Dr. Chang is a Radiology Resident and Dr. Huang is an Assistant Radiologist in the Division of Musculoskeletal Imaging and Intervention, Department of Radiology, Massachusetts General Hospital, Boston, MA. In addition, Dr. Huang is an Instructor of Radiology at Harvard Medical School, Boston, MA.
This article is based on “MR of articular cartilage lesions,” presented at Sports Medicine 2010: Advances in MRI and Orthopaedic Management, Department of Continuing Education, Harvard Medical School, Boston, MA, May 9, 2010.
Osteoarthritis is a highly prevalent disease in the United States
population, with approximately 75% of persons over age 65 having
radiographic evidence of degenerative changes, and nearly two-thirds of
routine knee magnetic resonance imaging (MRI) demonstrating articular
cartilage damage.1 Therefore, careful evaluation of the articular cartilage is an important part of the knee MRI examination.
Basic imaging principles
Routine
2-dimensional imaging of the knee includes fast spin-echo (FSE) T2-
and/or FSE proton density (PD)-weighted coronal and sagittal sequences,
with or without fat suppression. The contrast between the high T2 signal
intensity joint fluid and the intermediate T2 signal intensity
cartilage helps to assess for surface irregularities and defects of the
cartilage.2 FSE PD-weighted images provide excellent anatomic
detail and evaluation of all structures, including cartilage, menisci,
ligaments, and subchondral bone.3,4 Fat suppression helps to
highlight marrow edema and cystic changes underlying cartilage lesions
and to eliminate chemical shift artifact seen at the marrow
(fat)-cartilage (water) interfaces.5
The 3-dimensional
spoiled gradient echo (SPGR) sequence with fat suppression yields higher
cartilage signal and spatial resolution and is therefore useful for
cartilage thickness and volume measurements. However, 3-dimensional SPGR
is not typically included in imaging protocols because of decreased
contrast between the cartilage and the adjacent joint fluid, long
imaging times, increased metallic artifact (in the case of a
post-surgical knee), and uneven fat suppression, even though it is
considered standard for morphologic imaging of cartilage.6
At
least one sequence in both sagittal and coronal planes is necessary to
prevent overcalling of lesions due to volume averaging in the direction
perpendicular to the slice plane because while in-plane resolution may
be 0.3 mm to 0.6 mm, slice thickness is typically 3 mm to 5 mm. Table 1
lists several MR cartilage imaging pitfalls and troubleshooting
techniques.7,8
MR imaging at 3.0 Tesla (T) versus 1.5 T improves signal-to-noise ratio, lesion detection, and grade assessment.9-11
Various other techniques have been developed to enhance the
signal-to-noise ratio between cartilage and its surrounding structures,12,13 and to evaluate the molecular changes in the cartilage to detect early cartilage injury6, 14-21
but these techniques are not routinely utilized. MR arthrography (MRA)
of the knee also helps to increase sensitivity for cartilage lesions and
for detection of intra-articular bodies and their donor sites, but it
is also not routinely performed. Indications for MRA include evaluation
of osteochondral defects for stability and evaluation of postoperative
menisci for retear.22-24
Normal appearance and cartilage lesions
Cartilage
is approximately 75% to 80% water by weight and therefore appears
slightly less hyperintense to joint fluid on T2-weighted images.21
Matrix collagen has a leaf-like structure with proteoglycans projecting
from a central hyaluronic acid backbone. The collagen leaves extend
perpendicularly from the bony surface and curve 90 degrees until they
are approximately horizontal or parallel to the bone at the articular
surface. The different angles and orientations of the proteoglycans
likely affect the water mobility within and the dipole-dipole
interactions of the collagen fibrils, which result in the MR appearance
of cartilage on a T2-weighted sequence as three poorly demarcated
layers: a) a low signal intensity, striated, deep layer (perpendicular
portion, ≈50% of thickness); b) a high signal intensity transitional
layer (curving portion, ≈40% of thickness); and c) a low signal
intensity superficial layer (horizontal portion, ≈10% of thickness)
(Figure 1). The orientation of the cartilage relative to the orientation
of the static magnetic field (B0) also affects the
thickness, signal intensity, and distinctness of these layers.
