mri of the knee in adults · 2015-12-10 · ﬁ bers. chronic, atraumatic mucoid (also known as...

© 2015 AAOS Instructional Course Lectures, Volume 64 61

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This chapter focuses on the use of MRI in evaluating periarticular knee tissues. Tumors, infection, and pediatric condi-tions are not specifi cally covered.

Normal and Abnormal Appearances of Soft TissuesNormal ligaments, tendons, capsules, and menisci should be hypointense on all MRI sequences (Figure 1, A and B). Traumatic injuries manifest as increased signal on T2-weighted (fl uid-weighted) and proton density– weighted sequenc-es; the increased signal is caused by ede-ma and fl uid retention. Sprains show

increased signal and ill-defi ned fi bers but no discontinuity. Tears demonstrate defects as bright as fl uid, sometimes with laxity or the buckling of residual fi bers. Chronic, atraumatic mucoid (also known as myxoid) degeneration shows increased signal and can confound sprain diagnoses; such degeneration often is seen in the anterior cruciate ligament (ACL), the proximal fi bular collateral ligament (FCL), the popliteus tendon insertion, and the menisci (Fig-ure 1, C and D). Differentiating acuity from degeneration requires consider-ation of a combination of information

on history of the injury and additional radiologic clues. This chapter’s authors routinely recommend radiographs prior to MRI.

Anterior Cruciate LigamentThe normal ACL is hypointense and taut, paralleling the intercondylar roof (Figure 1, A). The anteromedial and posterolateral bundles often are indis-tinguishable proximally but visible dis-tally, where strands of increased signal presumably relate to the interdigitation of fat1 (Figure 1, B).

Complete ACL tears are diagnosed with up to 98% accuracy.2 The diag-nostic criteria include a fl uid-fi lled gap across the ligament, often with laxity of the residual fi bers (Figure 2), that can be appreciated in all three imag-ing planes. Although historically best detected on sagittal plane images, this chapter’s authors recommend confi r-mation on axial and coronal images, particularly in the setting of partial tears. Acute tears in adults have a dis-crete gap at the midsubstance in 70% of all tears and proximal in 20% of all tears; distal tears are the least common.1

MRI of the Knee in Adults

Dennis C. Crawford, MD, PhDMichael R. Hirota, MD

Erik W. Foss, MD

Dr. Crawford or an immediate family member serves as a paid consultant to or is an employee of Histogenics and serves as an unpaid consultant to Community Tissue Services; has received research or institutional support from Community Tissue Services, Histogenics, Moximed, and Zimmer Biologics. Neither of the following authors nor any immediate family member has received anything of value from or has stock or stock options held in a commercial company or institution related directly or indirectly to the subject of this chapter: Dr. Hirota and Dr. Foss.

AbstractMRI of the knee is a crucial component for evaluating symptomatic patients. An awareness of normal and abnormal appearances assists in clinical decision making. Chronic degen-erative changes and focal traumatic injuries can sometimes be confused with one another, so differentiation is crucial. As technolog y continues to evolve, identifying early disease and preventing disease progression will become an integral part of MRI interpretation.

Instr Course Lect 2015;64:61–73.

Orthopaedic Medicine and Practice

62 © 2015 AAOS Instructional Course Lectures, Volume 64

Chronic, complete tears of the ACL result in the resorption of fi bers in up to 42% of patients and will produce an “empty notch” sign3,4 (Figure 3). Resid-ual fi bers also may scar onto bone or the posterior cruciate ligament (PCL), thus mimicking an intact ACL. However, the ACL will be diminutive in caliber, lax, and attached to nonanatomic sites within the intercondylar notch.

Secondary signs of ACL tears of-ten aid in diagnosis. Bone bruises are common in the lateral compartment in both the midfemoral condyle and the posterior tibia, although they may occur in the medial femoral condyle.4

Anterior tibial translation may manifest in several ways. The PCL may appear buckled (Figure 4, A). A vertical line from the midposterior margin of the

lateral condyle will lie more than 5 to 7 mm posterior to the lateral tibia.5,6

The FCL may be abnormally vertically oriented and completely visualized on a single coronal image7 (Figure 4, B).

Partial ACL tears can be visualized, but published diagnostic criteria are limited.8 A partial tear can be inferred when a focal fl uid-intense defect is seen in a portion of the ligament. A sprain is suggested in the setting of acute trauma by diffuse T2-hyperintensity through-out the ACL, without focal fl uid signal or ligament thickening.

