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British Journal of Radiology (2003) 76, 777-787
© 2003 British Institute of Radiology
doi: 10.1259/bjr/51504520
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Review article

Imaging hyaline cartilage

D R Jeffrey, MRCP, FRCR and I Watt, FRCP, FRCR

Department of Clinical Radiology, Bristol Royal Infirmary, Bristol BS2 8HW, UK


   Introduction
Top
 Introduction
What is hyaline cartilage?
 Where is it found...
 What abnormalities occur in...
 How can we image...
 Future developments
 Conclusion
 References
 
Hyaline cartilage is a crucial tissue, vital to our daily activities as mobile and supple human beings. Cartilage permits friction free joint articulation, yet it is remarkably robust and durable, whilst being avascular and bereft of nerve supply. However, it is the tissue whose apparent failure is associated with one of the scourges of older life in our Western culture – osteoarthritis. This review sets out to examine this tissue, and to explore what we as radiologists can image and understand. Increasingly, research attention is being paid to hyaline cartilage as novel means of repair are being explored and chemotherapeutic interventions are focused to enhancing the repair and endurance of it into old age [1].


   What is hyaline cartilage?
Top
 Introduction
 What is hyaline cartilage?
Where is it found...
 What abnormalities occur in...
 How can we image...
 Future developments
 Conclusion
 References
 
Structure
Hyaline cartilage is a highly specialized type of connective tissue that occurs on the articular surfaces of bones and within the major airways. Three types of cartilage exist: hyaline, elastic and fibrous, differing in the composition of their matrix or ground substance. Hyaline cartilage is the most widely distributed type of cartilage within the human body. Macroscopically it has a translucent, bluish-white appearance, its name being derived from the Greek hyalos meaning glass.

Molecular
All connective tissues comprise a mixture of cells and intercellular, or ground, substance. Cartilage differs from other forms of connective tissue by virtue of the firmness of the ground substance. This enables it to act as a supportive structure and to bear mechanical stress. Cartilage cells, or chondrocytes, are derived from mesenchymal cells which form part of the undifferentiated loose connective tissue of early embryonic life. Chondrocytes are capable of synthesising and secreting the ground substance that surrounds them. As hyaline cartilage contains no blood vessels, lymphatics or nerves, the properties of the ground substance must allow diffusion of nutrients and waste products to and from the chondrocytes. The latter, located in small lacunae, have multiple short processes extending into the surrounding matrix effectively increasing their surface area.

The ground substance is composed of a mixture of amorphous (non-formed) and fibrous (formed) components. The amorphous component predominantly contains proteoglycans. These consist of polysaccharide chains (glycosaminoglycans) such as keratan sulphate and chondroitin sulphate, which are covalently bound to a protein core. These core proteins are in turn non-covalently bound to a long filament of hyaluronic acid to form large proteoglycan aggregates (Figure 1Go). Their principle function is to retain water, which is bound to the negatively charged glycosaminoglycans (GAGs), and represents 75% of the total volume of the ground substance. The formed component of the ground substance is composed of collagen fibres that constitute 50% of the dry weight of cartilage. The collagen fibres interact electrostatically with the GAGs to form a cross-linked matrix. The main type of collagen fibre in hyaline cartilage is type II collagen which consists of three alpha-1 (type II) chains [{alpha}1(II)]3. This differs from the more common type I collagen, which occurs in skin, tendons and bone, in that it contains higher levels of hydroxylysine and is thus more hydrophilic.



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  		Figure 1. Schematic representation of the molecular organization of an aggregated proteoglycan molecule.

 
Histological
Histological analysis of hyaline cartilage using polarised light microscopy and transmission electron microscopy reveals a zonal anatomy (Figure 2Go). The thin superficial or tangential zone contains densely packed collagen fibrils which are orientated parallel to the articular surface. Below the superficial zone is a transitional zone containing obliquely orientated collagen fibrils, which gradually change with depth to become perpendicular in orientation. The deepest and largest zone is the radial zone, in the upper two thirds of which the collagen fibrils are perpendicularly orientated, whilst in the lower third there are also numerous curved obliquely orientated fibrils. Below the radial zone is a thin calcified layer of cartilage (the "tide mark") anchoring the collagen bundles to the underlying bone [2]. The exact function of each of these zones is not known. The water concentration differs slightly between the zones, being 82% in the superficial zone and 76% in the radial zone [3]. The superficial zone is impermeable to water and has a lower proteoglycan concentration than the other zones. This allows higher permeability for fluid flow within the superficial zone itself. The superficial zone may therefore function as a soft cushion, absorbing and distributing the impact of a compressive force. Only prolonged loading forces are purported to be transmitted to the deeper zones [4].



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  		Figure 2. H&E (haemotoxylin and eosin) stain of hyaline cartilage (left) demonstrating chondrocytes surrounded by ground substance. Hyaline cartilage stained to show collagen fibrils (right) illustrating a zonal anatomy.

 

   Where is it found and what does it do?
Top
 Introduction
 What is hyaline cartilage?
 Where is it found...
What abnormalities occur in...
 How can we image...
 Future developments
 Conclusion
 References
 
Anatomy and function
Although hyaline cartilage is the main constituent of most of the early skeleton, its location is subsequently restricted to certain specialized sites. In the adult skeleton, hyaline cartilage covers the articular surfaces of opposing bone ends in synovial and cartilaginous joints. It occurs also within the costal cartilages and the major airways. Within diarthrodial (movable) joints, hyaline cartilage provides a low friction, wear-resistant surface and acts as an avascular hydrodynamic shock absorber. When a joint is compressed, water is redistributed through the cartilage cushion to absorb the compressive force whilst the overall cartilage volume may remain unchanged [4].


