The Knee : Topics in Magnetic Resonance Imaging

Secondary Logo

Journal Logo

Review Articles

The Knee

Morrison, William B. MD*; Major, Nancy MD

Author Information
Topics in Magnetic Resonance Imaging 24(4):p 193-203, August 2015. | DOI: 10.1097/RMR.0000000000000059
  • Open


Sports injuries at the knee are very common, not only in contact sports such as football but also in sports with jumping and pivoting. In addition, overuse injuries can affect the tendons, ligaments, and bone with degeneration, friction, and stress response. Radiologists and sports medicine professionals should be familiar with the range of injury occurring at the knee and patterns of injury that can be used to predict other more subtle pathology. These topics and others will be discussed.

Magnetic resonance imaging (MRI) of the knee is one of the most frequently performed magnetic resonance examinations of the musculoskeletal system. Magnetic resonance imaging provides detail of small intraarticular structures such as the meniscus and cartilage as well as information about the soft tissues and ligaments. It is the ideal global examination, particularly in the acutely injured individual who may have a challenging physical examination because of swelling and/or pain.

To make a proper diagnosis, the structures in the knee need to be adequately visualized. A proper protocol design is imperative for accurate interpretation and assistance to our referring clinicians for proper treatment. Magnetic resonance imaging is useful in distinguishing surgical from nonsurgical treatment. Therefore, a fluid-sensitive sequence is imperative to diagnose pathology in the ligaments and tendons and to locate abnormal fluid collections within the soft tissues. T1-weighted imaging is very useful for identifying conditions within the marrow. A proton density sequence, particularly in the sagittal plane, is the ideal way to determine meniscal pathology. Fat suppression is a mainstay in musculoskeletal imaging to make subtle foci of increased T2 signal more conspicuous. Consequently, imaging performed using a fluid-sensitive sequence with fat suppression allows for visualization of ligaments and tendons/muscles.


When evaluating any examination, it is important to have a standard search pattern that is used consistently. It does not matter whether it is different from that described in a textbook or used by a coworker; whatever is chosen should allow for evaluation of all structures and should use the same pattern on each case, assuring that pathology is not overlooked. This is especially important for MRI particularly in a joint where there is a combination of large and small structures requiring evaluation.

Soft Tissues

Evaluation of the soft tissues can assist in making the diagnosis. Subcutaneous edema can indicate trauma mechanism: focal subcutaneous edema may represent recent impact. Extraarticular fluid collections can also reveal a pattern of joint pathology and can help explain the patient's pain.

Joint Effusion and Synovial Plicae

Joint effusion is very common, and although nonspecific, its presence should suggest presence of trauma, internal derangement, or inflammatory arthritis. Rounding of the joint recesses is a sign of excess fluid. Hyperintensity of fluid on T1-weighted images or a fluid-fluid level is associated with hemarthrosis in the setting of acute trauma (Fig. 1). A sharply defined supernatant of fat signal represents a lipohemarthrosis, in which case an intraarticular fracture should be suspected. Complexity of the fluid is a sign of synovial proliferation; this is a nonspecific finding but generally indicates chronic disease, either noninflammatory (ie, internal derangement, pigmented villonodular synovitis) or inflammatory (ie, septic arthritis, rheumatoid arthritis). An unexplained effusion or mass-like synovial proliferation without traumatic or degenerative explanation should prompt suspicion of inflammatory arthritis (Fig. 1).

Joint fluid and synovium. A, Sagittal T2-weighted fat-suppressed image shows a fluid-fluid level (arrows) with a fat signal supernatant representing a lipohemarthrosis. This usually indicates presence of an intraarticular fracture. B, Axial T2-weighted fat-suppressed image with extensive synovial proliferation (arrows) at the margins of the joint in a patient with rheumatoid arthritis. Note difference in signal between synovium (arrows) and joint fluid (arrowhead).

During development, the knee is formed from 3 compartments; the remnants of their junctions are the plicae1: superior, inferior, and medial (Fig. 2). The superior plica arcs over the patella within the suprapatellar recess and is rarely symptomatic; if large and fenestrated, it can obstruct, becoming a 1-way valve effect presenting as a mass above the patella. The medial plica extends vertically through the medial patellofemoral joint and is most often symptomatic as it can cause a painful snapping and clicking. The inferior plica (also called the ligamentum mucosum) originates in the triangular fat pad (Hoffa's fat pad) adjacent to the patellar tendon, extending to the proximal anterior cruciate ligament (ACL). It can become thickened and inflamed with repetitive stress as can be seen in running and jumping activities. On MRI, the plica appears as a thicker low-signal band with fluid signal surrounding it as it courses through the fat pad to the ACL. The result of this inflammation can be anterior knee pain.

Synovial plica. Axial T2-weighted fat-suppressed image demonstrates a medial plica (arrow) extending into the patellofemoral joint.

Cystic Lesions

The popliteal cyst (“Baker cyst”) is a synovial cyst; the synovial lining of the joint herniates between the semimembranosis and medial head of the gastrocnemius posteromedially.2 Because Baker cysts are contiguous with the joint, they may contain loose bodies, synovial proliferation, and debris that may also be found within the joint space (Fig. 3). These cysts are generally indicative of chronic or recurrent joint effusions and as such imply internal derangement (ie, meniscal tear) or chronic joint inflammation (ie, rheumatoid arthritis). As they enlarge, they can rupture or leak synovial fluid into surrounding tissues and become painful. Clinically, a ruptured popliteal cyst can mimic venous thrombosis. Conversely, popliteal vein thrombosis can cause surrounding soft tissue edema mimicking other pathology3; this should be suspected when associated enlargement and heterogeneous signal are noted in the vein (Fig. 3).