Therefore, since much of the cartilage surfaces of the knee are curved
(eg, the femoral condyles), appearance of the articular cartilage
varies. The uniformity of the collagen fiber orientation at the
articular and the bony surfaces helps to elucidate the reason magic
angle phenomenon affects cartilage (Figure 2), and the curvature of the
collagen fibers also helps to explain the curved appearance of many
cartilage lesions.5,25-27
Chondromalacia, or cartilage
softening, without surface cartilage defect is the earliest stage of
cartilage injury and may appear on MRI as focal areas of increased
signal intensity on T2-weighted images (Figure 3). This finding is
nonspecific, as it is often seen in asymptomatic patients; concurrent
underlying marrow signal abnormality increases its specificity.7,28,29
Cartilage
defects appear as synovial fluid-filled, T2 hyperintense gaps that
disrupt the articular surface. The International Cartilage Repair
Society (ICRS) has standardized the evaluation of articular cartilage
injury based on the depth of the lesion. The lesion can be described as a
superficial defect or surface irregularity (Figure 4),
partial-thickness defect (Figure 5), or full-thickness defect (Figure
6). If spatial resolution allows, it may be possible to further
subdivide partial thickness defects into low-grade and high-grade
partial thickness defects depending on whether the lesion involves less
than 50% or 50% to 99% of the full cartilage thickness. Partial and
full-thickness
lesions may be associated with flap formation (Figure 7).
Numerous
classification schemes exist for grading cartilage lesions, most of
which take into account the size (area) and/or depth of the lesion. The
ICRS has developed one such system, in which lesions are graded 0 to 4
based on depth of the lesion (Table 2). Grade 1 and 2 lesions have
excellent prognosis. Grade 2 and 3 lesions may benefit from cartilage
debridement or other more conservative surgical measures. Grade 4
lesions extend into the subchondral bone and may require bone grafting
if bony cavitation is extensive. Subchondral marrow edema is more likely
to be associated with higher-grade lesions30 and, in the setting of acute trauma, indicates that the lesion may be full thickness.
Since
the grading of cartilage lesions is largely a matter of local practice
preference and no one classification scheme is overwhelmingly used over
all others, our practice reports the size, depth, and location of the
cartilage lesion to allow the referring physicians to fit the lesion
into their own grading system.
MRI has been shown to be an accurate method for detection of cartilage lesions. Bredella et al2
reported that the sensitivity, specificity, and accuracy of combined
axial and coronal FSE T2-weighted sequences with fat suppression
compared with the gold standard of arthroscopy were 94%, 99%, and 98%,
respectively. In their study, 64% of the lesions were given the same
grade as that shown during arthroscopy. Ninety percent of lesions were
within one grade between MRI and arthroscopy, and the majority of the
lesions undergraded on MR imaging. Potter et al4 reported
that the sensitivity, specificity, and accuracy of FSE PD-weighted
sequences compared with arthroscopy were 87%, 94% to 95%, and 92% to
93%, respectively. In general, MRI underestimates the true dimensions of
a cartilage defect due to volume averaging and challenges of imaging a
curved surface.31
Cartilage disease can be separated
into 3 broad categories: acute chondral or osteochondral injury,
osteoarthritis, and inflammatory arthritis. There are some
distinguishing characteristics of each category. An acute lesion has
sharp margins oriented perpendicular to the bone surface, occurs on
weight-bearing surfaces, and has subjacent bone marrow edema (Figure 8).23,26
The fractured cartilage may break off as a “loose” fragment; searching
for these intra-articular bodies on knee MRI in acute chondral injury is
imperative because of the implications for surgery.
In
osteoarthritis, early proteoglycan loss leads to expansion of the
residual proteoglycans and increased cartilage water content, which may
appear as increased cartilage thickness on MRI. This edematous cartilage
deforms more easily and is therefore more susceptible to mechanical
stress and cartilage damage. Eventually, the cartilage matrix fragments.