   What abnormalities occur in hyaline cartilage?
Top
 Introduction
 What is hyaline cartilage?
 Where is it found...
 What abnormalities occur in...
How can we image...
 Future developments
 Conclusion
 References
 
Radiologically, hyaline cartilage can undergo one of three pathological processes. It can become thinned, thickened or calcify.

Thinning
Thinning of hyaline cartilage is a normal occurrence with age and occurs due to alterations in proteoglycan synthesis as well as proteoglycan degradation [5]. The ground substance becomes less efficient at retaining water. Proliferation of chondrocytes and the formation of chondrophytes at the joint margins correct secondary instability [6]. It is these structures which, following enchondral ossification, form the well-recognised marginal osteophyte, a hallmark of osteoarthritis. However, minor joint margin spurs simply reflect this loss of hyaline cartilage integrity as part of the age related change, and such small spurs might be regarded as normal findings. Pathological thinning of hyaline cartilage may occur as part of any arthropathy or following joint trauma.

Arthropathy
Hyaline cartilage swelling is one of the earliest changes in an arthropathy [7]. This is due to proteoglycan loss and disruption of the collagen network that allows residual proteoglycan aggregates to expand and attract more water. The altered biomechanics mean that the oedematous cartilage is susceptible to further deformation with repeated mechanical stress. In osteoarthritis, degradation of collagen occurs in the superficial and mid zone [8]. This leads to fissuring, pitting and flaking of the articular cartilage with the development of vertical clefts that may extend down to subchondral bone (Figure 3Go). Fluid and debris are forced into these fissures and pieces of cartilage break away, leading to exposure of underlying bone. Subchondral bone cysts and eburnation of the bone surface result, since synovial fluid is toxic to bone marrow.



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  		Figure 3. Double contrast CT arthrogram of the patellofemoral joint indicating a fissure within the hyaline cartilage of the patella (arrow).

 
In inflammatory and septic arthritides, diffuse destruction of superficial hyaline cartilage occurs due to the proteolytic effect of inflammatory mediators and cytokines in synovial fluid. Collagen degradation occurs primarily around the chondrocytes in the mid and deep zones. This reflects, at least in part, chondrocytic response to inflammatory mediators. The abnormal matrix predisposes to further cartilage damage. In both these scenarios, hyaline cartilage may undergo a series of repair mechanisms including osteophyte formation and cartilage calcification (chondrocalcinosis).

Hyaline cartilage thinning, especially in small joints of the hands and feet, is the hallmark of relapsing polychondritis (Figure 4Go) [9]. In this condition, specific pathological change is directed to type II collagen, both in joints and the tracheobronchial rings, causing softening and destruction of both.



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  		Figure 4. Conventional radiograph of a hand in a patient with relapsing polychondritis demonstrating thinning of the hyaline cartilage (arrows).

 
Trauma
Hyaline cartilage can become thinned or destroyed as a result of fractures involving the articular surface of bone. Chondral or osteochondral fractures have been demonstrated at arthroscopy in 9–20% of patients with acute haemarthrosis of the knee (Figure 5Go) [10, 11]. Hyaline cartilage damage occurs in 40–60% of patients with acute anterior cruciate ligament tears, most commonly involving the lateral femoral condyle (Figure 6Go) [12]. Osteochondral fractures of the talar dome occur in approximately 2–6% of ankle ligament sprains [13]. The articular surface may also be disrupted during subluxation or dislocation particularly of the patellofemoral joint.



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  		Figure 5. Conventional lateral radiograph of a knee. There is an osteochondral fracture involving the lateral femoral condyle (large arrow) with a separate osteochondral body within the suprapatellar pouch (small arrow).

 


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  		Figure 6. (a) Conventional lateral radiograph of a knee in a patient with a torn anterior cruciate ligament. There is an osteochondral defect on the lateral femoral condyle (arrow). A joint effusion is also present. (b) Sagittal proton density weighted (repetition time/echo time 3680/15 ms) MRI of the same patient demonstrating the osteochondral defect (arrow).

 
Trauma to the articular cartilage may involve cartilage alone or be associated with subchondral bone abnormalities (Figure 7Go). In adults, lesions are usually confined to the cartilage, whereas in adolescents osteochondral fractures more commonly occur. This may be due to a stronger anchorage between hyaline cartilage and bone at the tide mark in younger individuals [14].



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  		Figure 7. (a) Coronal STIR (repetition time (TR)/echo time (TE) 4655/30 ms) MRI of a knee. There is an osteochondral defect with surrounding bone marrow oedema (arrow). (b) Coronal proton density weighted (TR/TE 3680/15 ms) MRI of the same patient again demonstrating the osteochondral defect (arrow).

 
Hyaline cartilage never heals fully once integrity has been lost. Defects are repaired by fibrocartilage that is biologically inefficient compared with hyaline cartilage [15]. Incongruity of an articular surface is a potent cause of premature osteoarthritis. Hyaline cartilage abnormalities are closely linked to restricted ranges of meniscal movement, although it is unclear which abnormality is cause or effect [16].