Mucoid degeneration in the ACL can be mistaken for a sprain. It manifests as thickening and diffuse intermedi-ate signal throughout the ligament, interspersed with thin, linear, well- defi ned strands of normal dark fi bers, an appearance that is similar to a celery stalk9,10 (Figure 1, C). In contrast, an ACL sprain should be of normal thick-ness and will usually lack well-defi ned, interdigitating fi bers.

A ganglion cyst can mimic an ACL tear. However, although ganglion cysts

Normal structures and mucoid degeneration. A, Sagittal, fat-sup-pressed, T2-weighted image of a normal anterior cruciate ligament (ACL) (arrows), which is homogeneously dark and taut and parallels the intercon-dylar roof. B, Coronal fat-suppressed, T2-weighted image of the ACL, the medial collateral ligament (MCL), and menisci. The distal ACL (thin arrow) shows linear striations of increased intensity as a result of the interdigitation of fat between the ACL bundles; this should not be mistaken for tearing. The normal MCL (arrowheads) is uniformly hypointense, without laxity. The normal medial meniscus (curved arrow) and lateral meniscus (thick arrow) are triangular in cross-section and uniformly hypointense. C, Sagittal fat-sup-pressed, T2-weighted image of ACL mucoid degeneration (arrows). ACL mucoid degeneration usually demonstrates ACL thickening and increased signal intensity, but distinct individual fi bers remain visible, in contrast with an acute traumatic injury that is usually accompanied by a lack of fi ber defi nition, surrounding edema, and joint effusion. D, Sagittal proton density–weighted image of medial meniscal mucoid degeneration (arrow). The intermediate- intensity, intrasubstance signal is amorphous in morphology, and the tissue surface remains intact. In contrast, a traumatic tear is linear and should show an articular surface defect.

Figure 1

Sagittal fat-suppressed, T2-weighted image of a complete ACL tear. Complete tears can be confi dently diagnosed when there is a visible fl uid-intensity gap in the ligament (arrow) and fi ber buckling (arrowheads). Note the edema in the pericruciate soft tissues and joint effusion.

Figure 2

MRI of the Knee in Adults Chapter 6


are as bright as fl uid, they will be well defi ned and typically lobular, and ad-jacent fi bers will be well defi ned with uniform hypointensity (Figure 5, A).

After ACL reconstruction, the graft should be taut and parallel the inter-condylar roof on sagittal images (Fig-ure 5, B).

Initially after surgery, the graft may show increased signal and enhancement as a result of revascularization, although it should not approach the same bright-ness of fl uid; the signal should decrease to expected dark ligamentous intensity after 24 months.11 In addition, in ham-string grafts, ingrowth of fi brovascular tissue will eventually occur between the individual bundles of the looped graft. Because fi brovascular tissue is slight-ly hyperintense on T2-weighted se-quences, this may produce a somewhat

striated appearance to the graft; this should not be mistaken for a longitu-dinal split tear.

MRI is useful for assessing ACL graft complications and reinjuries. A graft tear is diagnosed in a similar fashion to that of a torn native ACL: a fl uid-fi lled gap across the graft tissue. For qua-drupled or doubled soft-tissue grafts, attention to change within individual bundles is necessary because damaged bundles may reside adjacent to normal bundles. The graft should be parallel to the intercondylar roof without contact-ing it directly. An anterior femoral or posterior tibial tunnel results in a ver-tically oriented graft appearance that is not parallel to the intercondylar roof. Similarly, midline tunnel placement for either the femoral tunnel or the tibial tunnel portends a vertical graft, which

also raises concern for associated ro-tational instability. Conversely, graft impingement with an anteriorly placed tibial tunnel is seen as an indentation of the distal graft by the anterior inter-condylar roof (Figure 5, C). Tunnel widening may occur, with variable-in-tensity tissue fi lling the space between the graft and bone. Cysts may form within the ACL graft, which are visible as well- defi ned, fl uid-intense foci with splaying of intact fi bers and sometimes extension into bone, the intercondylar notch, or pretibial soft tissues.12

Focal arthrofi brosis (also known as a cyclops lesion) after ACL reconstruc-tion occurs in 1% to 10% of patients and can be visualized on MRI with 85% accuracy.13,14 It is usually localized along the anterior margin of the distal ACL graft as a discrete rounded or oval lesion

Coronal, fat-sup-pressed, T2-weighted images of a complete (grade 3) medial collateral ligament tear (MCL) demonstrates a fl uid-intense defect in the proxi-mal MCL (black arrow); no visible intact fi bers are seen in this area (or in images more anteriorly and posteriorly). This patient also had a complete anterior cruciate ligament tear, which can be inferred from the complete lack of normal, dark fi bers in the intercondylar notch (curved arrow). Note the normal, intact, and homogeneously dark iliotibial band (white arrows).