Cartilage lesions in osteoarthritis tend to be shallower and have wide,
horizontal, or obtuse margins with respect to the bone surface (Figure
9). Because synovial fluid is toxic to bone marrow, subchondral cysts
form if the defect extends to the subchondral bone surface. Lesions
typically occur in the weight-bearing portions of the joint and result
in nonuniform joint space narrowing, one of the hallmarks of
osteoarthritis. Chondrocalcinosis in osteoarthritis indicates attempts
at repair in response to a prior insult.22,32,33
In
inflammatory arthritis, cartilage loss is more diffuse and uniform. The
enzymes produced by the pannus cause cartilage breakdown. The pannus
also forms a physical barrier for diffusion of nutrients to
chondrocytes, further promoting chondrocyte death. Focal lesions are
less common. Inflammatory changes of the subchondral bone and
chondrocalcinosis are also seen.26
In osteochondritis
dissecans (OCD), the primary role of MRI is to determine stability of
the defect. Findings suggestive of instability include torn overlying
articular cartilage, undercutting of osteochondral fragment with fluid
signal, osteochondral defect with fluid-filled cavity, and cystic change
(5 mm or larger) deep to the lesion (Figure 10). The ICRS has developed
a grading system for OCD lesions (Table 3), but it requires
arthroscopic probing for definitive lesion classification. However,
lesions found to be stable by MRI have been found to have a good
clinical outcome, while articular surface defects detected by MRI
predict a poor clinical outcome.34
Factors leading to accelerated cartilage damage
The
cartilage, menisci, ligaments, and bony structures in the knee all
contribute to distribution of the load forces in the knee. Therefore,
abnormalities of any one of those structures invariably leads to the
early degeneration of the other structures.27
Meniscal tear
Preoperative
detection of a cartilage flap associated with a meniscal tear is
important in presurgical planning for the surgeon and modulating
expectations for length of rehabilitation time for the patient.35
Cartilage loss following menisecectomy may be accelerated (Figure 11);
therefore, meniscal debridement has largely replaced total meniscectomy
in the surgical management of meniscal tears to preserve stability and
function and to delay the onset of osteoarthritis.20,36 MRI
is helpful in imaging the postoperative knee because it can be
clinically difficult to distinguish between a meniscal retear, a
chondral lesion, or an osseous lesion as the source of symptoms in the
post-meniscectomy knee.
ACL tear
The mechanism
of injury in anterior cruciate ligament (ACL) ruptures includes
significant axial loading. The articular cartilage transmits these
forces, and this initial impact results in cartilage changes that often
lead to accelerated osteoarthritis, despite immediate stabilization of
the knee with ACL reconstruction (Figure 12). The sulcus terminalis on
the lateral femoral condyle and the posterolateral tibial plateau—also
the location of the “kissing contusions” associated with ACL tears—are
the most common locations for these cartilage lesions.
Early
cartilage injury and chondromalacia may or may not be visible on visual
inspection during arthroscopy but can be detected through probing during
arthroscopy and can be seen as increased signal intensity on
T2-weighted images. More severe trauma or chronic repetitive trauma may
result in an osteochondral lesion, which appears as the “deep lateral
femoral notch sign” at the sulcus terminalis.35,37
Cartilage surgery
Advances
in cartilage surgery include bone marrow stimulation through
microfracture, osteochondral autograft or allograft transplantation,
autologous chondrocyte implantation, and fixation with bio-absorbable
pins. Regardless of the type of procedure being performed, routine MRI
after cartilage surgery should address these concerns:
- Graft quality.
The graft ideally should fill in the defect and be level with the
articular surface. The signal intensity of the graft should match the
signal intensity of the adjacent native cartilage. A failed graft may
appear fragmented, demonstrate surface irregularity, or be resorbed.
- Graft incorporation.
A well-incorporated graft will be practically seamless with the
adjacent cartilage. A poorly incorporated graft may demonstrate
persistent fluid signal separating the graft and the bone, new
subchondral cyst formation, and/or new adjacent sclerosis.
- Native cartilage quality.
Accelerated osteoarthritis, including cartilage loss and other
cartilage lesions, may form as the consequence of altered mechanics from
the primary cartilage injury.
- Other. Joint synovitis or adhesions near the repair site may cause the patient symptoms unrelated to the cartilage graft itself.
By approximately 1 to 2 years following surgery, the defect should
appear smooth and well-filled by the reparative tissue (Figure 13).24,38
Future directions
Physiologic
imaging aims to detect cartilage lesions before they are visible as
surface defects. For example, delayed gadolinium-enhanced MRI of
cartilage (dGEMRIC) identifies areas of
decreased cartilage proteoglycan content.15 T2-mapping detects areas of increased tissue hydration within cartilage.39
Other developing techniques include T1ρ mapping, sodium MRI, and
diffusion imaging, all of which take advantage of the physiologic
properties of cartilage to show microscopic changes in the cartilage
ultrastructure before gross damage to the cartilage surface is apparent.
