MRI Web Clinic — November 2010

Osteoarthritis (OA) of the Knee
Gabrielle Bergman, M.D.

Clinical History: A 55 year-old woman presents with right knee pain. There has been no known injury. A meniscal tear is suspected.  (1a) Axial proton density with fat saturation, (1b) sagittal proton density with fat saturation and (1c) coronal proton density with fat saturation images are provided. What are the findings? What is your diagnosis?

1a
1b
1c
Figure 1:

(1a) Axial proton density with fat saturation, (1b) sagittal proton density with fat saturation and (1c) coronal proton density with fat saturation images

 

Findings

2a
Figure 2:

The axial proton density image with fat saturation shows loss of patellar articular cartilage focally at the median ridge and adjacent medial and lateral facets (long arrows). There is no articular cartilage loss at the lateral trochlea (short arrow). At the medial trochlear region (arrowhead), the intermediate signal represents pre-femoral fat pad, mimicking articular cartilage. The trochlear cartilage normally extends further proximally at the lateral aspect.

 

3a
Figure 3:

The sagittal proton density image with fat saturation, obtained near trochlear midline, illustrates the moderate (partial-thickness) articular cartilage loss, with subarticular bone marrow edema (arrow). At the most proximal patella, the articular cartilage remains normal (arrowhead). At the trochlear aspect, the prefemoral fat pad (arrowhead) contacts the patella. At the medial trochlea further distally, there was a small region of partial-thickness cartilage loss (not shown).

 

4a
Figure 4:

On coronal proton density image with fat saturation, mild (partial-thickness) articular cartilage loss is shown also in the medial compartment, femoral aspect (arrow). The vague region of signal loss at the lateral tibial plateau articular cartilage (arrowhead) is artifactual. The menisci are normal.

 

Answer

Osteoarthritis at patellofemoral and medial compartments. No meniscal tear.

Introduction

Osteoarthritis (OA) is a joint disorder that involves degeneration of articular cartilage, with limited inflammation manifested by synovitis, and with changes also at the subchondral bone. It has been stated that “there is nothing worth saying about osteoarthritis, except that it is common, hurts, and causes disability”, expressing the long held view that OA is an inevitable part of ageing. However, very extensive clinical and research work in orthopedics, joint biomechanics, and biochemistry/rheumatology has since led many to regard OA not as a disease of cartilage but rather as a process resulting from imbalance in the stresses affecting the entire joint1.

OA is maybe the most common of all human medical afflictions. It is estimated that as many as half of all those who have osteoarthritic joint changes, by imaging or clinical exam, are not symptomatic or have minimal symptoms. In certain locations, especially the CMC joint of the thumb, the hip and knee joints, OA is known to often cause significant disability. Recent studies of OA of the knee have shown that OA involvement of the patellofemoral joint compartment, either isolated or together with medial compartment OA, is associated with more pain and lower function level than when OA is limited to the medial or lateral tibiofemoral compartments2,3.

Etiologic Factors

In addition to being very common in humans, and having been identified in skeletal remains from thousands of years ago, OA is also frequent in other mammalian species. Still, OA has not been well understood in terms of its cause. The long held concept of OA as an inevitable feature of old age, or caused by long and hard work as a simple “wear-and-tear” phenomenon similar to the slow gradual wear down of treads of a car tire with a predetermined mileage limit, has been found to be entirely inaccurate. Instead of accepting OA as a disease limited to or even likely starting in articular cartilage (“primary” or idiopathic OA), several conceptual models have been proposed, with either a more mechanical or a more metabolic emphasis. One model describes OA as a process resulting from imbalance in the mechanical stresses affecting the entire joint, causing articular cartilage matrix degradation to dominate over matrix synthesis, thereby preventing cartilage self-repair and resulting in chondral loss4. Other proposed models see OA as a systemic metabolic disorder, in which circulating factors linked to altered lipid and glucose metabolism, or dysregulated tissue turnover in many tissues with common mesenchymal origin, may explain the diversity of pathophysiological changes found in generalized OA, including an association with obesity and with vascular disease5.