Periarticular fluid and edema: popliteal fossa. A, Axial T2-weighted fat-suppressed image shows a Baker cyst (arrow) connecting to the joint capsule and extending between the medial gastrocnemius (MG) and semimembranosus (SM). Note semitendinosus (ST) more posteriorly. Baker cysts commonly rupture, connoted by surrounding edema, in this example extending anteromedially (arrowheads). B, Axial T2-weighted image (left image) reveals a fluid-like lesion (arrows) in the popliteal soft tissues above the knee; if a cystic-appearing lesion cannot be connected to the joint, there should be increased suspicion for neoplasm. T1-weighted post-Gadolinium image (right image) shows heterogeneous enhancement (arrows) consistent with a solid neoplasm, in this case a synovial sarcoma. C, Axial T2-weighted fat-suppressed image shows enlargement of the popliteal vein (arrow) containing heterogeneous signal, with surrounding edema in the popliteal fossa, compatible with venous thrombosis.

However, various soft tissue malignancies are also common around the knee including synovial cell sarcomas and malignant fibrous histiocytomas; a T2 hyperintense lesion cannot be assumed to represent a cyst (Fig. 3). Contrast or ultrasound can be useful to document cystic nature, but malignant tumors can also have cystic or necrotic components. The important distinguishing feature is that tumors do not communicate with the joint; if a T2 hyperintense lesion can be demonstrated to have a neck extending to the joint, it can be confidently called a synovial cyst or ganglion. If not, concern should be raised regarding nonarticular etiologies including malignancy.

A fluid collection superficial to the patellar tendon, within the prepatellar bursa, can be a cause of anterior knee pain. Prepatellar bursitis can result from repetitive trauma from kneeling and is usually an easy clinical diagnosis (Fig. 4). However, a recently popularized lesion, Morel-Lavallée can simulate bursitis and is relatively common in this location.4 Morel-Lavallée lesion is an “internal degloving” phenomenon resulting from a shearing injury. The fascia becomes separated from underlying tissue, and a hematoma or seroma forms, preventing healing. This can become a chronic condition requiring surgical management. To differentiate Morel-Lavallée from routine bursitis, look for large-size, sharp, or acute margins with the fascia and persistence despite conservative treatment (Fig. 4).

Prepatellar fluid. Sagittal T2-weighted fat-suppressed image in a patient with anterior knee pain. Fluid and edema are present in the prepatellar soft tissues (arrows). Most likely, this represents bursitis. However, if there has been an injury (and if the margins of the fluid are not rounded), the differential includes Morel-Lavallée syndrome, a fascial shearing injury.

Pes anserinus (Latin for “goose's foot”) bursitis results from inflammation of the sac deep to the 3 tendons: the gracilis, sartorius, and semitendinosus inserting on the medial tibial shaft. The clinical symptoms of clicking and medial knee pain may mimic a meniscal tear. Magnetic resonance imaging can aid with the diagnosis and thus the appropriate treatment; edema in this location is commonly caused by inferior extension or rupture of a Baker cyst.

Ganglion cysts are also common at the knee, extending off the joint in various locations. Ganglion cysts are typically lobulated, with a narrow neck to a joint recess. These may extend into the bone (“intraosseous ganglion”) and should not be mistaken for neoplasia. Differential diagnosis includes a parameniscal cyst, arising from a meniscal tear. The latter will demonstrate a neck to the meniscal substance at the site of tear.

Extensor Mechanism

The quadriceps muscles and tendon, the patella, and the patellar tendon comprise the extensor mechanism. Normally, the quadriceps tendon on axial images demonstrates a stippled appearance because of insinuation of fat within the tendon slips. Ill-defined edema, adjacent suprapatellar fat pad edema, and tendon thickening help differentiate tendon pathology from normal fiber separation. Focal fluid signal is diagnostic of a tear.5 Quadriceps tendon tears are more common among middle-aged people who participate in running or jumping sports (Fig. 5).

Extensor mechanism. A, Sagittal T2-weighted fat-suppressed image shows a complete tear of the quadriceps tendon with fluid signal at the tear site (arrows). Observe thickening of the retracted tendon (arrowhead) representing underlying tendinosis. B, Sagittal T2-weighted fat-suppressed image of the knee of a basketball player reveals thickening of the proximal patellar tendon consistent with patellar tendinosis. Interstitial tearing is present (arrow). Note peritendinitis with edema extending along the tendon (arrowheads). C, Sagittal T1-weighted image demonstrates chronic changes related to previous Osgood-Schlatter disease, with irregular ossification of the tibial tuberosity (long arrows) and thickening of the distal patellar tendon (short arrow).