While for most patients the morphologic imaging sequences may suffice,
physiologic imaging may be useful for more detailed or longitudinal
evaluation of surgical procedures (ie, cartilage implants, medial
meniscal repair for prevention of osteoarthritis progression) or
pharmacologic therapies.6,15,21,35
Conclusion
Cartilage
lesions are very commonly seen on knee MRI imaging. Current imaging
techniques accurately diagnose and grade cartilage lesions, and
developing techniques for physiologic imaging show promise for
longitudinal evaluation of normal, degenerated, and postsurgical
cartilage. As medical and surgical therapies improve, MRI will play an
increasing role in diagnosis and management of knee cartilage lesions,
and familiarity with lesion terminology and accurate descriptions of
cartilage lesions will enhance communication between radiologists and
referring physicians.
References
- Disler DG, McCauley TR, Kelman CG, et al. Fat-suppressed
three-dimensional spoiled gradient-echo MR imaging of hyaline cartilage
defects in the knee: Comparison with standard MR imaging and
arthroscopy. AJR Am J Roentgenol. 1996;167:127-132.
- Bredella MA, Tirman PF, Peterfy CG, et al. Accuracy of T2-weighted
fast spin-echo MR imaging with fat saturation in detecting cartilage
defects in the knee: Comparison with arthroscopy in 130 patients. AJR Am J Roentgenol. 1999;172:1073-1080.
- Sonin AH, Pensy RA, Mulligan ME, Hatem S. Grading articular
cartilage of the knee using fast spin-echo proton density-weighted MR
imaging without fat suppression. AJR Am J Roentgenol. 2002;179:1159-1166.
- Potter HG, Linklater JM, Allen AA, et al. Magnetic resonance imaging
of articular cartilage in the knee. An evaluation with use of
fast-spin-echo imaging. J Bone Joint Surg Am. 1998;80:1276-1284.
- Disler DG, McCauley TR. Clinical magnetic resonance imaging of articular cartilage. Top Magn Reson Imaging. 1998;9:360-376.
- Gold GE, Hargreaves BA, Stevens KJ, Beaulieu CF. Advanced magnetic resonance imaging of articular
cartilage. Orthop Clin North Am. 2006;37:331-347, vi.
- Hayes CW, Conway WF. Evaluation of articular cartilage: Radiographic and cross-sectional imaging techniques. Radiographics. 1992;12:409-428.
- Waldschmidt JG, Rilling RJ, Kajdacsy-Balla AA, et al. In vitro and
in vivo MR imaging of hyaline cartilage: Zonal anatomy, imaging
pitfalls, and pathologic conditions. Radiographics. 1997;17:1387-1402.
- Masi JN, Sell CA, Phan C, et al. Cartilage MR imaging at 3.0 versus that at 1.5 T: Preliminary results in a porcine model. Radiology. 2005;236:140-150.
- Link TM, Sell CA, Masi JN, et al. 3.0 vs 1.5 T MRI in the detection
of focal cartilage pathology--ROC analysis in an experimental model. Osteoarthritis Cartilage. 2006;14:63-70.
- Kijowski R, Blankenbaker DG, Davis KW, et al. Comparison of 1.5- and
3.0-T MR imaging for evaluating the articular cartilage of the knee
joint. Radiology. 2009;250:839-848.
- Hargreaves BA, Gold GE, Lang PK, et al. MR imaging of articular cartilage using driven equilibrium. Magn Reson Med. 1999;42:695-703.
- Hargreaves BA, Gold GE, Beaulieu CF, et al. Comparison of new sequences for high-resolution cartilage imaging. Magn Reson Med. 2003;49:700-709.
- Gold GE, McCauley TR, Gray ML, Disler DG. What’s new in cartilage? Radiographics. 2003;23: 1227-1242.
- Burstein D, Velyvis J, Scott KT, et al. Protocol issues for delayed
Gd(DTPA)(2-)-enhanced MRI (dGEMRIC) for clinical evaluation of articular
cartilage. Magn Reson Med. 2001;45:36-41.