Thickening
Hyaline cartilage thickness may be increased in acromegaly, hypothyroidism and some mucopolysaccharidoses (Figure 8Go). It may also appear relatively thick in chronic non-inflammatory erosive conditions such as gout or pigmented villonodular synovitis. Increased thickness of hyaline cartilage in acromegaly, however, must not be perceived to be beneficial. Such over thick cartilage fails rapidly, resulting in early osteoarthritis.



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  		Figure 8. Conventional radiograph of a hand in a patient with acromegaly. There is increased joint space width at the metacarpophalangeal and interphalangeal joints.

 
Calcification
Cartilage calcification, or chondrocalcinosis, occurs due to crystal deposition in hyaline or fibrocartilage. The most common type of crystal to be deposited is calcium pyrophosphate dihydrate (CPPD), although occasionally it may be calcium hydroxyapatite. This is often an incidental finding and occurs with increasing frequency with age (Figure 9Go). It may, however, be associated with an acute episode of inflammation (pseudogout) or degenerative disease. As CPPD is produced at least partly by active chondrocytes, its presence in a joint may indicate an ability to undergo reparative change. There is evidence that individuals who deposit CPPD tend to develop hypertrophic osteoarthritis reflecting an overall tendency to undergo bone formation in response to insult. In contrast, hydroxyapatite deposition is associated with relative osteopaenia and a destructive type of osteoarthritis. MRI has been shown to be more sensitive than plain radiography in the detection of hyaline cartilage calcification [17] although in practical terms the latter is the most practical means of assessment.



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  		Figure 9. Conventional radiograph of a knee demonstrating chondrocalcinosis (arrows).

 

   How can we image hyaline cartilage?
Top
 Introduction
 What is hyaline cartilage?
 Where is it found...
 What abnormalities occur in...
 How can we image...
Future developments
 Conclusion
 References
 
Plain radiography
Conventional radiographs have limited value in imaging hyaline cartilage as they can provide only an indirect assessment [18]. However, for patients with known or suspected articular disorders, clinicians request plain radiographs more commonly than any other imaging modality. Radiologists therefore spend a great deal of time attempting to assess quality and quantity of hyaline cartilage on conventional radiographs. Normal hyaline cartilage is not radio-opaque and is thus not visible on a plain film. Its thickness may be inferred by the distance between two opposing bone ends, but other soft tissues such as inflamed synovium or joint fluid may equally well occupy this distance. Similarly, loss of joint space width may be due to damage to other intra-articular structures such as knee menisci rather than hyaline cartilage loss [19]. Minor degrees of hyaline cartilage damage, such as superficial ulceration, may be present with normal joint space width. Further, there may be considerable variation between observers in evaluating early osteoarthritis on plain radiographs [20].

Measurements of joint space width on conventional radiographs are imprecise and prone to error. Precision of joint space width measurement can be improved by positioning the joint in the functional anatomical position, centring the X-ray beam on the joint space and measuring in a plane orthogonal to the joint surfaces [21]. The minimum joint space width gives the most accurate assessment of hyaline cartilage thickness and should ideally be measured in the weight-bearing position for load-bearing joints such as the hip and knee [22]. It has been shown that the tibiofemoral joint space width may vary by up to 2 mm between weight bearing and non-weight bearing films of the knee [23]. Several studies have demonstrated that positioning the weight bearing knee in 30–45° of flexion enables the most reproducible assessment of joint space width in the medial femorotibial compartment [24, 25] whilst lacking reproducibility of measurement in the lateral or patellofemoral compartments. Precision has been further enhanced by the use of dedicated microfocal radiography and computer enhanced measurement techniques [26]. Even so, such apparatus is not widely available, and accuracy is still only reliable in the medial tibiofemoral compartment. Weight bearing, or functional images of other joints is not useful, although some authors recommend weightbearing images of the hip to assess hyaline cartilage loss in the more minor phases of disease especially [22].

Ultrasound
Ultrasound plays a minimal role in the imaging of hyaline cartilage. High frequency ultrasound has been shown to provide accurate measurements of hyaline cartilage thickness in vitro [27]. However, in vivo, the small acoustic window that exists in large joints in most patients limits evaluation of intra-articular structures. Accessibility may be further reduced by the presence of osteophytes in osteoarthritic joints. Ultrasound may be a useful tool in assessing hyaline cartilage damage in children although it is less sensitive than MRI [28]. It can also be useful in the detection of cartilage calcification in joints not easily assessed by plain radiography, such as the patellofemoral joint [29]. Superficial structures are more readily assessed by ultrasound and one study has demonstrated high accuracy for ultrasound assessment of cartilage cap thickness in exostoses [30]. The main strength of ultrasound is the evaluation of periarticular structures such as ligaments, tendons and muscle [31, 32]. Arthroscopic ultrasound may provide more detailed assessment of hyaline cartilage, but is obviously an invasive procedure.

Radionuclide radiology
99Tcm scintigraphy can be used as an indirect measurement of hyaline cartilage damage by virtue of the associated bony changes. It is a very sensitive test for early physiological abnormality. For example, increased uptake occurs at joint margins in the early stages of osteoarthritis (Figure 10Go) [33]. These appearances are non-specific however. Scintigraphy provides no direct assessment of hyaline cartilage. None the less, skeletal scintigraphy remains the single best predictor of outcome in groups of patients with osteoarthritis [34], and the pattern of isotope uptake (generalized, subchondral or marginal) may reflect various aspects of the disease process [35].



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  		Figure 10. Isotope bone scan of a knee demonstrating increased uptake at the margin of the medial femorotibial compartment with corresponding conventional radiograph (below).