Figure 3

A, Sagittal, fat-suppressed, T2-weighted image of an intact posterior cruciate ligament (PCL) in the setting of anterior tibial translation. The PCL is homogeneously dark and well defi ned (arrowheads). However, it appears slightly buckled, instead of following the expected smooth arc from the femur to the tibia (dashed line), which is compatible with secondary anteri-or tibial translation related to a complete anterior cruciate ligament (ACL) tear (not shown). Note the marrow edema in the posterior tibia caused by a bone contusion (curved arrow). B, Coronal, fat-suppressed, T2-weighted image of a normal proximal fi bular collateral ligament (FCL) in the setting of anterior tibial translation. The normal ligament (white arrows) is homogeneously dark. Because the FCL is normally obliquely oriented, it should not be completely visible on a single coronal image; in this case, the ligament is seen in its en-tirety on one coronal image because of anterior tibial translation (the vertical FCL sign) resulting from a complete ACL tear (not shown).

Figure 4



abutting the anterior margin of the dis-tal graft (Figure 5, B). A cyclops lesion may show hypointense, intermediate, hyperintense, or mixed signal intensity

on T2- and proton density–weighted images.14

The postoperative evaluation should include an assessment of the graft fi x-ation devices. Bioabsorbable interfer-ence devices are visible as hypointense, threaded structures and should be con-tained within or directly adjacent to the osseous tunnel. Fixation device migra-tion into the joint space or extra-articu-lar tissues and/or device fragmentation is typically visible on MRI sequences; intra-articular migration can occasion-ally cause a “kissing” osteochondral erosion.15 Extra-articular migration may show reactive edema or fl uid in adjacent soft tissues.

Posterior Cruciate LigamentThe normal PCL, which is approxi-mately twice as thick as the ACL, is seen in all three imaging planes, and follows a gentle curving arc from

femoral to tibial attachment (Fig-ure 4, A and Figure 6). The criteria for PCL injuries differ from those of ACL injuries because the PCL is prone to stretching and elongation after trau-ma and may not demonstrate a discrete, fl uid-intense defect.16 An injured PCL may show increased diameter, measur-ing 7 mm or more anteroposterior in its vertical portion, with intermediate signal intensity on both T2- and pro-ton density–weighted sequences17 (Fig-ure 7). If the PCL shows uniformly dark signal intensity on proton density– weighted images, it is almost assuredly normal.18,19 PCL osseous avulsions can be seen on MRI but may be more vis-ible on radiographs.

Medial Collateral LigamentThe medial collateral ligament (MCL) is the most commonly injured ligament in the knee. It is composed of three layers:

A, Sagittal fat-suppressed, T2-weighted image of an anterior cruciate ligament (ACL) ganglion cyst. An intraligamentous ganglion cyst will show well-defi ned single or multiple fl uid-intense internal foci and overall ligament enlargement (arrow); the cyst also may extend beyond the margins of the ligament. However, well-defi ned, intact fi bers should remain visible (arrowheads). The curved arrow points to a focus of tibial marrow change deep to the ACL attach-ment, most likely a traction-type change that is not uncommonly seen deep to the ACL and posterior cruciate ligament attachments. B, Sagittal fat-suppressed, T2-weighted image of an intact bone-tendon-bone ACL graft with focal arthrofi -brosis (cyclops lesion). A mixed-intensity, lobular mass sits along the anterior margin of an ACL graft (arrowheads); this is a common location and appearance for a cyclops lesion. The ACL graft is normal in signal, is intact, and parallels the intercondylar roof (thin arrows). Signal abnormalities proximal and distal to the graft are the result of metallic artifact from interference screws (thick arrows). C, Sagittal proton density–weighted image of ACL graft impingement. An osseous spur along the anterior margin of the intercondylar roof (arrow) contacts and displaces the ACL graft (arrowhead). Im-pingement also can result from a normal intercondylar roof when the tibial tunnel is placed too far anteriorly.

Figure 5

Sagittal, fat-sup-pressed, T2-weighted image of a normal posterior cruciate ligament (PCL). The normal PCL (arrows) is homogeneously dark on all sequences and follows a gentle, curving arc from its femoral to its tibial attachments.