- Lammentausta E, Kiviranta P, Nissi MJ, et al. T2 relaxation time and delayed gadolinium-enhanced
MRI of cartilage (dGEMRIC) of human patellar cartilage at 1.5 T and 9.4 T: Relationships with tissue mechanical properties. J Orthop Res. 2006;24:
366-374.
- Bashir A, Gray ML, Hartke J, Burstein D. Nondestructive imaging of human cartilage glycosaminoglycan concentration by MRI. Magn Reson Med. 1999;41:857-865.
- Reddy R, Insko EK, Noyszewski EA, et al. Sodium MRI of human articular cartilage in vivo. Magn Reson Med. 1998;39:697-701.
- Recht M, Bobic V, Burstein D, et al. Magnetic resonance imaging of articular cartilage. Clin Orthop Relat Res. 2001;(391 Suppl):S379-S396.
- Recht MP, Kramer J. MR imaging of the postoperative knee: A pictorial essay. Radiographics. 2002;22:765-774.
- Van Breuseghem I. Ultrastructural MR imaging techniques of the knee
articular cartilage: Problems for routine clinical application. Eur Radiol. 2004;14:184-192.
- Gagliardi JA, Chung EM, Chandnani VP, et al. Detection and staging
of chondromalacia patellae: Relative efficacies of conventional MR
imaging, MR arthrography, and CT arthrography. AJR Am J Roentgenol. 1994;163:629-636.
- Chung CB, Isaza IL, Angulo M, et al. MR arthrography of the knee: How, why, when. Radiol Clin North Am. 2005;43:733-746, viii-ix.
- Miller TT. MR imaging of the knee. Sports Med Arthrosc. 2009;17:56-67.
- Goodwin DW, Zhu H, Dunn JF. In vitro MR imaging of hyaline cartilage: Correlation with scanning electron microscopy. AJR Am J Roentgenol. 2000;174:405-409.
- Jeffrey DR, Watt I. Imaging hyaline cartilage. Br J Radiol. 2003;76:777-787.
- Burstein D, Bashir A, Gray ML. MRI techniques in early stages of cartilage disease. Invest Radiol. 2000;35:622-638.
- Rose PM, Demlow TA, Szumowski J, Quinn SF. Chondromalacia patellae: Fat-suppressed MR imaging. Radiology. 1994;193:437-440.
- Mosher TJ, Dardzinski BJ, Smith MB. Human articular cartilage:
Influence of aging and early symptomatic degeneration on the spatial
variation of T2--preliminary findings at 3 T. Radiology. 2000;214:259-266.
- Kijowski R, Stanton P, Fine J, DeSmet A. Subchondral bone marrow
edema in patients with degeneration of the articular cartilage of the
knee joint. Radiology. 2006;238:943-949.
- Brittberg M, Winalski CS. Evaluation of cartilage injuries and repair. J Bone Joint Surg Am. 2003;85-A Suppl 2:58-69.
- Dardzinski BJ, Mosher TJ, Li S,et al. Spatial variation of T2 in human articular cartilage. Radiology. 1997;205:546-550.
- Kleemann RU, Krocker D, Cedraro A, et al. Altered cartilage
mechanics and histology in knee osteoarthritis: Relation to clinical
assessment (ICRS Grade). Osteoarthritis Cartilage. 2005;13:958-963.
- De Smet AA, Ilahi OA, Graf BK. Untreated osteochondritis dissecans
of the femoral condyles: Prediction of patient outcome using
radiographic and MR findings. Skeletal Radiol. 1997;26:463-467.
- Potter HG, Foo LF. Magnetic resonance imaging of articular cartilage: Trauma, degeneration, and repair. Am J Sports Med. 2006;34:661-677.
- Cicuttini FM, Forbes A, Yuanyuan W, et al. Rate of knee cartilage loss after partial meniscectomy. J Rheumatol. 2002;29:1954-1956.
- Johnson DL, Urban WP, Caborn DN, et al. Articular cartilage changes
seen with magnetic resonance imaging-detected bone bruises associated
with acute anterior cruciate ligament rupture. Am J Sports Med. 1998;26:409-414.
- Choi YS, Potter HG, Chun TJ. MR imaging of cartilage repair in the knee and ankle. Radiographics. 2008;28:1043-1059.
- Kelly BT, Potter HG, Deng XH, et al. Meniscal allograft
transplantation in the sheep knee: Evaluation of chondroprotective
effects. Am J Sports Med. 2006;34:1464-1477.