The older OA classification also includes “secondary” OA, resulting from another distinct disorder, such as pseudogout/CPPD, ochronosis and others causing selective tissue deposits that lead to quality changes within cartilage, and the accepted risk factors for OA including post-traumatic joint instability, joint malalignment, obesity, genetic predisposition, and also senescent changes increasingly frequent with advancing age.

Interestingly, high but not excessive level of activity does not predispose a normal joint to develop OA, but may be considered beneficial, considering that the lack of any vascularity within cartilage makes intermittent loading an important factor promoting cartilage metabolism. Studies have shown that long distance middle aged and older runners develop OA with similar but not higher incidence as in the general population6. Furthermore, a very sedentary life style is a risk factor for development of OA, with a proposed mechanism attributing this to the lack of muscle strength and coordination4.

5a
Figure 5:

Medial compartment OA, with full-thickness articular cartilage loss at both femoral and tibial aspects, exposing the pink vascularized underlying bone (arrow). Note the slightly yellowish white appearance of the normal adjacent cartilage (asterisk), and the normal cartilage at the lateral femoral condyle and trochlea.

 

 

The central feature of osteoarthritis, breakdown of hyaline articular cartilage, shows a focal involvement usually at the region of highest concentration of transmitted force (5a). Diffuse and smooth loss of cartilage throughout a joint is not characteristic of OA; indeed a cartilage biopsy taken a short distance from a full-thickness lesion may be histologically normal. In addition there is a variable degree of inflammatory reaction, in part caused by breakdown products from cartilage and mediated by the synovium; some of these break-down products can be measured not only in joint fluid but also in the blood of an individual with OA in an active phase.

Up to 90% of forces across the knee joint are routinely absorbed by active mechanisms when the knee flexes, mainly through opposing muscles distributing the impact over time and over surface4. In addition, much of articular impact is absorbed by the trabecular bone immediately deep to the cartilage4. In normal joints, the actual load per articular cartilage surface area during use has been found to be remarkably constant within most joints, around 23 kg/cm square, both in large weight-bearing joints and in small joints in the hand and fingers6. When this load is significantly exceeded, the chondrocytes in cartilage react, with various extent of degradation dominating synthetic activity. Chondrocytes, like osteocytes in bone, have been found to serve as both mechano-sensors and osmo-sensors, altering their metabolism in response to local physicochemical changes in the microenvironment. This recent discovery elegantly links extracellular environment events to intracellular signaling cascades.

 

6a
Figure 6:

This 3D graphic representation demonstrates the densely packed large proteoglycan aggregates "trapped" between the bundles of collagen, both produced by the chondrocytes. In the background note the organization of collagen fibers, with an overall "upside-down U" configuration (Benninghoff's arcades) leading to parallel fibers along the main articular force vector at the deep regions of cartilage, while at the joint surface the fibers are parallel to the surface. This organization is thought to be reflected in the MR signal from different regions of articular cartilage.

 

When evaluating the MR imaging features of OA, it is beneficial to have a conceptual understanding of the basic components, architecture, and physiology of articular (hyaline) cartilage and adjacent tissues (6a). Cartilage is a highly specialized tissue, one of the very few avascular and aneural tissues in the body. Hyaline cartilage always exists in a thin layer, from a fraction of a mm, up to 5-6mm in maximal thickness at the mid-patella which is usually the thickest hyaline cartilage in the body. Importantly, cartilage contains no distinct laminar structures, but instead there is a particular functional arrangement of collagen fibril orientation, chondrocyte prevalence, proteoglycans, and water content, with predictable gradual variations from the surface to the deep aspect of cartilage. The orientation of the collagen fibers (Benninghoff,s arcades) include parallel thick collagen bundles at the surface, oblique orientation at the mid-section, and radial collagen bundles at the deep layers (6a). The presence of collagen fiber cross-linking is strongly associated with function and imparts the characteristic strength and resilience. The dense collagen meshwork functions to “trap” the extremely large proteoglycan molecules that represent some of the largest molecules in the body, combining into aggregates with molecular weight up to 100 million (compare to water MW of 18). Inside cartilage, these proteoglycan molecules are highly compressed to1/1000 of the size they would have outside of cartilage, and indeed if the collagen interfibrillar ties rupture, this allows proteoglycan expansion to force the matrix apart, producing swelling and fissuring, characteristic early manifestations of OA. These large proteoglycan molecules are highly negatively charged, and during weight bearing when cartilage is compressed, they are made to move even slightly closer together, further repelling each other, and thereby maintain volume and then re-expand, contributing to the tremendous cartilage resilience manifested by tolerance of high load and high repetition mechanical stresses. In addition, when cartilage is compressed such as in the knee during motion, a minute amount of fluid is squeezed from the surface layers of cartilage onto the contact surfaces, with the lubrication further lowering the friction. Hyaline cartilage has one of the lowest friction coefficients known, approximately 1/3 of the friction between two melting ice cubes, lower than what has been recreated in man-made mechanical devices7.