The patellar tendon is normally uniform in thickness and black in signal. Thickening (focal or diffuse) and intermediate T1 and T2 signal represents patellar tendinopathy (Fig. 5). This classically occurs in athletics associated with jumping sports. In this population, especially basketball players, interstitial tears at the proximal patellar tendon are common. Distal patellar tendon pathology is often related to residual effects of previous Osgood-Schlatter disease6: distal patellar tendon pathology related to excessive traction during development, with pain and bursitis associated with tendinosis and irregular ossification adjacent to the tibial tuberosity. Symptoms and residual MRI findings can continue into adulthood (Fig. 5). An analogous condition, also related to jumping activities, known as Sindig-Larsen-Johannsen disease occurs at the proximal patellar tendon.

Patellar Tracking Disorders

Patellar maltracking is a common source of anterior knee pain, especially in females.7–10 The etiology is multifactorial and therefore difficult to characterize simply (Fig. 6). Findings that can predispose to maltracking include patella alta (high-riding patella; ie, in extension, the articular cartilage of the patella barely covers the cartilage of the trochlea), a shallow trochlear sulcus, a prominent Q angle (the angle between the quadriceps and patellar tendon), weakening of the medial supporting structures (especially the medial patellofemoral ligament [MPFL]), and tightening of the lateral fascia (see ‘iliotibial [IT] band friction syndrome’). Q angle may be measured on MRI as the “TT-TG” distance or tibial tuberosity—trochlear groove offset with greater than 20-mm relative lateralization of the tuberosity considered abnormal. Chronic patellar maltracking can be seen as subluxation or tilt of the patella and lateral patellofemoral cartilage loss. Soft tissue edema may be seen at the superolateral aspect of Hoffa's fat pad. Acute injury can manifest as frank lateral patellar dislocation.

Patellar maltracking. A, Sagittal T2-weighted fat-suppressed image demonstrating patella alta defined as patellar tendon length (A) divided by patellar length (B) resulting in a ratio greater than 1.2, which can be associated with maltracking. Patellar maltracking is often associated with soft tissue edema at the superolateral aspect of Hoffa's fat (arrow). B, Three axial T2-weighted fat-suppressed images of the same patient with a diagnosis of patellar maltracking. Note lateralization of the patella with a cartilage defect (arrowhead). The trochlear sulcus (black lines) is shallow, and there is a prominent tibial tuberosity–trochlear groove (TT-TG) offset predisposing to lateral patellar subluxation.

Patellar dislocation is one of the conditions in musculoskeletal imaging in which the radiologist plays an essential role.11 Typically, the dislocation is transient, the patella quickly snapping back into position. The patient reports sudden onset of pain with associated anterior knee swelling; this can be mistaken for a joint effusion. In addition, the patient is often in too much pain to undergo a full physical examination. Referring doctors, even orthopedic surgeons, may have no idea that the patient recently dislocated.

Patellar Dislocation

The most specific MRI sign of patellar dislocation is bone bruising at the inferomedial patella and the anterolateral femoral condyle (Fig. 7). However, occasionally, bone marrow edema is only present at one location or neither. Other signs include edema at the medial supporting structures, including the medial retinaculum at the patellar attachment and the MPFL at the medial femoral condyle.12 Edema at the latter can mimic a grade 1 medial collateral ligament (MCL) sprain. When patellar dislocation is identified on MRI, care should be taken to evaluate the articular cartilage, which can become delaminated (separated) and displaced; most commonly, this occurs at the sites of impaction at the medial patella and the anterior aspect of the lateral femoral condyle. Injury to the MPFL should be identified (which can lead to recurrent dislocation), in addition to underlying factors described earlier predisposing to maltracking.

Patellar dislocation. A, Axial T2-weighted fat-suppressed image shows bone bruising at the medial patella (arrowhead) and at the lateral femoral condyle (arrow) representing impaction injury from transient lateral patellar dislocation. B, Sagittal T2-weighted fat-suppressed image through the medial aspect of the knee in a different patient with recent transient patellar dislocation. Arrows identify edema and disruption of the MPFL, which normally courses from the adductor tubercle (AT) to the patella below the vastus medialis obliquus muscle (VMO).

Medial Collateral Ligament

The MCL injury can be a result of a contact or noncontact injury occurring when the knee is forced inward with a valgus mechanism.13,14 Injuries are most common in athletes during sporting activities when the knee is bent. When an MCL injury occurs with an ACL tear and a medial meniscus tear as well, it is referred to as the “unhappy triad.”

The MCL originates on the medial aspect of the distal femur and inserts on the medial aspect of the proximal tibia. The medial meniscus is attached to the deep layer of the MCL. Grade 1 sprain is seen as fluid signal superficial to the MCL; however, more commonly, edema superficial to the MCL is related to other conditions such as a ruptured Baker cyst or hyperemia related to medial meniscal tear.15,16 Grade 2 sprain represents partial disruption of fibers with T2 signal within the MCL substance. Grade 3 sprain is a complete tear, which is most common at the proximal aspect (Fig. 8). Fortunately, the MCL has a blood supply and therefore has a high potential for healing without surgery, if injured in isolation.

Medial collateral ligament. A, Coronal STIR image shows a normal appearing MCL (arrowheads) coursing from the medial femoral condyle past the joint to the pes anserinus. Superficial edema (arrows) may represent a grade 1 sprain; however, causes for edema in this location in the absence of acute injury include ruptured Baker cyst and patellar dislocation. B, Coronal STIR image of a patient with true valgus injury and a high-grade partial tear (grade 2 sprain) of the MCL (arrow). Note osteochondral impaction injury at the lateral femoral condyle (arrowhead).