Figure 6



a poorly visualized superfi cial fascial layer, a middle layer composed of super-fi cial MCL fi bers (10 to 11 cm in length), and a deep layer composed of the medi-al joint capsule and the meniscofemoral and meniscotibial ligaments.20

Most MCL sprains and tears occur proximally and are visible on coronal and axial images (Figures 3, 8, and 9). Inspection of the ligament on axial im-aging may help distinguish a complete tear from a partial tear. MCL buck-ling is a secondary sign of a tear and is common in complete tears. Menis-cocapsular separation is subtle and is seen as a focal discontinuity of the me-niscotibial and/or meniscofemoral lig-aments. Other fi ndings include medial meniscal displacement relative to the capsule, with edema and irregularity of the peripheral meniscal margin along its capsular attachment.21

Chronic and remotely healed MCL injuries are relatively indistinguishable and show thickening and fi brosis of the ligament substance, which tend to be proximal, tapering distally to normal thickness. A Pellegrini-Stieda lesion refers to chronic, posttraumatic ossifi -cation at the femoral attachment, which is visible as marrow signal intensity ad-jacent to the medial epicondyle.

Iliotibial BandThe iliotibial band (ITB) is normally hypointense, and the deeper soft tissues are intermediate to low signal. The ITB is separated from the underlying lateral femoral epicondyle by fat, connective tissue, and two layers of synovial lining. In ITB friction syndrome, impingement at the epicondyle may occur, which is manifested as tendinopathy and under-lying edema or adventitial bursal fl u-id1,22 (Figure 10, A). Traumatic tears are uncommon and typically occur in

the posterior tendon midsubstance, being manifested by a fl uid-intense discontinuity and, with acute injuries, surrounding soft-tissue edema23,24 (Fig-ure 10, B).

Posterolateral CornerThe posterolateral corner complex in-cludes several structures variably visi-ble on MRI. The FCL and the biceps femoris tendon are best evaluated in

Sagittal proton density– weighted image of a posterior cru-ciate ligament (PCL) tear. The PCL (arrowheads) is abnormally bright. Because the PCL has a higher propensity for stretching rather than discretely tearing, no fl uid-fi lled liga-ment defect is visible in this case.

Figure 7

Fat-suppressed, T2-weighted axial image shows absence of most of the expected medial collateral ligament (MCL) fi bers (arrow), with surrounding soft-tissue edema. Small remnants of MCL tissue (arrowheads) were noted to be discontiguous on more proximal images.

Figure 8

A, Coronal, fat-suppressed, T2-weighted image of a partial (grade 2) medial collateral ligament (MCL) tear demonstrates that the prox-imal MCL is too thin, and there is abnormal edema superfi cial and deep to the middle layer (black arrow), but intact fi bers remain, which are compatible with a partial tear. Note the bucket-handle tear of the medial meniscus, as shown by the small and irregular meniscal body (curved arrow) and the bucket handle fl ipped into the intercondylar notch (thick arrow). Compare the torn, in situ medial meniscal body with the normal lateral meniscus. B, Axial image shows that the proximal MCL fi bers are thinner than expected (arrows); a small amount of underlying fl uid-intensity signal (arrowhead) is compatible with partial tearing of the undersurface fi bers at the femoral attachment.

Figure 9



the axial and coronal planes; the pop-liteus tendon should be well visualized in all three planes. The popliteofi bular ligament is inconsistently seen.25 The rest of the arcuate complex is diffi cult to separate from surrounding tissue in normal joints and is often obscured af-ter posterolateral trauma.

The FCL and the popliteus tendon may avulse from their bony attach-ments, which occurs in up to 40% of knees with multiple ligament injuries.26 Such injuries show discontinuity and laxity of fi bers and may include osse-ous avulsion fragments. Up to 96% of popliteus tendon injuries occur at the myotendinous junction, not the femoral insertion, and are best seen on axial im-ages;27 a strain will be seen as feathery, nonfocal edema in the myotendinous junction, and a tear will demonstrate a fl uid-intense defect. Complete tears usu-ally result in retraction and clumping.24

A complete tear usually shows laxity of the residual fi bers and large amounts of surrounding edema and hemorrhage (Figure 11). Fibular attachments of the FCL and the biceps femoris tendon fre-quently form a conjoined tendon, thus

singular distal FCL or biceps femoris tendon injuries are diffi cult to distin-guish, and combined injuries are com-mon.28 Avulsions of the fi bular head may occur, so correlation with radio-graphs is essential where osseous frag-ments may be more conspicuous.