Clinical Presentation

The aching joint pain of OA is characteristically worsened by weight-bearing activity and relieved by rest. Also common is joint stiffness which is usually worse in the morning, and mild edema and tenderness. Other symptoms include a catching or grinding sensation on joint movement, periarticular protuberances (periarticular mucous cysts mainly at the small joints of the fingers, and marginal osteophytes at any joint with OA), and later joint malalignment may develop. The clinical and histo-chemical findings of low-grade inflammation coupled with the degenerative processes have led many OA researchers to return to use of the term “osteoarthritis” after a period when the term “arthrosis” had been preferred.

Just as with MRI findings of intervertebral disc herniations and with meniscal tears at the knee, not all OA lesions detected by MR imaging are associated with clinical symptoms. Ongoing symptomatology may be absent even when advanced changes of OA are present on imaging exams. When symptoms are present, they are not likely to be generated within the articular cartilage, which is avascular and aneural, instead symptoms are mediated by other joint components including the synovium, joint capsule, and subchondral bone. Another variable feature of OA is the rate of progression of the joint degeneration, which may proceed over months or years, or may remain without progression for many years. Changes most frequently progress slowly over years, and longitudinal MR imaging studies have estimated the average yearly loss of cartilage with OA of the knee to 4-6% of total cartilage volume.

Imaging

MR imaging represents a dramatic improvement in the evaluation of joint involvement by OA. Radiographic evaluation is limited to demonstrating changes in bony mineralization affecting architecture and density, a “mineral map”, while MRI can directly show detailed morphology of the articular cartilage and also of all mineralized and non-mineralized joint structures.

Extensive literature exists regarding ongoing efforts to develop MR sequences and imaging methods specifically to further optimize cartilage evaluation, with the aim of improving clinical evaluation, as well as to provide replicable and detailed information for use in longitudinal follow-up research studies of the effects of novel surgical or pharmacological therapies8,9.

Artifacts influence the MR image of articular cartilage, and need to be recognized to avoid interpretation errors. Chemical shift artifact, related to mismapping in the frequency-encoded axis at junctions between tissues with fat and water, such as junction of bone marrow and cartilage (due to its high water content), makes the cortex look artifactually thick or thin (7a) on images without fat saturation. In reality, the subchondral cortex normally has a thickness of approximately 1/6 of that of overlying articular cartilage. Truncation artifact can cause an appearance suggesting sharply defined layers within cartilage; the presence of these layers is not compatible with the histology of articular cartilage. Likely due to the arcade-like arrangement of collagen fibers within cartilage (6a), there will be low signal at both the surface and the deep layers of articular cartilage, and variably higher signal in the midzone, related to anisotropy and the effects of magic angle artifact. The loss of signal may vary depending on the orientation of the cartilage region relative to the long axis of the magnetic field. In addition to the collagen fiber orientation in cartilage, proteoglycans and water concentrations in different regions have been shown to influence cartilage signal variations10.

7a
Figure 7:

This sagittal T1-weighted image of normal articular cartilage demonstrates the chemical shift artifact, with subtle mismapping in the x-axis of this image for signal from fat relative to signal from water, with fat shifted slightly to the right on this image, making the cortex next to cartilage at the trochlea (to the left) look artifactually thicker (long arrow), and the cortex posteriorly (to the right) on both the lateral femoral condyle and the patella look artifactually thinner (arrowheads).