Lateral Collateral Ligament Complex

The lateral collateral ligament (LCL) complex is composed of 3 structures that are readily identifiable on MRI.17 The biceps femoris tendon is the most posterior of the structures, more anterior is the fibular collateral ligament (referred to as the LCL “proper”), and the most anterior structure is the IT band. The first 2 structures combine into the “conjoined tendon” and insert onto the head of the fibula, whereas the IT band inserts onto a bony prominence of the anterolateral tibia called Gerdy tubercle. Edema between the IT band and the lateral femoral condyle can be seen in patients with tightening of the lateral fascia, known as “IT band friction syndrome”.18 This condition is especially common in athletes, particularly runners and cyclists. Painful snapping and lateral pain characterize this condition, which may also be associated with lateral patellar maltracking (with lateral patellar tilt and eventual chondrosis) and proximally at the tensor fascia lata, hip snapping, and greater trochanteric bursitis (Fig. 9).

Lateral collateral ligament complex. A, Coronal T2-weighted fat-suppressed image with IT band (arrowheads) coursing past the lateral femoral condyle. Edema (arrow) between the band and the condyle can be seen in patients with IT band friction syndrome. B, Normal posterolateral corner structures. Coronal T2-weighted fat-suppressed image through the posterior knee shows the fibular collateral ligament (FCL); the biceps tendon (BT); and the conjoined tendon (CT) at their coalescence. Also in view are the popliteus tendon (PT); the popliteal-fibular ligament (PFL) and geniculate vessels (GV). C, Posterolateral corner injury on a coronal STIR image. There is a complete tear of the conjoined tendon (long arrows) and popliteal fibular ligament with retraction of the fibular collateral ligament (arrowheads). Note also a radial tear of the medial meniscus (double arrow) with extrusion.

Injury to the LCL occurs with a varus stress of the knee when the foot is planted on the ground. The LCL can also be injured if the knee is forced into hyperextension or forced into excessive rotation. A complete LCL complex tear is an uncommon injury occurring in isolation. It often occurs with a traumatic injury that involves multiple knee ligaments or the knee joint capsule, associated with a posterolateral corner injury.19,20

The posterolateral corner is composed of additional structures along with the fibular collateral ligament and biceps femoris. The arcuate ligament is a Y-shaped low-signal structure that extends from the fibular styloid process to the lateral femoral condyle with one of the arms of the Y extending to the joint capsule; this structure is not consistently seen on MRI. The popliteal-fibular ligament is a strong lateral knee stabilizer. It is a low-signal structure located superficial to the popliteus tendon, originating from the popliteus tendon sheath inserting on the fibula deep to the conjoined tendon (Fig. 9).

Injuries to the posterolateral corner often occur in association with an anterior and/or posterior cruciate ligament (PCL) tear. It is important for the radiologist to recognize a posterolateral corner injury (Fig. 9). Failure to diagnose and treat this injury is associated with failure of the ACL reconstruction and persistent instability of the knee.

Anterior Cruciate Ligament

The majority of ACL injuries occur while playing agility sports, with the most often reported sports being basketball, soccer, skiing, and football.21 Most ACL injuries are sustained through noncontact mechanisms, most commonly “pivot shift” or hyperextension. A smaller percentage of injuries are a result of a direct blow. Females have up to 4 times the incidence of ACL tear as male counterparts in the same sports; the reason is unclear but is likely multifactorial.22

The normal ACL is obliquely oriented parallel to the roof of the intercondylar notch with origin at the lateral femoral condyle and insertion at the tibial spines. The 2 bundles (anteromedial and posterolateral) make it appear striated on sagittal images (Fig. 10), which can be a pitfall for diagnosis of a tear; coronal T2-weighted images provide better visualization of bundle anatomy. Orientation (parallel to the intercondylar notch, also called Blumensaat line) as well as the taut appearance and low-signal fibers signify a normal ACL. Another pitfall is mucoid degeneration,23 which results in intermediate signal, occasionally with enlargement and ACL ganglion cyst formation (Fig. 10). If the ACL is not parallel to the intercondylar notch with an “empty notch sign,” acute or chronic tear can be considered (Fig. 11). Discontinuity of fibers and edema associated with typical bone bruises is a sign of acute or subacute injury.24,25 Over time, the torn ACL if untreated may resorb, appearing as if there was never a ligament; these patients often have significant instability and are prone to rapidly developing osteoarthritis. If the fibers fuse to the PCL, the ligament will appear low in signal but directed horizontally instead of along the intercondylar notch; these patients may have few symptoms and may not develop arthritis as rapidly (Fig. 11).