 
CT arthrography
Plain CT has no role in the imaging of hyaline cartilage. CT arthrography, however, allows good visualization of hyaline cartilage due to the contrast between low-density cartilage and high-density intra-articular contrast medium (Figure 11Go). Open cartilage defects fill with contrast material and are seen as areas of high density. CT arthrography of the knee has been shown to be highly sensitive and specific for open lesions of patellar cartilage in patients with intermediate or advanced chondromalacia patellae, although its sensitivity for early lesions is poorer [36–38].



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  		Figure 11. CT arthrogram of the patellofemoral joint. An open cartilage defect is seen on the patella which fills with intra-articular contrast medium. There is also thinning of the hyaline cartilage on the medial patellar facet (arrow).

 
MRI
MRI is currently the most promising method of imaging hyaline cartilage in vivo. It has the advantages of high spatial resolution, good soft tissue contrast and multiplanar imaging whilst being non-invasive, well tolerated and is widely available within the UK. Early attempts to study hyaline cartilage using MRI were hampered by poor spatial resolution and insufficient soft tissue contrast between hyaline cartilage and surrounding tissues. However, the advent of higher field strength magnets, dedicated surface coils and new pulse sequences has led to considerable advances in this field.

Normal hyaline cartilage
Normal hyaline cartilage was originally thought to have a simple homogeneous appearance on MRI [39–41]. Subsequent studies, however, described a bilaminar appearance on spin echo sequences in hyaline cartilage in bovine patellae [4, 42]. It was postulated that this appearance was due to the difference in water content between the superficial and deep laminae. The superficial hyperintense lamina was thought to represent the tangential and transitional zones described histologically. The deep low signal lamina was thought to represent the radial zone. However, the difference in water content between the zones is small, being 82% in the superficial zone and 76% in the deep zone. Another possible explanation for the laminar appearance is the different orientation of collagen fibres within each zone, which would have an effect on magnetic susceptibility [3]. During the last decade, numerous other studies have described a trilaminar appearance of normal human hyaline cartilage in both knees and other joints using a variety of spin echo and gradient echo pulse sequences [36, 43–47]. Various attempts have been made to correlate the MRI appearances with the histological structure of hyaline cartilage but currently no consensus of opinion agrees as to what the laminae truly represent. Indeed, it has been suggested that the trilaminar appearance described on 3D SPGR (spoiled gradient recall) sequences is predominantly due to truncation artefact rather than zonal anatomy as it varies with a reduction in pixel dimension [48].

Fine resolution MRI using high field strength magnets (4.7 T) demonstrates vertical striations within hyaline cartilage of normal knee joints, which are most prominent in weight-bearing areas (Figure 12Go). These are thought to correspond to the structural heterogeneity demonstrated on histological section (areas of alternating light and dark staining) due to the presence of areas of high collagen and high proteoglycan content that exist in weight bearing areas [49]. These can be observed on clinical MR images of the femoral condyles, especially using fast spin echo techniques.



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  		Figure 12. High resolution imaging of the normal knee joint. Sagittal fat suppressed 3D gradient echo image (repetition time/echo time 50/11 ms) was obtained at a field strength of 4.7 T and shows vertical striations within hyaline cartilage. These are most prominent in weight-bearing areas.

 
MRI may be used to assess hyaline cartilage thickness. However, thickness measurements are prone to interobserver and intraobserver error due to several factors. The deepest, basal layers of hyaline cartilage blend with the zone of provisional calcification (tide mark). The T2 relaxation time here is so short that it cannot be measured, or visualized using clinically available magnets [50]. This inherently reduces the accuracy of MR assessed hyaline cartilage thickness and perhaps, early pathological change. The relative thinness of hyaline cartilage compared with its area and the complex curvilinear arrangement of hyaline cartilage over articular surfaces are important factors in thickness measurement. Approximate error rates of 10% between MR and histologically calculated hyaline cartilage thickness in the proximal tibia have been quoted [51]. Most investigations have evaluated the femorotibial and patellofemoral surfaces that have relatively thick hyaline cartilage. Whilst thickness values of 4 mm and 3.7 mm in the medial and lateral femorotibial joints have been quoted [52], hyaline cartilage is much thinner on most other joint surfaces such as the humeral head (1.2 mm) [45] and the femoral head (1.8 mm) [53]. In these locations, measurements are likely to be less accurate as the thickness of hyaline cartilage is relatively small compared with a routine pixel size. Cartilage thickness at specific sites within a joint may also vary as a function of weight bearing. Diurnal studies using healthy young volunteers demonstrate that cartilage thickness decreases in load bearing regions of the knee after a period of weight-bearing, whilst overall volume measurements remain constant [54]. Longitudinal measurements of hyaline cartilage thickness are thus liable to error due to misregistration of the point of measurement and changes in thickness due to normal daily activity.

Compared with measurement of hyaline cartilage thickness, volume assessment within a joint may be a more accurate method of gauging hyaline cartilage loss. Several studies have demonstrated that MRI is capable of producing accurate and reproducible measurements of hyaline cartilage volume in the knee [55–58]. Initially, accuracy of measurement was thought to be about ±10%, however, more recent studies suggest that this error rate is now much less, perhaps as little as 2.5% in routine practice. Another potent cause of error lies in the measurement algorithm supplied by the maker of the MR scanner, although this can be normalized by the use of a phantom.