MenisciThe normal meniscus should be well defi ned on sagittal and coronal imaging and is best visualized on T2-weighted sequences. Tiny, linear vessels visu-alized within the vascularized outer third of the meniscus appear as linear hyperintensities and do not extend to the articular surface. Normal menisci are otherwise homogeneously dark and triangular in cross-section (Figure 12). The anterior and posterior roots should be visibly intact on both sagittal and coronal sequences. The meniscal body should not extend beyond the tib ial plateau; otherwise, it is extruded. Ex-trusion greater than 3 mm is associated with severe meniscal degeneration, extensive or complex tears, large ra-dial tears, and meniscal root tears29 (Figure 13).

The criteria for diagnosing meniscal tears depend on the type of tear. For longitudinal vertical or horizontal tears, a discrete linear signal hyperintensity should be seen within the meniscus on either two consecutive images in one plane or two images in two different planes (the two-slice rule), unequivocal-ly contacting the articular surface on at least one image30 (Figure 14, A). This generates positive predictive values of 94% for medial meniscal tears and 96% for lateral meniscal tears. A radial tear can be more diffi cult to identify but needs to be seen on only one image. The inner edge of the meniscus should be sharply defi ned in cross-section; with

A, Coronal, fat-suppressed, T2-weighted image of iliotibial band (ITB) friction syndrome. There is abnormal fl uid and edema deep to the ITB (arrow), and the ITB is intact. B, Coronal proton density–weighted image of a complete ITB tear. The ITB is discontiguous (curved arrow), and the proximal fi bers are buckled and slightly retracted (arrow).

Figure 10

Coronal, fat-suppressed, T2-weighted image of a posterolateral corner injury. The fi bular collateral ligament (FCL) and the biceps femoris tendon are completely torn. The only visible FCL fi bers are severely buckled (arrowhead). Only a few abnormal biceps femoris tendon fi bers are seen (short arrows). No FCL or biceps femoris tendon fi bers are seen attaching to the fi bular head (long arrow). There is a large amount of soft-tissue edema around the posterolateral corner. The proximal popliteus tendon (curved arrow) is intact but only partially visualized on this image.

Figure 11



radial tears, the donor edge will be fo-cally blunted (Figure 14, B).

If a meniscal tear is identifi ed, the surgeon should search for a displaced fl ap or fragment. Medial bucket-handle tears displaced into the intercondylar notch are identifi able as an elongated, hypointense structure parallel to the PCL; this is known as the double-PCL sign. Large, lateral fl ap tears can dis-place anteriorly above or in front of the anterior horn; these are seen on sagittal images as a markedly small posterior horn and a large—or even double—an-terior horn. Small, displaced fl ap tears are more diffi cult to visualize; medial meniscal tears may displace into the superior or inferior recesses of the me-dial joint space (Figure 14, C) or less frequently posteriorly adjacent to the PCL; lateral meniscal tears displace less frequently, usually laterally or into the popliteus haitus.31

Traumatic tears must be differenti-ated from degeneration and degener-ative tears. Menisci typically undergo mucoid degeneration with aging (Fig-ure 1, D); although this was once thought to be a precursor of future de-generative tearing, some studies sug-gest that it is an incidental fi nding that sometimes spontaneously resolves.32 A degenerative tear can look severely abnormal, with a mixture of mucoid degeneration and tearing, loss of the normal triangular shape, and extrusion (Figure 13). Importantly, adjacent de-generative joint disease (DJD) often accompanies meniscal degeneration.

It is challenging to assess a repaired or a partially resected meniscus for any retearing. Because healed fi brovascu-lar tissue is bright on T2- and proton density– weighted sequences, it can be confused with a tear. Following menis-cal repair, a residual hyperintensity at

the healed tear interface can be seen for up to 12.9 years;33 following a partial meniscectomy, residual linear signal ab-normalities may represent healed tissue rather than tearing. Thus, comparison with a prior MRI is essential. If the

linear signal abnormality is similar to that of the preoperative study, it likely represents fi brovascular tissue; if differ-ent, it may represent a new tear.

The evaluation of a meniscal repair or a prior meniscectomy may be aided by

Coronal, fat-suppressed, T2-weighted image of normal medial (arrow) and lateral (curved arrow) meniscal bodies. In cross section, the menisci should be dark, triangular, and similar in size. The peripheral third of the meniscus may show some linear bright signal corresponding to vascularity, but the signal should not contact an articular surface. The peripheral margins of the meniscal bodies do not extend beyond the tibial plateau (otherwise extrusion is present). The medial meniscofemoral and meniscotibial ligaments are partially visible (arrowheads).