 

8a
Figure 8:

A coronal proton density image demonstrates artifactually thick subchondral cortex and artifactually thin articular cartilage, at a thickness ratio of 2:1, caused by T2 signal loss at the intermediate and deep regions of the cartilage at both femoral and tibial aspects, with the resulting low signal in cartilage blending with the low signal from the subchondral bone (arrows). The normal ratio of thickness of subchondral bone to articular cartilage is approximately 1:6.

 

MRI features characteristic of OA include focal loss of articular (hyaline) cartilage, osteophytes, subchondral marrow lesions, and joint effusion. Frequently seen with OA and with a probable association are meniscal tears, especially meniscal extrusion, and periligamentous edema at the MCL11.

    • Articular cartilage loss: The main feature of OA is articular cartilage loss, which can range from surface fissuring (H), to surface fraying/mild loss (9a), to moderate loss (9b), and full-thickness loss (9c). Several of these features generally can be found at any one time in a knee with OA. The size of the resulting focal defects can vary significantly, and the location can vary although certain patterns prevail. These cartilage abnormalities all involve the articular surface of cartilage, with variation in the depth of involvement. With traumatic shear injury to cartilage, an injury may occur that does not communicate with the articular cartilage surface, usually with a linear extent of a couple of mm along the cartilage-bone interface, with signal of fluid, described as delamination (9d) at the transition region between cartilage and the stiffer underlying cortical bone. Articular cartilage defects have been found to have a high frequency of association with pain in several but not in all clinical studies12,13

 

9a
9b
9c
9d
Figure 9:

Images illustrating articular cartilage fissuring (9a), surface fraying and mild loss (9b), moderate loss (partial-thickness) (9c), and severe loss (full-thickness) (9d). Fissuring (9a) represents disruption at right angle to the cartilage surface, and may extend to partial (arrow) or full thickness of cartilage. Surface fraying often results in an undulating (9b, arrow) or jagged contour, sometimes with subtle fissuring. Moderate loss can be difficult to identify correctly, as signal loss at deeper cartilage layers may cause this to look like full-thickness loss (9c, arrow); compare with adjacent normal cartilage (arrowhead). With full-thickness loss, the exposed bony margin is often sharply defined (9d, long arrows), outlined by joint fluid, compared to adjacent partial-thickness loss (K, arrowheads).

 

10a
Figure 10:

A proton density axial image shows a delamination injury (arrow) to cartilage at the cartilage-bone interface at the medial patellar facet, after trauma to the knee.

 

Cartilage fissuring is characteristically seen on MRI images as linear defects with high signal perpendicular to the cartilage surface, with the high signal attributed to fluid within the fissure or to fluid imbibition in the cartilage along the fissure. The MRI finding of low-signal fissuring (11a,11b) at the patella and midline trochlea, with short well-defined linear signal abnormalities seen on images in more than one plane, has recently been shown to correspond to arthroscopically or arthrographically verified fissures14. The cause of the low instead of high signal in these lesions has not yet been clarified. However, care should be taken not to mistake the frequent ill-defined artifactual regions of low-signal in cartilage for low-signal fissuring (4a).

 

11a
11b
Figure 11:

Sagittal proton density image with fat saturation demonstrates a linear low-signal abnormality at the patellar median ridge (11a, arrow), which was seen also on coronal and axial images (not shown), and which was on subsequent arthroscopy shown to represent a cartilage fissure. An axial proton density image shows similar linear low signal extending from the cartilage surface at the midline trochlea (11b, arrow), compatible with a fissure.