Normal ACL and mucoid degeneration. A, Sagittal proton density weighted fat-suppressed (left image) and coronal T2-weighted fat-suppressed (right image) images show the normal appearance of the ACL. Note striated pattern of the bundles on sagittal images (long arrow) related to volume averaging effect. On coronal images, the anatomy of the separate bundles is evident consisting of the anteromedial (arrowhead) and posterolateral (short arrow) bundle. B, Sagittal T2-weighted fat-suppressed image demonstrating mucoid degeneration of the ACL (arrows) with intermediate signal and expansion diffusely. This may be associated with cruciate ganglion cysts and cystic change at the ACL origin or insertion (arrowheads).
The ACL tear. A, Sagittal proton density-weighted fat-suppressed image shows focal fluid signal within the ACL proximally with disruption of some fibers but with preservation of normal orientation of the ACL along the intercondylar notch roof. These findings are compatible with a partial ACL tear. B, Sagittal proton density-weighted fat-suppressed image (left image) demonstrates a complete acute tear of the ACL with disruption of fibers at the midportion (arrow). Coronal T2-weighted fat-suppressed image (right image) shows an “empty notch” sign with fluid signal (arrow) replacing low-signal ligament. Note the normal PCL (arrowhead). C, Sagittal T2-weighted fat-suppressed image of a patient with remote injury. The ACL (arrowheads) is horizontally oriented (ie, not paralleling the roof of the notch, known as Blumensaat line) consistent with previous tear. Distal fibers are fused to the PCL (arrow).

The ACL is not repaired but rather is reconstructed with a graft, harvested from the patient's own patellar tendon (“bone-tendon-bone” autograft, results in the strongest graft, usually reserved for athletes and younger patients), hamstring autograft, or cadaveric allograft.

Posterior Cruciate Ligament

Posterior cruciate ligament tears are much less common than ACL tears, and they are usually partial unlike ACL tears, which are usually complete. Mechanism is typically either hyperextension (which can also cause ACL tears) and direct blow to the anterior tibia (“dashboard injury”). On sagittal images, the PCL is black in signal and of uniform width (Fig. 12). Alteration in signal intensity and sudden change in caliber are the clues to a PCL tear.24,25 Therefore, suspect a PCL tear if it demonstrates intermediate or high signal on T2-weighted images. Tears most commonly occur at the “genu” or curved region at the midportion. Posterior cruciate ligament tear with associated edema can make the low-signal meniscofemoral ligaments anterior (Humphry ligament) and posterior (Wrisberg ligament) to the PCL appear to stand out (“Humphry sign”) (Fig. 12).

Posterior cruciate ligament tear. Sagittal T2-weighted fat-suppressed image shows partial disruption of the PCL (long arrow). Note that the edema in the midportion of the PCL enhances visualization of the anterior meniscofemoral ligament (arrowhead) known as Humphry sign. Anterior knee impaction with forced posterior tibial translation (“dashboard injury”) is suggested by anterior soft tissue edema (short arrows).


The meniscus is a pair of C-shaped, fibrocartilaginous structures that have primary responsibility of shock absorption and load transmission within the joint space. They are attached to the tibial plateau at anterior and posterior “root” attachment and at the capsular margins. The attachments of the medial meniscus are tighter, allowing for relatively more mobility of the lateral meniscus. Generally, the medial and lateral menisci are subdivided into 3 sections, the anterior horn, the body, and the posterior horn.

Menisci are best imaged on proton density sequences with primary evaluation in the sagittal plane and a secondary search in the coronal plane. The appearance of each meniscus is mostly low signal with intermediate signal in the center and periphery often seen related to degeneration or vascularity. Diagnosis of meniscal tear is based on visualization of signal contacting the superior or inferior surface or abnormal morphology (ie, truncation in the absence of previous surgery).26–28 However, the anterior root attachments may have a striated appearance normally. In addition, the insertion of the meniscofemoral ligament at the posterior horn of the lateral meniscus is an additional pitfall.

On sagittal images of the medial meniscus, the posterior horn is larger than the anterior horn. This observation is important because it will allow for identification of subtle tears and flipped fragments. The anterior and posterior horns of the lateral meniscus are similar in size. Thus, the posterior horn of either meniscus should not be smaller than the anterior horn. The implication is that there is meniscal tissue missing and a tear with displaced fragment or postsurgical changes can be suggested.

Tears should be characterized by location and extent (eg, posterior horn and body of the medial meniscus) as well as morphology. Morphology can be divided into longitudinal and radial types, that is, longitudinal along the circumference of the meniscus and radial perpendicular to its circumference. Longitudinal tears are subdivided into vertical, oblique, and horizontal orientations. Radial tears that are curved are often referred to as “parrot beak” tears because of their shape. Vertical tears can extend around the meniscal substance resulting in a centrally flipped fragment known as a “bucket handle tear.” Flipped fragments are common and can be seen with various tear configurations; they can be a source of pain and locking and should be identified when present.29 Tears with multiple components that cannot be easily classified are typically referred to as “complex” tears. However, the predominant component or any unstable aspect should always be described (ie, a radial tear, flipped fragment or tear at the root attachment) (Fig. 13).

Meniscal tear. A, Sagittal proton density image depicts a vertical tear (arrow) of the posterior horn of the medial meniscus. This type of tear is prone to displacing as a bucket-handle fragment. B, Coronal STIR image shows an oblique longitudinal tear (long arrow) to the undersurface of the body of the medial meniscus. A small fragment (white arrowhead) is flipped into the adjacent meniscotibial recess. Secondary signs of meniscal tear include perimeniscal edema (black arrows) and linear subchondral bone marrow edema (short arrow). C, Coronal and sagittal T2-weighted images show complex tear of the medial meniscus consisting of a radial tear at the posterior horn (long arrows) near the root attachment as well as a horizontal tear (short arrows) extending to the body. Secondary signs of meniscal tear are evident including adjacent chondrosis (arrowhead) and meniscal extrusion (lines and double head arrow).

