Subchondral insufficiency fractures of the knee: review of imaging findings

Introduction

Insufficiency fractures are the result of repetitive physiologic stress (load) on bone that is weakened by non-tumorous disease, most commonly deficient mineral content (osteoporosis/osteopenia) or less likely decreased elastic resistance (osteomalacia) (1).

Subchondral insufficiency fractures typically occur around large weight-bearing synovial joints (i.e. hips, knees, ankles), in multiple locations. They may also occur in other sites, as in the metatarsal heads prior to the development of Freiberg’s infraction.

In the knee these types of fractures are called subchondral insufficiency fractures of the knee (SIFK), and can involve both femoral condyles and tibial plateaus. The weight-bearing surface of the medial femoral condyle is the most commonly reported location (2–5).

Patients are usually elderly, female, overweight, or osteoporotic. Insufficiency fractures have also been reported in renal and liver transplant recipients, post chemo- or radiation therapy, in patients with systemic lupus erythematosus, and after long-term corticosteroid usage (2–5). The typical clinical presentation is acute onset of knee pain that gradually worsens, without a history of trauma. Sometimes concomitant conditions responsible for abnormal stress on the bone are also present (e.g., meniscal tears or prior arthroscopic surgery in the knee) (3–7). Once a subchondral insufficiency fracture has occurred, there is increased risk of secondary osteonecrosis, subchondral collapse, and rapidly progressive osteoarthritis (4–9).

Recently a new relationship has been suggested between SIFK and the entity historically called spontaneous osteonecrosis of the knee (SONK). SONK is now considered a misnomer, as this term was commonly used to describe different conditions with a similar radiological presentation, such as osteonecrosis related to primary vascular insults, sequelae of acute or chronic trauma, and also SIFKs (4–6). Part of this confusion was probably due to the fact that focal osteonecrosis can be found both pathologically and radiologically as a consequence of subchondral fractures (10–13).

Histopathology

Histopathologic findings of SIFK have previously been classified into three groups based on morphologic characteristics (5). Group I is characterized by a subchondral fracture disconnecting bone trabeculae in the epiphysis, with no evidence of antecedent osteonecrosis. There is extensive callus formation and granulation tissue surrounding the fracture, which is not seen in primary (classic) osteonecrosis. Group II demonstrates a subchondral fracture with focal fracture-related osteonecrosis located between the fracture line and the articular surface (subchondral plate). Group III shows detachment of the subchondral fracture from the underlying bone, with displacement of articular cartilage and release of necrotic tissue into the joint space. In contradistinction, primary osteonecrosis associated with corticosteroid therapy or systemic diseases (i.e. sickle cell disease, alcoholism, pancreatitis), demonstrates “wedge-shaped” infarct areas (4–6).

Imaging findings

Initially, radiographs can be normal or show only a decrease in bone density (7). A patient, particularly if elderly, osteoporotic, or overweight, with severe knee pain and a negative radiograph should raise suspicion of SIFK. Magnetic resonance imaging (MRI) is the technique of choice for an early diagnosis. The MRI appearance of SIFK is dominated by marrow edema and subchondral architectural changes that sometimes can be very subtle (Fig. 1). SIFK is initially identified as a focal irregular, serpiginous subchondral low-signal intensity band on all pulse sequences, with intense surrounding bone marrow edema pattern (4–6,14). This band histopathologically reflects the fracture line, repair tissue (callous formation) and compression of trabeculae. On T2-weighted (T2W) images this line is always hypointense (Fig. 2), partially differentiating it from traumatic fracture lines, which can display both high and low signal intensity on T2W images. Another characteristic feature described in the early phases of SIFK is a homogeneous high signal intensity of the bone between the subchondral surface and the fracture line on gadolinium-enhanced images. This corresponds to a segment that is generally alive and shows repair tissue. With SIFK progression, worsening osteochondral displacement, subchondral collapse, and secondary osteonecrosis can be seen (Figs. 3–5). Saucerized defects develop along involved articular surfaces (Fig. 6). OPEN IN VIEWER

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Fig. 2.

Coronal (a) and sagittal (b) intermediate-weighted fat-saturated, (c) coronal, and (d) sagittal proton density MR images demonstrate an insufficiency fracture (arrows) within the medial tibial plateau, with surrounding reactive marrow edema. An irregular, serpiginous subchondral fracture line is appreciable, with low signal on both sequences.

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Fig. 3.

Sagittal intermediate-weighted fat-saturated (a), T1-weighted (b), and proton density (c) MR images demonstrate a subchondral insufficiency fracture (arrows) within the medial femoral condyle, with surrounding reactive marrow edema. There is a separate osteochondral fragment (curved arrows) with underlying collapse. Notice the radial tear through the posterior horn of the medial meniscus.

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Fig. 4.

Frontal knee radiographs at 3-month intervals (a, b, c) show subchondral fracture in the medial femoral condyle, with worsening secondary osteonecrosis and articular surface collapse in the medial compartment (curved arrows). Coronal proton density fat-saturated (d), coronal T1-weighted (e), and sagittal proton density fat-saturated (f) MR images of the same patient at onset of symptoms (presentation) demonstrate a small subchondral insufficiency fracture (arrows) within the medial femoral condyle, with surrounding reactive marrow edema.

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Fig. 5.