 

  • Subarticular bone marrow lesions: A large number of clinical studies now support the notion that the presence of a subarticular bone marrow lesion makes an OA lesion of cartilage more likely to be associated with the clinical finding of pain. While the well-known radiographic feature of subarticular sclerosis can occasionally be seen as low signal on MRI images (9d), the vast majority of subarticular bone marrow lesions in OA do not have low but instead high, or mixed intermediate and high, signal (2a,3a,12a,12b,13a,13b). This has in histological correlation studies been shown to correspond to marrow fibrosis with interspersed regions of trabecular necrosis, debris and repair features very similar to those of osteonecrosis, with associated variable hyperemic response. Also frequently seen histologically are subchondral cystic change and degenerative microcysts15,16. Subarticular bone marrow lesions occur in both OA patients with and without pain, but with a significantly higher frequency reported in symptomatic patients. While larger subarticular lesions show stronger association with the presence of pain (but not with the severity of pain), they also in longitudinal studies predicted progression of OA17. In a large longitudinal study, absence of bone marrow lesions at baseline or follow-up was associated with a decreased risk of further cartilage loss, and it was also found that although many subarticular bone marrow lesions slowly progress, this was not always the case, and indeed subarticular bone marrow lesions may regress or fully resolve, as in nearly 50% of their cases18.

 

 

12a
12b
Figure 12:

Sagittal T1-weighted (12a) and STIR (12b) images demonstrate well-defined subchondral bone marrow lesions in OA with subchondral cysts and marrow edema at the patellofemoral compartment (arrows), severe (full-thickness) articular cartilage loss, and osteophyte formation.

 

 

13a
13b
Figure 13:

Sagittal T1-weighted (13a) and STIR (13b) images show a spectrum of less-well defined subarticular marrow lesions in OA, with replacement of marrow fat signal with minimal edema and hemispheric configuration at the posterior femur (arrowhead), mainly low signal at the tibial subchondral lesion (short arrow), and mild bone marrow edema at the trochlear and distal femoral locations (long arrows).

 

 

 

  • Osteophytes: These fibro-cartilage-capped bony outgrowths appear mainly at articular margins in OA, are commonly but not always present in OA, and when present can vary in size between locations and individuals. Osteophytes may form very early or later in OA, and may be a source of pain and loss of function, in the knee specifically related to limitation of joint mobility, but may also be present without causing symptoms, and may even have positive effects by increasing the joint contact surface (12a,12b,14a)17. More rarely seen mainly with very advanced OA are intra-articular osteophytes, occurring at the articular surface. Osteophytes are not entirely specific for OA, and a relationship of non-progressing osteophytes to joint instability has been previously suggested. More recent research has shown that osteophytes have a close resemblance to healing fracture callus, and that a specific growth factor when introduced into a joint in experimental animals induces osteophyte formation; expression of this growth factor is observed in human osteophytes, suggesting that growth factors may cause precursor cells in the periosteum at a joint margin to produce osteophytes19.

 

 

14a
Figure 14:

Coronal T1-weighted image demonstrating marginal osteophytes (arrows) in a patient without articular cartilage loss at the medial and lateral compartments. Advanced OA was present at the patellofemoral compartment of this knee (not shown).

 

  • Joint effusion: One of the features in MRI studies of OA that has shown a positive correlation with the presence of symptoms is a joint effusion. In addition, effusions have been found to be more frequent with more advanced OA9. The synovial inflammation in patients with OA has been shown to contribute to the pathogenesis of OA through formation of various catabolic and pro-inflammatory mediators such as cytokines, prostaglandins and nitric oxide, altering the balance of cartilage matrix degradation and repair.
  • Meniscal tears, especially extrusion of the meniscus (15a), have shown a strong association with progression of symptomatic OA of the knee9,12,20. The incidence of meniscal tear found on MRI examinations in patients with symptomatic OA has been reported in different studies at 52-92%, and it has been found that in advanced OA there are essentially always severe meniscal lesions such as complex tears with deformity or severe destruction13. The cartilage-protective function of an intact meniscus is well known, with significant increases in the incidence of OA of the knee demonstrated in studies of meniscectomy populations3.

 

 

15a
Figure 15:

A coronal proton density image with fat saturation in a patient with OA of the medial compartment demonstrates severe loss of femoral articular cartilage (arrow). Partial extrusion from the joint is noted at the medial meniscal body (arrowhead).