Secondary signs can be useful for diagnosis of meniscal tear when findings are equivocal. These include meniscal extrusion, adjacent subchondral bone marrow edema, adjacent cartilage loss, perimeniscal edema, and parameniscal cyst formation.30

Articular Cartilage

Hyaline cartilage is intermediate in signal on all sequences, relatively hyperintense if fat suppression is used. Therefore, a fat-suppressed sequence of virtually any type (T1, PD, GRE, T2) can be used to image articular cartilage morphology, the only other factor being titrating signal intensity of joint fluid such that it optimizes visualization of fissures and defects. In general, a fat-suppressed proton density sequence offers the best versatility, with excellent visibility and resolution of the cartilage while offering evaluation of the menisci, ligaments, and bone marrow as well.

Cartilage abnormality (“chondrosis”) in a practical fashion can be divided into diffuse or generalized pathology (Fig. 14) and focal lesions.31–34 Diffuse pathology is commonly seen in long-standing conditions such as chronic ACL tear or chronic meniscal tear, characterized by various degrees of thinning/fissuring/surface fraying with marginal osteophyte formation, with subchondral edema and cystic change. Treatment of diffuse cartilage pathology is typically either conservative (ie, nonsteroidal anti-inflammatory drugs, steroid injection, viscosupplementation) or aggressive (arthroplasty); therefore, very specific descriptors are not warranted above locations and severity of the findings. In contrast, focal cartilage lesions may be treated with localized therapy (ie, microfracture, osteochondral autograft transplantation, cartilage transplantation) especially in younger patients; a more thorough description of the lesion(s) is necessary. This includes the specific location, size in 2 dimensions, margins (sharply defined vs rounded), and depth (partial thickness vs full thickness) as well as any subchondral changes. Classification systems are available (Outerbridge, Noyes, ICRS), which can be applied; however, description as that mentioned previously is arguably better for communication than applying a grade. Sharp edges (“shoulders”) of a cartilage defect generally imply a more acute lesion. Fluid signal beneath the cartilage indicates delamination or a chondral flap, which basically means full-thickness cartilage loss with an unstable fragment; delamination may not be apparent on arthroscopic probing, and so location and extent should be identified. In addition, location and size of intraarticular bodies should be added to the report. These are most commonly found in the joint recesses and may even extend into ganglia and Baker cysts.

Cartilage. A, Axial T2-weighted fat-suppressed image showing normal appearance of patellofemoral cartilage on trochlear (short arrows) and patellar (arrowheads) surfaces. Note normal heterogeneity as well as low signal between the cartilage surfaces (long arrow) representing exclusion of water between like-charged cartilage tissue. B, Axial T2-weighted fat-suppressed image demonstrates a full-thickness fissure (arrow) at the lateral patellar facet, with reactive subchondral bone marrow edema (arrowheads). C, Axial T2-weighted fat-suppressed image shows a chondral flap (arrow) at the lateral patellar facet. D, Coronal proton density weighted fat-suppressed image shows generalized cartilage wear in the lateral compartment (arrowheads) with areas of focal fissuring and flap formation (white arrows). Note complex tear of the adjacent lateral meniscus with extrusion (black arrow).

Osteochondral lesions (OCLs) (previously known as “osteochondritis dissecans”) can be found anywhere in the knee joint, although the process has been classically identified at the medial femoral condyle adjacent to the intercondylar notch.35 As with other cartilage abnormalities, there are numerous grading schemes, all with different characteristics emphasized. Description, as with other findings, is more useful than grading along a particular scheme. Lesions should be described much like other focal cartilage lesions, in terms of the size, location, as well as status of the cartilage and underlying subchondral bone. Osteochondral lesions can be additionally divided into stable or unstable lesions (Fig. 15). Stable lesions have intact overlying cartilage; intact cartilage acts as a “cast,” facilitating healing of the subchondral bone. Unstable lesions have one or more of the following characteristics: a focal cartilage defect; black T1 signal in the subchondral bone indicating necrosis; collapse of the articular surface; fluid dissecting beneath the osseous fragment; and a flap or detachment of the fragment.

Osteochondral lesion. Coronal proton density weighted fat-suppressed image demonstrates an OCL (long arrow) at the lateral aspect of the medial femoral condyle. The lesion shows signs of instability including fluid (short arrow) extending under the fragment and cystic change (arrowhead) deep to the lesion.

When a necrotic osseous fragment is present or when the lesion is at the lateral aspect of the medial femoral condyle, it is easy to characterize it as an OCL. However, it is often difficult to decide when to identify focal chondrosis with reactive subchondral edema or cystic change in other locations as an OCL. In general, the terminology is not important; communication of findings is the essential aspect of a report, and the differentiation is largely academic.

Bone Marrow

Contusion Patterns

As mentioned earlier, with reference to patellar dislocation, there are specific patterns of bone contusion that can indicate the mechanism of injury (Fig. 16). This can be used to predict associated soft tissue (ie, meniscal, ligament, and tendon) injuries.36

Bone bruising and injury mechanism. A, Sagittal T2-weighted fat-suppressed image through the lateral aspect of the joint shows bone bruising at the lateral femoral condyle (long arrow) and posterolateral tibial plateau (short arrow) representing a “pivot shift” injury mechanism typically associated with ACL tear. B, Sagittal T2-weighted fat-suppressed image through the medial aspect of the joint demonstrates bone bruising (arrows) at the medial femoral condyle and anteromedial tibial plateau representing a “hyperextension” injury mechanism, which can result in ACL and/or PCL tear.