Although most studies have been carried out in the knee, accurate measurements of hyaline cartilage volume within other joints including metacarpophalangeal joints have been published [44]. Quantification becomes less accurate, however, as the volume of hyaline cartilage within the joint decreases. Thus a 14% loss of hyaline cartilage volume can be detected on the metacarpal surface of a joint, but a loss of 27% on the smaller phalangeal surface would be required for detection [44]. The validity of MRI as a tool for assessing small volume changes or volume changes in small joints is therefore uncertain. Even in larger joints such as the knee, the use of volume based assessments may need revision. Longitudinal studies in osteoarthritis and rheumatoid disease suggest that little overall volume change occurs in a 1 year and 3 year review period [59]. This may be because, in population studies, relatively few patients do actually have disease progression over these time frames. Alternatively, areas of cartilage loss may be obscured by areas in which cartilage thickens, albeit with not necessarily normal tissue. Newer approaches thus will focus on the use of comparative area/thickness maps that may permit specific areas of change to be identified.

Abnormal hyaline cartilage
Thinning of hyaline cartilage with age is a normal phenomenon and MRI demonstrates an inverse relationship between hyaline cartilage thickness and age in the medial femorotibial compartments of male patients [60]. Abnormal hyaline cartilage may be manifest by changes in signal characteristics or morphology or both [61]. Any change in water content due to swelling or fibrillation may result in altered signal intensity. Cartilage abnormalities may appear as areas of increased or decreased signal intensity, but an awareness of artefacts such as chemical shift and the magic angle phenomenon is important in interpretation.

The use of pulse sequences optimized for hyaline cartilage visualization allows surface irregularities and focal defects to be detected with a high degree of sensitivity and specificity. This is particularly the case in the patellofemoral joint as it can be examined with a small field of view and thus high spatial resolution. Many studies have compared the accuracy of different pulse sequences for detection of hyaline cartilage abnormalities [39, 62–64]. T1 weighted conventional spin echo sequences have high signal to noise ratio and good spatial resolution but poor contrast between cartilage and joint fluid [65]. T2 weighted spin echo sequences have the advantage of the T2 effect of joint fluid acting as a surrogate contrast agent within the joint, producing good contrast between relatively hypointense cartilage and hyperintense joint fluid. More recently fast spin echo techniques have been developed which provide both good signal to noise ratio and high spatial resolution, with images being obtained in only a fraction of the time required for conventional spin echo sequences. Normal cartilage appears diffusely low in signal intensity, in contrast to the adjacent high signal joint fluid, and focal surface defects are readily detected [66, 67]. Gradient echo sequences allow volume (3D) acquisition within reasonable imaging times and this improves spatial resolution because thin slices can be acquired. Signal to noise ratio is also better than with spin echo sequences for a given slice thickness [68, 69]. In steady state gradient echo sequences such as GRASS (gradient-recalled acquisition in the steady state) or FISP (fast imaging with steady state precession) T2 weighted images are obtained, in which cartilage is hyperintense and joint fluid even more so. Spoiled gradient echo sequences such as SPGR (spoiled GRASS) or FLASH (fast low angle shot) provide T1 weighted images with better contrast between cartilage (hyperintense) and intra-articular fluid (hypointense). Fat suppression can be used with all sequences, which improves contrast between cartilage and surrounding structures [70, 71]. When fat suppression is combined with a 3D spoiled gradient echo sequence, cartilage is the only bright articular structure (Figure 13Go). Ultimately, the choice of pulse sequence is often a matter of personal preference. However, the 3D spoiled gradient echo sequence with fat suppression has the highest reported accuracy rate for the detection of hyaline cartilage abnormalities (Figure 14Go) [43]. More sophisticated methods of analysis of 3D data, such as image segmentation, can be used to generate surface maps of the articular contours. This can aid detection of surface irregularities and focal defects [55].



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  		Figure 13. Value of 3D gradient echo imaging with fat suppression for imaging hyaline cartilage. (a) Sagittal orientation and (b) axial orientation of the patellofemoral joint using 3D gradient echo FLASH sequence with fat suppression (repetition time/echo time 47/11 ms, flip angle 40°). Hyaline cartilage is hyperintense whilst all other structures are hypointense.

 


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  		Figure 14. Axial 3D gradient echo FLASH (repetition time/echo time 47/11 ms, flip angle 40°) MRI of the patellofemoral joint demonstrating thinning of the hyaline cartilage on the medial patellar facet (arrow).

 
The intra-articular injection of a 2 mmol gadolinium solution to produce direct MR arthrograms increases the sensitivity of detection of cartilage abnormalities. MR arthrography has been shown to be more sensitive than standard 3D T2 weighted gradient echo sequences for the detection of cartilage lesions [72] and there is no statistical difference between the sensitivity of MRA FISP and MRA T1 weighted sequences. Its use is limited by the fact that it is an invasive procedure and is often reserved for cases in which the diagnosis is in doubt.


   Future developments
Top
 Introduction
 What is hyaline cartilage?
 Where is it found...
 What abnormalities occur in...
 How can we image...
 Future developments
Conclusion
 References
 
During the last 5 to 10 years new treatments have been developed for chondral defects, particularly those resulting from trauma. Conventional treatments such as drilling, microfractures and abrasion arthroplasty promote generation of fibrocartilage with its inferior mechanical properties. New techniques are now available which aim to fill chondral defects with hyaline cartilage. These include autologous osteochondral arthroscopically implanted grafts (mosaicplasty) taken from donor sites that are partially or non-weight bearing. Early follow up studies show promising results in the treatment of osteochondral defects in both the knee and ankle [73, 74]. Autologous chondrocyte implantation offers a tissue engineered alternative to transplantation and may become more widely used in the future.