Figure 12

Coronal, fat-suppressed, T2-weighted image of degenerative joint disease. There is full-thickness cartilage loss along both sides of the medial compartment (arrows), with underlying degenerative marrow change in the medial femoral condyle. There are degenerative changes of the medial meniscal body, consisting of mucoid degeneration (intermediate intrasubstance signal; curved arrow) and medial extrusion (displacement of the meniscus beyond the medial tibial plateau). Cartilage fi ssuring and ulcerations also are seen in the lateral compartment (arrowheads).

Figure 13



a direct MRI arthrogram (dMRA). Ex-tension of gadolinium contrast (bright signal) into the meniscal substance is compatible with retears. The evaluative pitfalls include contrast not insinuating into a defect and small tears where the signal is not visible. Conventional MRI is equivalent to dMRA for diagnosing a recurrent tear if prior repair or resection involves less than 25% of the meniscal tissue; when resection exceeds 25%, dMRA is more accurate for diagnosing

a recurrent tear.34 Of note, although commonly used in practice and general-ly accepted as routine, the FDA has not approved gadolinium contrast material for MRA, so its use must be considered off-label for such applications.

Osteochondral Degenerative ChangesIn the setting of adult sports medi-cine, fi ndings suggestive of DJD have important implications in decisions

about therapeutic recommendations. Whereas traumatic articular cartilage lesions will show sharply marginated defects surrounded by relatively normal cartilage (Figure 15), chronic cartilage degeneration usually appears as regions of generalized chondral thinning and irregularity (Figure 13). Signs of DJD in bone include osteophytes, subchon-dral cysts, sclerosis, and ill-defi ned bone marrow with hyperintensity on T2- and proton density–weighted images.

A, Sagittal, fat-suppressed, T2-weighted image of a vertical meniscal tear. The linear hyperintense signal in the peripheral third of the lateral meniscal posterior horn contacts the femoral articular surface (white arrow); the signal abnormality was visible on more than one image, confi rming the diagnosis. Note the bone marrow edema in the lateral femoral condyle (black arrow) representing a bone contusion related to an anterior cruciate ligament tear (not shown). A normal popliteus tendon (curved arrow) is partially visualized coursing through the popliteus hiatus. B, Coronal, fat-suppressed, T2-weighted image of a radial tear of the lateral meniscus. There is focal blunting of the inner third of the lateral meniscal body (arrow), which returned to a normal sharp free edge on adjacent images and is compatible with a radial tear. Note the sharp free edge of the normal medial meniscal body. C, Coronal, fat-suppressed, T2-weighted image of a displaced medial meniscal tear. The inner third of the meniscal body is blunted (arrowhead), which is compatible with a tear. There is abnormal meniscal-intensity signal in the superomedial joint recess, which represents the displaced fl ap/fragment (arrow).

Figure 14

A, Axial, fat-suppressed, T2-weighted image of a full-thickness cartilage fi ssure. A linear hyperintensity (arrow) extends down to the hypointense subchondral bone plate (arrowhead). Underlying ill-defi ned marrow hyperintensity is compatible with degenerative marrow change. B, Coronal, fat-suppressed, T2-weighted image of cartilage delamination. A focal linear hyperintensity is seen along of the base of the medial femoral condylar cartilage (arrow).

Figure 15



The ill-defi ned hyperintensity often seen in DJD is described as the bone marrow edema pattern. This phenom-enon of hyperintense signal is not nec-essarily simply marrow edema, but is composed of marrow edema, necrosis, fi brosis, trabecular remodeling, and bleeding.35 Sadaat et al36 suggested that bone marrow edema patterns are sec-ondary to increased perfusion related to fi brovascular ingrowth. Other investi-gators have attempted to correlate bone marrow edema patterns and symptoms with varying and contradictory results. Some studies have reported no cor-relation, one found an increased inci-dence in bone marrow edema patterns in symptomatic patients, and another reported increasing bone marrow ede-ma patterns associated with worsening

pain.37-40 In addition, bone marrow ede-ma lesions may increase in size and/or number, whereas others may decrease.38

Patellofemoral CompartmentLateral patellar dislocation injuries have a characteristic appearance and demonstrate injury to the medial pa-tellofemoral ligament (MPFL), often with associated signs of patellofemoral contusion. Injury at the patellar inser-tion occurs 50% to 90% of the time and 25% at the femoral attachment.41,42 Two-thirds of the time, there is a partial tear at the patellar insertion.43 Acutely, the MPFL demonstrates fi ber discon-tinuity and buckling, generally accom-panied by a large amount of edema along the anteromedial aspect of the knee. In the setting of patellar osseous

avulsion, marrow edema and an osse-ous fragment are seen adjacent to the medial patella; femoral avulsions occur less frequently.