A contusion pattern that is fairly specific for an ACL tear includes bone marrow edema in the central portion of the lateral femoral condyle and posterior lateral (and often medial) tibial plateau. This is the result of a rotational injury that causes the lateral femoral condyle to impact the posterolateral tibial plateau, referred to as a “pivot shift” mechanism. Children and adolescents may demonstrate the classic bone contusion pattern of injury to the lateral femoral condyle and posterolateral tibial plateau and demonstrate an intact ACL. This is presumed because of the laxity of ligaments in this population. In adults, this pattern is nearly 100% specific for ACL injury.

Hyperextension mechanism can injure the ACL and/or the PCL and may result in tibiofemoral dislocation. Matching (“kissing”) bone bruises are found at the anterior aspect of the femoral condyles and tibial plateau, more commonly medial than lateral. Bone contusions at the anterior lateral femoral condyle and inferomedial patella are indicative of a recent patellar dislocation.

More severe injury mechanism can result in a fracture; differentiation between a bone bruise and fracture is generally determined by cortical interruption and linear signal associated with bone marrow edema, with the fracture line best seen on T1-weighted images. However, very often, impaction of the articular surface from mechanisms described earlier creates linear signal abnormality with depression of the articular surface, but the pattern does not fit the terminology and treatment protocol of a fracture. In this situation, the term osteochondral impaction injury is usually applied.

As mentioned earlier, true fractures are characterized by linear marrow signal and cortical interruption associated with bone marrow edema. Description of location, extent, and concomitant soft tissue injury is important; correlation with history is essential as well. Subacute fractures can be indistinguishable from stress fractures, and history (ie, no specific injury, change in activity level) may reveal the true etiology.

Stress Injury and Other Marrow Findings

Subchondral stress fractures are common in older patients with osteopenia. Contact forces across the articular surfaces can increase suddenly related to meniscal tear or meniscal surgery, especially at the medial aspect of the joint. Previously referred to as SONK (spontaneous osteonecrosis of the knee), subchondral fracture should be suggested when intense bone marrow edema is present, associated with linear low signal paralleling the articular surface, or crescentic low signal at the surface (Fig. 17). Although the injury arises from altered mechanics and not ischemia, continued stress can result in collapse of the articular surface and true osteonecrosis.37,38

Subchondral stress fracture. Coronal STIR image shows intense bone marrow edema (short arrow) in the medial femoral condyle with a subchondral crescent of low signal (arrowheads) consistent with a stress fracture, previously (and inaccurately) referred to as spontaneous osteonecrosis of the knee (SONK). Observe meniscal tear (long arrow) with extrusion that resulted in abnormal contact forces leading to the fracture.

Other marrow abnormalities require a detailed differential, particularly with reference to the level of concern for malignancy. A multimodality approach is essential, especially incorporating radiographs. This topic is beyond the scope of this chapter. However, any focal medullary lesion with signal isointense to the muscle on T1-weighted images (ie, without fat content) requires additional attention. Lesions containing fat are generally considered benign such as hematopoietic marrow or “burned out” lesions.


Sports injuries of the knee are very common, and the radiologist should be familiar with the range of pathology that can occur. New conditions continue to be described, while understanding of established conditions evolves. Therefore, continuing education is essential for effective communication with referring physicians.