Delayed gadolinium enhanced MRI of cartilage (dGEMRIC) has recently been proposed as a means of measuring glycosaminoglycan concentration. Using this technique, T1 values are directly related to GAG concentration within cartilage. This may be a useful imaging tool to monitor osteochondral grafts and chondrocyte implants [75].


   Conclusion
Top
 Introduction
 What is hyaline cartilage?
 Where is it found...
 What abnormalities occur in...
 How can we image...
 Future developments
 Conclusion
References
 
The amazing biomechanical strengths of hyaline cartilage result in years of frictionless subtle movement of our limbs. The tissue is subject to various forms of trauma, for the most part recovering spontaneously. However, hyaline cartilage gradually fails with age and the relationship between this process and those governing true osteoarthritis remain to be unravelled. Newer therapies are in the process of evaluation and at least for focal pathology, may soon result in effective repair. Imaging, particularly MRI, has a vital role to play in evaluating both normal and pathological tissue, and imminently, in the assessment of novel medical and surgical therapies.

Received for publication June 10, 2002. Revision received June 10, 2003. Accepted for publication July 17, 2003.


   References
Top
 Introduction
 What is hyaline cartilage?
 Where is it found...
 What abnormalities occur in...
 How can we image...
 Future developments
 Conclusion
 References
 