Sagittal proton density fat-saturated (a), sagittal proton density (b), and coronal proton density fat-saturated (c) MR images demonstrate a focus of subchondral osteonecrosis within the medial femoral condyle (arrows), with surrounding reactive marrow edema. Coronal proton density fat-saturated (d) image shows full-thickness radial tear at the posterior root of the medial meniscus (curved arrow), suggesting a previous stress-insufficiency fracture as a possible, though not clearly recognizable, cause of osteonecrosis in this knee. See the smooth, low-signal intensity line circumscribing the necrotic portion and somehow mirroring the contour of the articular surface, that represents repair tissue. In this case we cannot call it a SIFK, since there are no clear imaging features of a subchondral fracture, and the osteonecrotic pattern prevails.

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Fig. 6.

Frontal knee radiograph (a), CT coronal reformation (b), coronal proton density fat-saturated (c), and coronal T1-weighted MR images demonstrate chronic subchondral insufficiency fracture with articular surface collapse, and saucerized defect (arrows) in the medial femoral condyle. There is diffuse full thickness chondral loss in the medial compartment (curved arrows) with tear of the medial meniscus.

Differential diagnoses when SIFK is suspected include primary osteonecrosis, traumatic fractures, and even osteomyelitis. Primary osteonecrosis in the knee has appearance similar to that well-described in the radiologic literature for the femoral head. Thus, to distinguish between this condition and SIFK, many of the criteria described for the hip can be helpful (4,5,8,12,14). As seen before, SIFK is generally seen in postmenopausal women with osteoporosis or overweight. On the other hand, primary osteonecrosis is generally seen in middle-aged patients, often with a history of corticosteroids intake or alcohol abuse, and unlike SIFK it is frequently associated with mild or vague and bilateral pain or with osteonecrosis in other sites (5,11,12). In the early stages, when treatments could still be useful to prevent further progression, their radiographic appearance is similar, typically showing no or minimal alterations. On MRI, both present a low intensity band on T1 with associated bone marrow edema. However, while in SIFK the band is generally irregular and convex or parallel to the articular surface, reflecting the fracture line, in osteonecrosis, since it represents repair tissue, it is generally smooth and circumscribes the necrotic segments, often looking as a mirror image of the articular surface (Fig. 5). Cases of SIFK have been described where the low signal intensity band appeared smooth and well delineated. On the other hand, subchondral fractures frequently superimpose to osteonecrosis, so the evidence of a fracture line does not automatically exclude primary osteonecrosis as the underlying cause, even though other radiologic features of osteonecrosis will be present (7,14–16). A homogeneously high signal intensity of the bone between the subchondral surface and the fracture line on T2W images sometimes seems to be helpful in the differential diagnosis between primary osteonecrosis and SIFK in the early phases. In SIFK this area corresponds to a segment that is generally alive and that shows repair tissue, while in osteonecrosis often there is no high signal intensity since it is totally necrotic. Only rarely may this region show high signal intensity even in osteonecrosis, if it has undergone repair by granulation tissue and appositional bone formation.

Another important condition to consider when dealing with SIFK is the “transient bone marrow edema syndrome”, a self-resolving syndrome still not completely understood, also called by many authors transient regional osteoporosis (15). Transient regional osteoporosis affects a different demographic, as it is commonly seen in healthy middle-aged men and in women in the third trimester of pregnancy, while the age of patients with SIFK is considerably higher. On plain radiographs regional osteopenia is present, without evidence of subchondral collapse. On MRI, reactive marrow edema is demonstrated with no appreciable fracture line or deformity of the epiphyseal contour (4,15,17). Recently, some authors have suggested that this condition could be related to extremely subtle subchondral fractures too, but evidences in the literature are still conflicting on this subject (17,18).

Disease outcome

Outcome of SIFK depends on the initial extent (size) of the subchondral fracture, the patient’s weight, the degree of osteopenia, as well as the early diagnosis and initial treatment. MRI is a key part of the treatment algorithm for early diagnosis.

Prompt aggressive conservative treatment with limitation of weight bearing can lead to subchondral fracture healing and remission of symptoms in early stages of the disease. Other non-operative treatments have been proposed, such as anti-inflammatory drugs, biphosphonates, and bone stimulators (4–6,11,12,16,19,20). However, a longitudinal study with controls comparing outcomes and treatment efficacies in SIFK has to our knowledge still to be published: this is important considering that SIFK is a variable and sometimes self-remitting condition.

Progressive subchondral collapse, osteochondral fragment detachment and fragmentation, and osteonecrosis indicate a poor prognosis. This progressive destruction of the weight-bearing surfaces of the joint can result in the need for surgical intervention. Various procedures have been proposed to achieve symptomatic relief, including unicompartmental and total knee arthroplasty or osteochondral allografts. Surgical decision-making is based upon the size, location and severity of the joint destruction, as well as patient and surgeon related factors (6,11,12,16).

Conclusion

In patients with SIFK an early aggressive conservative treatment can reduce the probability of progression to subchondral collapse and osteonecrosis. In order to get an early diagnosis, it is crucial to be familiar with this relatively common disease. For a radiologist dealing with spontaneous knee pain, particularly in overweight people and/or postmenopausal women, and standard radiographs revealing evidence of osteopenia, SIFK should be suspected. MRI can then be worth considering. On MRI, the diagnosis of SIFK is suggested when there is focal compression of subchondral trabeculae with intense surrounding marrow edema.