 

Terminology for cartilage defects on MR images: Cartilage loss on MR images is often described differently by different radiologists, reflecting a lack of an accepted and easy to use terminology or grading scheme. The grading schemes created for research evaluations are not always suitable for clinical work. There is a need to coordinate terminology used with MRI with that used with arthroscopic exams, which is a surface-limited exam while MRI is cross-sectional and does not readily offer a feel for what the surface will look like through an arthroscope. Use of Grades 1 through 4, without added descriptive terminology, may not be sufficiently clear to all readers of clinical MRI exam reports. Use of the description “cartilage loss” has been proposed, as shown above (9b,9c,9d).

Use of the term “chondromalacia” is frequent in clinical imaging, but not entirely correct. This combination of chondro from cartilage and malacia meaning “soft”, is used by arthroscopists probing cartilage and finding regions where the surface can be slightly depressed and may have surface fraying. It has then been adapted to also describe abnormal-appearing cartilage on MR images. Some orthopedic authors have suggested that the term “chondromalacia” be abandoned altogether due to the issue that it holds different meanings for different readers21; or that it is limited to use in the specific cases of chondromalacia patellae or “runner’s knee” with reversible cartilage softening occurring in in young individuals.

Differential diagnosis

Chondromalacia patellae, or “runner’s knee”, is a diagnosis referring to retropatellar knee pain in adolescents and young adults. Symptoms are aggravated by either activity (especially walking down stairs) or by prolonged sitting, and are associated with the arthroscopic finding of softened articular cartilage at the patellar facets. The cartilage is often not structurally permanently damaged, and healing may occur over a sometimes very long period of time, usually with patellar cartilage return to normal, while in some cases there will be progression to cartilage defects, subarticular bone marrow lesions, osteophytes and the features of OA22.

Trauma: Acute trauma can cause osteochondral injury with features very similar to OA, with focal cartilage loss and sometimes, but not always, also subarticular bone marrow edema. If the cartilage defect has well-defined right angle margins (16a), with marrow edema deep to the defect, this suggests a traumatic etiology, and other joint injuries may be present as well.

16a
Figure 16:

On a sagittal proton density image with fat saturation, obtained after acute injury to the knee in a 14 year-old male, a full-thickness articular cartilage defect 28 mm in length at the lateral femoral condyle is seen to have well-defined angular margins (arrows), with associated subarticular marrow edema. A corresponding size intra-articular body was present nearby, along midline trochlea (not shown).

 

Rheumatoid arthritis: A principally different type of arthritis, erosive inflammatory, RA is associated with bony erosions located at the peripheral bare area of a joint, with bone marrow edema at the erosion if there is active inflammation, or without bone marrow edema if not active. RA does not cause osteophyte formation, but is associated with synovitis and often severe synovial thickening (pannus formation). The articular cartilage loss in RA is not localized as in OA, but more diffuse and is related to enzymatic action on the cartilage surface; it may progress to an end-stage joint with loss of all articular cartilage.

Osteonecrosis: At an earlier stage, osteonecrosis of the knee can be seen as a subarticular bone marrow lesion with normal overlying articular cartilage. Later, if collapse has occurred and progressed to loss of articular cartilage and joint degeneration, it may be difficult or impossible to identify the underlying osteonecrosis/AVN, with the MRI features identical to those of advanced OA.

Insufficiency fracture of the femoral condyles: A subcortical insufficiency fracture of the medial or lateral femoral condyle or tibial plateau presents as a low signal fracture line immediately deep to the subchondral cortex, with associated often intense bone marrow edema, with intact subchondral cortex and articular cartilage (17a,17b). An insufficiency fracture may progress to articular collapse, with flattening/fracture of the subchondral cortex and injury leading to loss of articular cartilage, with some features similar to those of OA.

17a
17b
Figure 17:

Coronal (17a) and sagittal (17b) proton density images with fat saturation show subarticular bone marrow edema at the medial tibial plateau, with a low signal insufficiency fracture line (arrow). Surface fraying and mild loss of articular cartilage is also present, compatible with pre-existing mild OA, and there is periligamentous edema at the MCL.