  1. Felson DT, et al. Osteoarthritis: new insights. Part 2: treatment approaches. Ann Intern Med 2000;133:726–37.[Abstract/Free Full Text]
  2. Rubenstein JD, et al. Effects of collagen orientation on MR imaging characteristics of bovine articular cartilage. Radiology 1993;188:219–26.[Abstract/Free Full Text]
  3. Modl JM, et al. Articular cartilage: correlation of histologic zones with signal intensity at MR imaging. Radiology 1991;181:853–5.[Abstract/Free Full Text]
  4. Lehner KB, et al. Structure, function, and degeneration of bovine hyaline cartilage: assessment with MR imaging in vitro. Radiology 1989;170:495–9.[Abstract/Free Full Text]
  5. Buckwalter JA, Rough PJ, Rosenberg LC. Age-related changes in cartilage proteoglycans: quantitative electron microscopic studies. Microsc Res Tech 1994;28:398–408.[CrossRef][Medline]
  6. Pottenger LA, Phillips FM, Draganich LF. The effect of marginal osteophytes on reduction of varus-valgus instability in osteoarthritic knees. Arthritis Rheum 1990;33:853–8.[Medline]
  7. Calvo E, et al. High-resolution MRI detects cartilage swelling at the early stages of experimental osteoarthritis. Osteoarthritis Cartilage 2001;9:463–72.[CrossRef][Medline]
  8. Dodge GR, Poole AR. Immunohistochemical detection and immunochemical analysis of type II collagen degradation in human normal, rheumatoid, and osteoarthritic articular cartilages and in explants of bovine articular cartilage cultured with interleukin 1. J Clin Invest 1989;83:647–61.
  9. Booth A, et al. The radiological manifestations of relapsing polychondritis. Clin Radiol 1989;40:147–9.[CrossRef][Medline]
  10. Vahasarja V, Kinnuen P, Serlo W. Arthroscopy of the acute traumatic knee in children. Prospective study of 138 cases. Acta Orthop Scand 1993;64:580–2.[Medline]
  11. Noyes FR, et al. Arthroscopy in acute traumatic hemarthrosis of the knee. Incidence of anterior cruciate tears and other injuries. J Bone Joint Surg Am 1980;62:687–95, 757.[Abstract/Free Full Text]
  12. Vellet AD, et al. Occult posttraumatic osteochondral lesions of the knee: prevalence, classification, and short-term sequelae evaluated with MR imaging. Radiology 1991;178:271–6.[Abstract/Free Full Text]
  13. Shea MP, Manoli A 2nd. Osteochondral lesions of the talar dome. Foot Ankle 1993;14:48–55.[Medline]
  14. Bohndorf K. Imaging of acute injuries of the articular surfaces (chondral, osteochondral and subchondral fractures). Skeletal Radiol 1999;28:545–60.[CrossRef][Medline]
  15. Chen FS, Frenkel SR, Di Cesare PE. Repair of articular cartilage defects: part I. Basic Science of cartilage healing. Am J Orthop 1999;28:31–3.[Medline]
  16. Kawahara Y, et al. MR assessment of meniscal movement during knee flexion: correlation with the severity of cartilage abnormality in the femorotibial joint. J Comput Assist Tomogr 2001;25:683–90.[CrossRef][Medline]
  17. Beltran J, et al. Chondrocalcinosis of the hyaline cartilage of the knee: MRI manifestations. Skeletal Radiol 1998;27:369–74.[CrossRef][Medline]
  18. Lund F, Nilsson BE. Radiologic evaluation of chondromalacia patellae. Acta Radiol Diagn (Stockh) 1980;21:413–6.[Medline]
  19. Gale DR, et al. Meniscal subluxation: association with osteoarthritis and joint space narrowing. Osteoarthritis Cartilage 1999;7:526–32.[CrossRef][Medline]
  20. Kellgren JH. Epidemiology of rheumatoid arthritis. Arthritis Rheum 1966;9:658–74.[Medline]
  21. Buckland W. Radiographic assessment of osteoarthritis: comparison between existing methodologies. Osteoarthritis Cartilage 1999;7:430–3.[CrossRef][Medline]
  22. Conrozier T, et al. The effects of position on the radiographic joint space in osteoarthritis of the hip. Osteoarthritis Cartilage 1997;5:17–22.[CrossRef][Medline]
  23. Leach RE, Gregg T, Siber FJ. Weight-bearing radiography in osteoarthritis of the knee. Radiology 1970;97:265–8.[Medline]
  24. Buckland-Wright JC, et al. Substantial superiority of semiflexed (MTP) views in knee osteoarthritis: a comparative radiographic study, without fluoroscopy, of standing extended, semiflexed (MTP), and schuss views. J Rheumatol 1999;26:2664–74.[Medline]
  25. Davies AP, et al. Plain radiography in the degenerate knee. A case for change. J Bone Joint Surg Br 1999;81:632–5.
  26. Buckland-Wright JC, et al. Accuracy and precision of joint space width measurements in standard and macroradiographs of osteoarthritic knees. Ann Rheum Dis 1995;54:872–80.[Abstract/Free Full Text]
  27. Myers SL, et al. Experimental assessment by high frequency ultrasound of articular cartilage thickness and osteoarthritic changes. J Rheumatol 1995;22:109–16.[Medline]
  28. El-Miedany YM, et al. Ultrasound versus MRI in the evaluation of juvenile idiopathic arthritis of the knee. Joint Bone Spine 2001;68:222–30.[CrossRef][Medline]
  29. Sofka CM, Adler RS, Cordasco FA. Ultrasound diagnosis of chondrocalcinosis in the knee. Skeletal Radiol 2002;31:43–5.[CrossRef][Medline]
  30. Malghem J, Vande Berg B, Noel H, Maldague B. Benign osteochondromas and exostotic chondrosarcomas: evaluation of cartilage cap thickness by ultrasound. Skeletal Radiol 1992;21:33–7.
  31. Friedman L, Finlay K, Jurriaans E. Ultrasound of the knee. Skeletal Radiol 2001;30:361–77.[CrossRef][Medline]
  32. Grobbelaar N, Bouffard JA. Sonography of the knee, a pictorial review. Semin Ultrasound CT MR 2000;21:231–74.[CrossRef][Medline]
  33. McAlindon TE, et al. Magnetic resonance imaging in osteoarthritis of the knee: correlation with radiographic and scintigraphic findings. Ann Rheum Dis 1991;50:14–9.[Abstract/Free Full Text]
  34. Dieppe P, et al. Prediction of the progression of joint space narrowing in osteoarthritis of the knee by bone scintigraphy. Ann Rheum Dis 1993;52:557–63.[Abstract/Free Full Text]
  35. McCrae F, et al. Scintigraphic assessment of osteoarthritis of the knee joint. Ann Rheum Dis 1992;51:938–42.[Abstract/Free Full Text]
  36. Gagliardi JA, et al. Detection and staging of chondromalacia patellae: relative efficacies of conventional MR imaging, MR arthrography, and CT arthrography. AJR Am J Roentgenol 1994;163:629–36.[Abstract/Free Full Text]
  37. Boven F, et al. The value of computed tomography scanning in chondromalacia patellae. Skeletal Radiol 1982;8:183–5.[CrossRef][Medline]
  38. Ihara H. Double-contrast CT arthrography of the cartilage of the patellofemoral joint. Clin Orthop 1985(198):50–5.
  39. Konig H, et al. Cartilage disorders: comparison of spin-echo, CHESS, and FLASH sequence MR images. Radiology 1987;164:753–8.[Abstract/Free Full Text]