1. Schindler OS. ‘The Sneaky Plica’ revisited: morphology, pathophysiology and treatment of synovial plicae of the knee. Knee Surg Sports Traumatol Arthrosc. 2014; 22: 247–262.
2. Herman AM, Marzo JM. Popliteal cysts: a current review. Orthopedics. 2014; 37: e678–e684.
3. Parellada AJ, Morrison WB, Reiter SB, et al. Unsuspected lower extremity deep venous thrombosis simulating musculoskeletal pathology. Skeletal Radiol. 2006; 35: 659–664.
4. Borrero CG, Maxwell N, Kavanagh E. MRI findings of prepatellar Morel-Lavallée effusions. Skeletal Radiol. 2008; 37: 451–455.
5. Sonin AH, Fitzgerald SW, Bresler ME, et al. MR imaging appearance of the extensor mechanism of the knee: functional anatomy and injury patterns. Radiographics. 1995; 15: 367–382.
6. Tuong B, White J, Louis L, et al. Get a kick out of this: the spectrum of knee extensor mechanism injuries. Br J Sports Med. 2011; 45: 140–146.
7. Kramer J, White LM, Recht MP. MR imaging of the extensor mechanism. Semin Musculoskelet Radiol. 2009; 13: 384–401.
8. Hayes CW. MRI of the patellofemoral joint. Semin Ultrasound CT MR. 1994; 15: 383–395.
9. Elias DA, White LM. Imaging of patellofemoral disorders. Clin Radiol. 2004; 59: 543–557.
10. Colvin AC, West RV. Patellar instability. J Bone Joint Surg Am. 2008; 90: 2751–2762.
11. Diederichs G, Issever AS, Scheffler S. MR imaging of patellar instability: injury patterns and assessment of risk factors. Radiographics. 2010; 30: 961–981.
12. Sanders TG, Morrison WB, Singleton BA, et al. Medial patellofemoral ligament injury following acute transient dislocation of the patella: MR findings with surgical correlation in 14 patients. J Comput Assist Tomogr. 2001; 25: 957–962.
13. De Maeseneer M, Shahabpour M, Pouders C. MRI spectrum of medial collateral ligament injuries and pitfalls in diagnosis. JBR-BTR. 2010; 93: 97–103.
14. House CV, Connell DA, Saifuddin A. Posteromedial corner injuries of the knee. Clin Radiol. 2007; 62: 539–546.
15. Blankenbaker DG, De Smet AA, Fine JP. Is intra-articular pathology associated with MCL edema on MR imaging of the non-traumatic knee? Skeletal Radiol. 2005; 34: 462–467.
16. Wen DY, Propeck T, Kane SM, et al. MRI description of knee medial collateral ligament abnormalities in the absence of trauma: edema related to osteoarthritis and medial meniscal tears. Magn Reson Imaging. 2007; 25: 209–214.
17. Bolog N, Hodler J. MR imaging of the posterolateral corner of the knee. Skeletal Radiol. 2007; 36: 715–728.
18. Muhle C, Ahn JM, Yeh L, et al. Iliotibial band friction syndrome: MR imaging findings in 16 patients and MR arthrographic study of six cadaveric knees. Radiology. 1999; 212: 103–110.
19. Geiger D, Chang EY, Pathria MN, et al. Posterolateral and posteromedial corner injuries of the knee. Magn Reson Imaging Clin N Am. 2014; 22: 581–599.
20. Malone WJ, Koulouris G. MRI of the posterolateral corner of the knee: normal appearance and patterns of injury. Semin Musculoskelet Radiol. 2006; 10: 220–228.
21. Vahey TN, Meyer SF, Shelbourne KD, et al. MR imaging of anterior cruciate ligament injuries. Magn Reson Imaging Clin N Am. 1994; 2: 365–380.
22. Prodromos CC, Han Y, Rogowski J, et al. A meta-analysis of the incidence of anterior cruciate ligament tears as a function of gender, sport, and a knee injury-reduction regimen. Arthroscopy. 2007; 23: 1320–1325.e6.
23. Bergin D, Morrison WB, Carrino JA, et al. Anterior cruciate ligament ganglia and mucoid degeneration: coexistence and clinical correlation. AJR Am J Roentgenol. 2004; 182: 1283–1287.
24. Stork A, Feller JF, Sanders TG, et al. Magnetic resonance imaging of the knee ligaments. Semin Roentgenol. 2000; 35: 256–276.
25. Roberts CC, Towers JD, Spangehl MJ, et al. Advanced MR imaging of the cruciate ligaments. Radiol Clin North Am. 2007; 45: 1003–1016, vi–vii.
26. Fritz RC. MR imaging of meniscal and cruciate ligament injuries. Magn Reson Imaging Clin N Am. 2003; 11: 283–293.
27. Fox MG. MR imaging of the meniscus: review, current trends, and clinical implications. Magn Reson Imaging Clin N Am. 2007; 15: 103–123.
28. Koenig JH, Ranawat AS, Umans HR, et al. Meniscal root tears: diagnosis and treatment. Arthroscopy. 2009; 25: 1025–1032.
29. Fodor DW, Vagal AS, Wissman RD, et al. Meniscal gymnastics: common and uncommon locations of meniscal flip and flop. Curr Probl Diagn Radiol. 2008; 37: 15–25.
30. Bergin D, Hochberg H, Zoga AC, et al. Indirect soft-tissue and osseous signs on knee MRI of surgically proven meniscal tears. AJR Am J Roentgenol. 2008; 191: 86–92.
31. Goodwin DW. MR imaging of the articular cartilage of the knee. Semin Musculoskelet Radiol. 2009; 13: 326–339.
32. Potter HG, Foo LF. Magnetic resonance imaging of articular cartilage: trauma, degeneration, and repair. Am J Sports Med. 2006; 34: 661–677.
33. Shapiro LM, McWalter EJ, Son MS, et al. Mechanisms of osteoarthritis in the knee: MR imaging appearance. J Magn Reson Imaging. 2014; 39: 1346–1356.
34. Jazrawi LM, Alaia MJ, Chang G, et al. Advances in magnetic resonance imaging of articular cartilage. J Am Acad Orthop Surg. 2011; 19: 420–429.
35. Zbojniewicz AM, Laor T. Imaging of osteochondritis dissecans. Clin Sports Med. 2014; 33: 221–250.
36. Patel SA, Hageman J, Quatman CE, et al. Prevalence and location of bone bruises associated with anterior cruciate ligament injury and implications for mechanism of injury: a systematic review. Sports Med. 2014; 44: 281–293.
37. Yao L, Stanczak J, Boutin RD. Presumptive subarticular stress reactions of the knee: MRI detection and association with meniscal tear patterns. Skeletal Radiol. 2004; 33: 260–264.
38. Gil HC, Levine SM, Zoga AC. MRI findings in the subchondral bone marrow: a discussion of conditions including transient osteoporosis, transient bone marrow edema syndrome, SONK, and shifting bone marrow edema of the knee. Semin Musculoskelet Radiol. 2006; 10: 177–186.


Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.