Transient impaction of the patella against the lateral femoral condyle often produces a bone marrow edema pattern in the medial patellar facet and the lat-eral femoral condyle (Figure 16, A). Chondral or osteochondral fragments may displace into the joint space. In a chronic injury, a torn MPFL may be diffi cult to see, but a sign of prior injury on MRI and radiographs is irregular-ity and/or an osseous fragment at the MPFL attachment to the patella.

The patellar and quadriceps tendons are hypointense structures often with a striated, marbled look at their insertions because of interspersed fi brovascular

Patellofemoral abnormalities. A, Axial, fat-suppressed, T2-weighted image of a medial patellofemoral ligament (MPFL) avulsion fracture. There is a fracture of the medial patella at the MPFL attachment (black arrow). A large amount of edema tracks along an ill-defi ned MPFL (arrowheads). There is characteristic lateral femoral condylar contusion edema (white arrow) from transient lateral patellar dislocation and associated impaction against the condyle. B, Sagittal, fat-suppressed, T2-weighted image of patellar tendinopathy. There is intermediate signal in the proximal patellar tendon (arrow), which should have the same hypointensity as in the distal tendon. Mild edema lies superfi cial and deep to the tendon. Note the normal quadriceps tendon (curved arrow); the linear hyperintense striations represent interdigitating fi brovascular tissue and should not be mistaken for tearing. C, Sagittal, fat-suppressed, T2-weighted image of a partial patellar tendon tear. There is a fl uid-intense defect in the proximal tendon involving the deep fi bers (arrow); the superfi cial fi bers are intact. There is intermediate signal in the proximal half of the tendon, which is compatible with underlying tendinopathy.

Figure 16



tissue (Figure 16, B), which can be mistaken for microtears. Tendinopathy of the patellar and quadriceps tendons appears as an abnormal intermediate signal with ill-defi ned fi bers and oc-casional thickening. The patellar and quadriceps tendons most common-ly tear near their patellar insertions44 (Figure 16, C). Axial images depict the remaining intact fi bers, and sagittal images demonstrate tendon retraction in complete tears. Patellar tendon lax-ity can be a useful secondary sign of a quadriceps tendon tear.

CartilageCurrently, the bulk of cartilage assess-ment is directed toward identifying visible, macroscopic defects. T2- and proton density–weighted sequences are used; hyaline cartilage is intermediate in signal intensity, whereas joint fl uid is bright, providing contrast along the

articular surface and enhancing the visualization of defects, which will typi-cally be bright. Normal cartilage shows homogeneous signal and a smooth sur-face (Figure 17).

Chondral defects can usually be cat-egorized as either traumatic or chronic degenerative lesions. Traumatic lesions tend to be focal and well defi ned and also demonstrate acute margins45 (Fig-ure 15). Underlying subchondral bone bruises may be present in the acute set-ting. Chronic degenerative lesions are typically larger and less well defi ned, with adjacent chondral thinning and/or surface irregularity (Figure 13). The opposing cartilage surface also may be affected (known as the “kissing le-sion”). Endochondral osteophytes may be present within the cartilage defect. Subchondral marrow changes (cysts and the bone marrow edema pattern) are often seen with deep partial- and full-thickness disease.

Following a cartilage repair pro-cedure, MRI can help demonstrate healing and identify any complica-tions. After repair or cellular-based replacement procedures, the lesion should ideally fi ll with hyaline tissue but more commonly fi lls with a mix of fi brocartilaginous tissue, maturing in 1 to 2 years. The composition of the repair tissue, surface characteris-tics, and signal intensity usually differ from normal hyaline cartilage.46 The Magnetic Resonance Observation of Cartilage Repair Tissue (MOCART) scoring system is designed to defi ne pertinent variables in the description of cartilage repair tissue.47 Hyperintense subchondral marrow signal should de-crease across time, although it may not completely disappear.48 In autologous osteochondral transplants, fi brocar-tilage tissue interposes in grout-like

fashion around the transplanted tis-sue, with ingrowth of normal marrow across the graft–native bone interface. Bone marrow T2-weighted hyperinten-sity around the interface should grad-ually decrease in the fi rst 12 months, although a mild amount of hyperinten-sity may persist around graft margins for up to 24 months.46,49 Worsening marrow edema and the development of cyst-like lesions and internal osteo-phytes is worrisome for graft failure.

