hip consist of the pubofemoral, ischiofemoral and iliofemoral ligaments that collectively encircle the hip joint [22] The pubofemoral ligament is located inferiorly and the ischiofemoral ligament is located posteriorly. The obturator externus bursa, which normally communicates with the inferior hip joint, arises from the area of the ischiofemoral ligament attachment and may be distended in patients with a hip effusion [23] The zona orbicularis is a compact set of fibers perpendicular to these capsular ligaments further reinforcing the superior, posterior and inferior capsule resulting in a narrow constriction at the femoral neck that is well seen with MR imaging [22].

The iliofemoral ligament is the strongest of the capsular ligaments and reinforces the anterior hip capsule. It has an inverted Y configuration, consisting of a horizontal superior band and a vertical inferior band. The superior band is well seen on axial MR images as it courses from the anterior acetabulum to insert on a tubercle on the anterior femoral neck. Injury to this portion of the iliofemoral ligament is a common finding in patients who have undergone transient posterior hip subluxation, typically occurring near its femoral insertion [24].

Unlike the shoulder, posterior subluxation/dislocation is more common at the hip than anterior instability. Transient posterior hip subluxation typically results from a fall on a flexed and adducted hip and is often clinically misdiagnosed as a hip sprain. Frank hip dislocation is typically the result of significant trauma such as motor vehicle accident, sports related injury or a significant fall. Males are more commonly affected than females. Correct diagnosis of this injury is essential to minimize future hip instability and reduce the risk of avascular necrosis.

Findings on MR that suggest transient posterior hip subluxation and dislocation include posterior acetabular rim marrow edema or fracture, posterior labral tearing or avulsion, and the presence of a significant effusion and/or hemarthrosis. (Fig. 6) Injury to the anterior and posterior capsule may be present, along with strain of the external rotator muscles, damage to the external rotator tendons, and edema in the fat surrounding the sciatic nerve posterior to the hip capsule [25] Injury to the obturator externus tendon in particular appears to be associated with concurrent damage to the deep branch of the medial circumflex artery to the femoral head and subsequent avascular necrosis [26]

Fig. 6

Posterior hip subluxation. Axial T2-weighted MR image of the left hip in a 9 year old female obtained following a soccer injury demonstrates avulsion of the posterior labrum with overlying soft tissue swelling. (arrow) There is also mild edema in the anterior hip capsule within the iliofemoral ligament, consistent with transient hip subluxation

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