  40. Yulish BS, et al. Chondromalacia patellae: assessment with MR imaging. Radiology 1987;164:763–6.[Abstract/Free Full Text]
  41. Reicher MA, Bassett LW, Gold RH. High-resolution magnetic resonance imaging of the knee joint: pathologic correlations. AJR Am J Roentgenol 1985;145:903–9.[Abstract/Free Full Text]
  42. Hayes CW, Sawyer RW, Conway WF. Patellar cartilage lesions: in vitro detection and staging with MR imaging and pathologic correlation. Radiology 1990;176:479–83.[Abstract/Free Full Text]
  43. Recht MP, et al. Abnormalities of articular cartilage in the knee: analysis of available MR techniques. Radiology 1993;187:473–8.[Abstract/Free Full Text]
  44. Peterfy CG, et al. Quantification of the volume of articular cartilage in the metacarpophalangeal joints of the hand: accuracy and precision of three-dimensional MR imaging. AJR Am J Roentgenol 1995;165:371–5.[Abstract/Free Full Text]
  45. Hodler J, et al. Assessment of articular cartilage thickness of the humeral head: MR-anatomic correlation in cadavers. AJR Am J Roentgenol 1995;165:615–20.[Abstract/Free Full Text]
  46. Disler DG, et al. Detection of knee hyaline cartilage defects using fat-suppressed three-dimensional spoiled gradient-echo MR imaging: comparison with standard MR imaging and correlation with arthroscopy. AJR Am J Roentgenol 1995;165:377–82.[Abstract/Free Full Text]
  47. Recht MP, Resnick D. MR imaging of articular cartilage: current status and future directions. AJR Am J Roentgenol 1994;163:283–90.[Abstract/Free Full Text]
  48. Erickson SJ, et al. Hyaline cartilage: truncation artifact as a cause of trilaminar appearance with fat-suppressed three-dimensional spoiled gradient-recalled sequences. Radiology 1996;201:260–4.[Abstract/Free Full Text]
  49. Foster JE, et al. Structural periodicity in human articular cartilage: comparison between magnetic resonance imaging and histological findings. Osteoarthritis Cartilage 1999;7:480–5.[CrossRef][Medline]
  50. Peterfy CG, Genant HK. Emerging applications of magnetic resonance imaging in the evaluation of articular cartilage. Radiol Clin North Am 1996;34:195–213, ix.[Medline]
  51. Kladny B, et al. Cartilage thickness measurement in magnetic resonance imaging. Osteoarthritis Cartilage 1996;4:181–6.[CrossRef][Medline]
  52. Hall FM, Wyshak G. Thickness of articular cartilage in the normal knee. J Bone Joint Surg Am 1980;62:408–13.[Free Full Text]
  53. Hodler J, et al. Knee joint hyaline cartilage defects: a comparative study of MR and anatomic sections. J Comput Assist Tomogr 1992;16:597–603.[Medline]
  54. Waterton JC, et al. Diurnal variation in the femoral articular cartilage of the knee in young adult humans. Magn Reson Med 2000;43:126–32.[CrossRef][Medline]
  55. Peterfy CG, et al. Quantification of articular cartilage in the knee with pulsed saturation transfer subtraction and fat-suppressed MR imaging: optimization and validation. Radiology 1994;192:485–91.[Abstract/Free Full Text]
  56. Eckstein F, et al. Accuracy of cartilage volume and thickness measurements with magnetic resonance imaging. Clin Orthop 1998(352):137–48.
  57. Kshirsagar AA, et al. Measurement of localized cartilage volume and thickness of human knee joints by computer analysis of three-dimensional magnetic resonance images. Invest Radiol 1998;33:289–99.[CrossRef][Medline]
  58. Piplani MA, et al. Articular cartilage volume in the knee: semiautomated determination from three-dimensional reformations of MR images. Radiology 1996;198:855–9.[Abstract/Free Full Text]
  59. Gandy SJ, et al. No apparent progressive change to knee cartilage volumes over one year in rheumatoid and osteoarthritis. in ISMRM. 2000. Denver, Colorado, USA.
  60. Dalla Palma L, Cova M, Pozzi-Mucelli RS. MRI appearance of the articular cartilage in the knee according to age. J Belge Radiol 1997;80:17–20.[Medline]
  61. Brown TR, Quinn SF. Evaluation of chondromalacia of the patellofemoral compartment with axial magnetic resonance imaging. Skeletal Radiol 1993;22:325–8.[Medline]
  62. Disler DG, et al. Fat-suppressed spoiled GRASS imaging of knee hyaline cartilage: technique optimization and comparison with conventional MR imaging. AJR Am J Roentgenol 1994;163:887–92.[Abstract/Free Full Text]
  63. Hardy PA, et al. Optimization of a dual echo in the steady state (DESS) free-precession sequence for imaging cartilage. J Magn Reson Imaging 1996;6:329–35.[Medline]
  64. Tervonen O, et al. MR imaging of knee hyaline cartilage: evaluation of two- and three-dimensional sequences. J Magn Reson Imaging 1993;3:663–8.[Medline]
  65. Loeuille D, et al. Review: Magnetic resonance imaging of normal and osteoarthritic cartilage. Arthritis Rheum 1998;41:963–75.[CrossRef][Medline]
  66. Potter HG, 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;80:1276–84.[Abstract/Free Full Text]
  67. Bredella MA, 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;172:1073–80.[Abstract/Free Full Text]
  68. Recht MP, et al. Accuracy of fat-suppressed three-dimensional spoiled gradient-echo FLASH MR imaging in the detection of patellofemoral articular cartilage abnormalities. Radiology 1996;198:209–12.[Abstract/Free Full Text]
  69. Cicuttini F, et al. Comparison and reproducibility of fast and conventional spoiled gradient-echo magnetic resonance sequences in the determination of knee cartilage volume. J Orthop Res 2000;18:580–4.[CrossRef][Medline]
  70. Totterman S, et al. MR fat suppression technique in the evaluation of normal structures of the knee. J Comput Assist Tomogr 1989;13:473–9.[Medline]
  71. Disler DG. Fat-suppressed three-dimensional spoiled gradient-recalled MR imaging: assessment of articular and physeal hyaline cartilage. AJR Am J Roentgenol 1997;169:1117–23.[Abstract/Free Full Text]
  72. Kramer J, Recht MP, Imhof H, Stiglbauer R, Engel A. Postcontrast MR arthrography in assessment of cartilage lesions. J Comput Assist Tomogr 1994;18:218–24.[Medline]
  73. Hangody L, et al. Mosaicplasty for the treatment of articular defects of the knee and ankle. Clin Orthop 2001;(391 Suppl):S328–36.
  74. Mendicino RW, Catanzariti AR, Hallivis R. Mosaicplasty for the treatment of osteochondral defects of the ankle joint. Clin Podiatr Med Surg 2001;18:495–513.[Medline]
  75. Gillis A, et al. Magnetic resonance imaging of relative glycosaminoglycan distribution in patients with autologous chondrocyte transplants. Invest Radiol 2001;36:743–8.[CrossRef][Medline]



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I S Boniatis, L I Costaridou, D A Cavouras, E C Panagiotopoulos, and G S Panayiotakis
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