Advanced Cartilage TechniquesMethods of assessment are rapidly advancing in the fi eld of cartilage imaging. A common technique adds a T2- weighted, three-dimensional, gradient-recalled echo sequence (Fig-ure 18, A), which has inherent high spatial resolution and can offer ex-quisite cartilage structure detail. Two drawbacks to gradient-recalled echo se-quences compared with conventional sequences include variable image qual-ity because of proprietary and variable MRI parameters and a high suscepti-bility to metallic artifact.

Molecular cartilage imaging research is aimed at identifying early disease and characterizing disease progression and repair. Rather than simply demon-strating macroscopic defects, new techniques attempt to show pathologic alterations in molecular composition and biochemical activity.

T2-mapping (Figure 18, B) is an advanced technique for imaging carti-lage by refl ecting collagen content and organization. Water molecules interact closely with hyaline cartilage macro-molecules; as disease and degeneration ensue, the cartilage matrix is disrupted, and the water molecules demonstrate different magnetic properties, which

Sagittal, fat-suppressed, T2-weighted image of normal cartilage. Cartilage should have homogeneous, intermediate signal intensity. Defects will usually have a fl uid-intense signal.

Figure 17



are manifested as increased T2 relax-ation time. A special T2-mapping se-quence can image these variations in T2 relaxation time and potentially identify areas of disease. Although T2 values have yet to be specifi cally correlated with the staging of osteoarthritis, some suggest that T2-mapping may provide a valuable tool for monitoring changes in both native cartilage and cartilage repair tissues.50,51

Delayed gadolinium-enhanced MRI of cartilage (dGEMRIC) and sodium imaging techniques refl ect glycos-aminoglycan concentration in hyaline cartilage (Figure 18, C). Glycosami-noglycans are negatively charged ions that are depleted in early degenerative disease. Thus, regions of degenerative cartilage have a relative positive charge. Gadolinium is a positively charged particle that, following injection, preferentially diffuses into the areas of normal (negatively charged) carti-lage, not diseased cartilage. Similarly, sodium imaging uses synovial fl uid’s inherent positively charged sodium ions

that—like gadolinium—preferentially diffuse into healthier cartilage. Using complex MRI sequences, the amount of gadolinium or sodium in the carti-lage can be quantifi ed. dGEMRIC has shown promise in terms of predict-ing the development of osteoarthritis and has been used to assess cartilage repair.52-55

T1-rho imaging is a means to assess proteoglycan, a component of normal healthy cartilage that imparts resis-tance to compressive loads. Analogous to T2-mapping, it images variations in the T1-rho relaxation time of cartilage, which is prolonged in areas of degen-eration. Although T1-rho imaging re-mains primarily a research technique at this time, it shows great promise for the early detection of cartilage degener-ation, showing signifi cant T1-rho pro-longation in patients with osteoarthritis and potentially greater sensitivity for cartilage degeneration compared with T2-mapping alone.56,57

These new techniques are evolving and, to date, have found limited clinical

implementation outside research set-tings. Special protocols, data evaluation software, and sometimes specialized hardware are generally required. Assess-ments may be time consuming, and the range of normal values for these poten-tially quantitative techniques remains nonstandardized. However, these devel-opments hold the promise of a more dy-namic method of understanding disease processes and the potential anatomic effi cacy of therapeutic intervention to alter natural history and repair injuries.

SummaryMRI is a crucial component for evaluat-ing the knees of symptomatic patients. Knowledge of normal and abnormal ap-pearances can assist in clinical decision making. Chronic degenerative changes and focal traumatic injuries can some-times be confused with one another. Continued technologic development will aid in identifying early disease and preventing disease progression and will become an integral part of MRI interpretation.

Advanced cartilage imaging. A, Sagittal three-dimensional, water selective (WATS), gradient-recalled echo image of normal cartilage with intermediate signal intensity. Note the sharp interface between cartilage and the adjacent subchondral bone and overlying joint fl uid. B, Sagittal T2-mapping image of cartilage adjacent to focal osteochondral transplants. Regions of interest are drawn along the cartilage, and software calculates the T2 values of the individual pixels; color-coded maps can then be produced. Diseased cartilage tends to have higher T2 values compared with healthy cartilage. C, A delayed gadolinium-enhanced MRI of cartilage (dGEMRIC) color map from the same patient as in Part B, which was taken 1 year after an osteochondral transplant. For dGEMRIC images, higher T1 values (blue) are associated with increased relative glycosaminoglycan content, whereas lower T1 values (red) indicate decreased glycosaminoglycan content.

Figure 18



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