 

Treatment and prognosis

Traditional OA therapies have consisted of analgesics as needed, exercise programs and physical therapy, sometimes the use of braces, and ergonomic or life style changes; there may be a need for surgery with correction of joint instability or malalignment, and possibly later with prosthetic replacement, especially at weight-bearing joints.

Not all cartilage lesions are indications for surgery, but smaller lesions in younger symptomatic individuals may benefit from open surgical drilling or microfracture (arthroscopic use of a pick), both aiming to breach the subchondral cortex at a cartilage lesion reaching into vascularized subchondral bone, thereby causing clot formation and within a few weeks leading to filling of the defect with cartilage. However, after maturation this cartilage consists mainly of fibrocartilage with less ability to hold up to stresses over time. In the last decade, other procedures have become available, if still mostly considered experimental by medical insurance companies. These include techniques using autologous cartilage transplants where a plug consisting of bone and cartilage is harvested from an expendable part of the joint and placed into the site of a prior defect, also the use of autologous chondrocyte implantation (ACI) where cartilage cells are harvested at arthroscopy, cultured in the lab, and re-introduced in solution into a cartilage defect, and held in place under a periosteal transplant cover. ACI can also be performed using a biodegradable scaffolding. Challenges have included attempting to induce the formation of hyaline-like cartilage as opposed to fibrocartilage, with hyaline-type cartilage with cross-linking required for holding up to the stresses of long term use.

Also ongoing is evaluation of multiple pharmacological “chondroprotective” substances23. The use of oral glucosamine and chondroitin sulphate, substances primarily derived from shellfish and available as dietary supplements, has been evaluated in several published blinded series, some supporting and others not supporting an association with clinical improvement of OA.

Conclusion

MR imaging provides excellent characterization of the articular changes in OA. This is valuable in the clinical management of patients with OA, facilitating accurate diagnosis, and providing information regarding location and severity of joint pathology. OA is expected to continue to be a significant medical problem in the future in view of the increased sports activity demands with related injuries and overuse in professionals and also in young individuals involved in sports, the high frequency of obesity in the population, and with a longer life expectancy.

Significant developments in the scientific understanding of OA, aided by the advances in MR imaging technology, have resulted in a paradigm shift for OA, now seen less as a disease limited to cartilage and rather as a “whole joint” and maybe even a “whole individual” process with complex series of molecular changes and interactions between tissues. The strong influence of structure on the MR image contrast indicates that MRI is ideally suited to the evaluation of cartilage tissue integrity, and new techniques hold promise for future detection capability related to very early changes of cartilage composition. MR diagnostic information is therefore likely to increasingly provide an important part of the basis for opportunities for future therapeutic interventions, aiming for more effective therapies for OA.

References

1 Developments in the scientific understanding of osteoarthritis. Abramson S, Attur M. Arthritis research and therapy 2009, 11:227 http://arthritis-research.com/content/11/3/227

2 Patellofemoral joint osteoarthritis: an important subgroup of knee osteoarthritis. Hinman, RS, Crossley KM. Rheumatology 2007, 46 (7): 1057-1062 http://rheumatology.oxfordjournals.org/content/46/7/1057.long

3 Patellofemoral osteoarthritis coexistent with tibiofemoral osteoarthritis in a meniscectomy population. Englund M, Lohmander LS. Annals of Rheumatic Diseases 2005, 64:1721-1726 http://ard.bmj.com/content/64/12/1721.abstract?ijkey=c63cbf12aa7c7ae6dd1ee1981942f90b7b7396c2&keytype2=tf_ipsecsha

4 Yet more evidence that osteoarthritis is not a cartilage disease. Brandt KD, Radin EL, Dieppe PA , van de Putte. Annals of Rheumatic Diseases 2006, 65(10):1261-64 http://ard.bmj.com/content/65/10/1261

5 Osteoarthritis: a problem of growth not decay? Aspden RM. Rheumatology 2008: 47(10): 1452-1460 http://rheumatology.oxfordjournals.org/content/47/10/1452.full

6 The risk of osteoarthritis with running and aging: a 5-year longitudinal study. Lane NE, Michel B, Bergman AG, Oehlert J et al. J Rheumatol. 1993 Mar;20(3):461-8

7 Personal communication: Pathophysiology of osteoarthritis. Sledge CB. Kovitz honorary lecture, Stanford University, CA, Dec. 14, 1989

8 MRI of articular cartilage: revisiting current status and future directions. Recht MP, Goodwin DW, Winalski CS, White LM.. AJR 2005: 185:899-914 http://www.ajronline.org/cgi/content/full/185/4/899

9 Cartilage imaging: motivation, techniques, current and future significance. Link TM, Stahl R, Woertler K. European Radiology 2006, 17(5): 1135-1146 http://www.springerlink.com/content/42n71222684333u2/fulltext.html

10 Short TE MR microscopy: Accurate measurement and zonal differentiation of normal hyaline cartilage. Freeman DM, Bergman AG, Glover G. Magnetic Resonance in Medicine 1997, 38:72-81

11 Is intra-articular pathology associated with MCL edema on MR imaging of the non-traumatic knee? Blankenbaker DG, De Smet AA, Fine JP. Skeletal Radiology 2005 34:462-467 http://www.ncbi.nlm.nih.gov/pubmed/15940487

12 Risc factors for progressive cartilage loss in the knee. Biswal S, Hastie T, Andriacchi TP, Bergman AG et al. Arthritis and Rheumatism 2002, 46(11):2884-2892

13 Osteoarthritis: MR imaging findings in different stages of disease and correlation with clinical findings. Link TM et al, Radiology 2003, 226:373-381 http://radiology.rsna.org/content/226/2/373.full

14 The cartilage black line sign: an unexpected MRI appearance of deep cartilage fissuring in three patients. Stevens T, Didusch DR, Balin JI, Gaskin CM. Skeletal Radiology online http://www.springerlink.com/content/u1616653861776p8/fulltext.html

15 Osteoarthritis of the knee: correlation of subchondral MR signal abnormalities with histopathologic and radiographic features. Bergman AG, Willen HK, Lindstrand AL, Pettersson HT. Skeletal Radiology 1994: 23:445-448 http://www.ncbi.nlm.nih.gov/pubmed/7992110?dopt=Abstract

16 Bone marrow edema pattern in osteoarthritic knees: correlation between MR imaging and histologic findings. Zanetti M, Bruder E, Romero J, Hodler J. Radiology 2000 215:835-40 http://radiology.rsna.org/content/215/3/835.fulltext.html

17 Bone marrow lesions in people with knee osteoarthritis predict progression of disease and joint replacement: a longitudinal study. Tanamas S, Wluka A, Pelletier J-P, Pelletier J et al. Rheumatology 2010 September published on line http://rheumatology.oxfordjournals.org/content/early/2010/09/07/rheumatology.keq286.abstract

18 Change in MRI detected subchondral bone marrow lesions is associated with cartilage loss: the M.O.S.T. Study. A longitudinal multicentre study of knee osteoarthritis. Annals of Rheumatic Diseases 2009 68(9):1461-1465 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2905622/

19 Osteophytes: relevance and biology. Van der Kraan PM, van den Berg WB. Osteoarthritis Cartilage 2007, 15(3):237-244. http://www.oarsi.org/pdfs/paper_selection/Mar_07.pdf

20 Meniscal tear and extrusion are strongly associated with progression of symptomatic knee osteoarthritis as assessed by quantitative MRI. Berthiaume M-J, Raynauld J-P, Martel-Pelletier J,et al. Annals of Rheumatic Diseases 2005, 64:556-563 http://ard.bmj.com/content/64/4/556.full

21 Patellar nomenclature: the Tower of Babel revisited. Grelsamer RP. Clinical Orthopedics and Related Research 2005: 436:60-65

22 Chondromalacia of the patella. Wheeless’ Textbook of Orthopedics on line. http://www.wheelessonline.com/ortho/chondromalacia_of_the_patella

23 Protective effects of licofelone versus naproxen on cartilage loss in knee osteoarthritis: a first multicentre clinical trial using quantitative MRI. Raynauld J-P et al. Annals of Rheumatic Diseases 2009:68:938-947

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