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Internal Derangement of the Knee: Cartilage and Osteochondral Injuries
Prevalence, Epidemiology, and Definitions
The term osteochondral lesion is used to describe a defect of the articular surface involving separation of the cartilage and the underlying bone, without making any pretense to etiology. Possible causes of osteochondral lesions are traumatic osteochondral lesions, osteochondritis dissecans, and insufficiency fractures of the subchondral bone. The underlying mechanism in all cases is believed to be repetitive and prolonged overloading or sudden compressive stress of the hyaline cartilage and the subchondral bone. These lesions are most often seen on the talus, the femoral condyles, and the elbow joint. Other, less frequently affected sites include other tarsal and metatarsal bones, the distal tibia, the acetabulum, the metacarpal bones, and the glenoid cavity.
The various etiologic entities of an osteochondral lesion are distinguished through a combination of clinical symptoms, patient history, and demographics, on the one hand, and imaging findings such as location of the lesion and associated structural abnormalities on the other hand. In early stages of the disease, symptoms are often obscure and functionality of the joint is rarely impaired, making imaging findings and demographics all the more important.
Injury to the articular cartilage in the knee is reported in 63% of arthroscopies, and the vast majority of these lesions are associated with other problems, such as anterior cruciate ligament injury (23%) and meniscal lesions. MRI of the knee shows a prevalence of hyaline cartilage defects similar to arthroscopy but reports solitary lesions in almost one fourth of patients. In immature knees, cartilage lesions are more common than meniscal or anterior cruciate ligament tears. All types of osteochondral lesions occur two to three times more often in men than in women, although the incidence in females is increasing as higher numbers of young women are participating in intensive sports.
Tenderness and joint effusion are variably present early on but become more apparent as the disease progresses. Quadriceps atrophy will be present if the injury becomes chronic. Intermittent knee swelling with activity is common. Catching, locking, grinding, and giving way may be intermittent at first but become more constant with the appearance of loose bodies.
Traumatic Chondral or Osteochondral Lesions
When shearing or rotational forces are transmitted from one congruent articular surface to another, fracture lines paralleling the surface can arise in the cartilage proper or in the subchondral bone. Depending on the depth of the fracture, chondral (cartilage alone) or osteochondral fragments (consisting of cartilage and underlying bone) can break away (see Fig. 29-1 ). In many cases the fracture line does not reenter the joint space but is deflected by the most superficial cartilage layer (lamina splendens, see later), which has strong collagen fibers paralleling the surface, and forms an intracartilaginous tear (see Fig. 29-2 ). After a variable amount of time subchondral cystic lesions can develop beneath these lesions. Their appearance can be explained by two mechanisms ( eFig. 29-1 ).
When compressive forces are transmitted over a joint, fracture lines are more perpendicular to the articular surface, and impaction of cartilage and subchondral bone occurs. These chondral or osteochondral fractures can occur on one or on both apposing joint surfaces and are surrounded by areas of bone marrow edema. The whole of fractures and edema is often referred to as a bone bruise.
Full-thickness clefts or fissures allow synovial fluid to reach the subchondral bone. In situations of elevated intraarticular pressure, it is thought that joint fluid is forced down these fissures and penetrates the subchondral bone, with subsequent resorption of trabecular bone and formation of cystic lesions. Another theory explaining the origin of these cystic lesions is focal posttraumatic osteonecrosis, with cyst formation occurring as necrotic trabeculae are removed by osteoclasts. Most likely, both mechanisms play a role in the formation of subchondral cysts.
In most cases the patient can easily recall the traumatic event. Tenderness, impaired function, joint effusion, and even hemarthrosis are seen in patients with acute (osteo)chondral fractures and allow some degree of distinction between trauma and other causes of osteochondral lesions.
Osteochondritis Dissecans
Osteochondritis dissecans most commonly involves patients between the ages of 10 and 20 years and is more prevalent in children, especially in active boys. This form of osteochondritis dissecans, called juvenile osteochondritis dissecans, includes patients with open metaphysis and has a higher rate of spontaneous healing. The causes of osteochondritis dissecans are still not fully understood, although there is an undeniable association with trauma, both repetitive and solitary. In 40% to 60% of cases, a significant history of trauma can be found. This trauma is believed to disrupt the blood supply to the subchondral bone, which can be tenuous in a rapidly growing person. Apparently, the medial femoral condyle is most susceptible because 80% to 85% of osteochondritis lesions in the knee are found there. The lateral aspect of the medial condyle is especially affected. This is probably due to microinjuries caused by repetitive impingement of the intercondyloid eminence against the medial condyle during internal rotation of the tibia. This abutment of the eminence against the osteochondral lesion explains the pain patients complain about when they rotate the tibia internally with extended knee. This sign was first described by Wilson and is sometimes seen in patients with osteochondritis. It does not, however, exclude other forms of osteochondral lesions.
The appearance of osteochondral lesions in other locations in the knee and the observation that both knees are affected in 20% to 30% of patients demonstrate, however, that trauma, repetitive or acute, is not the only possible cause. Increased intraosseous pressure, similar to that seen in osteonecrosis, has been described in osteochondritis dissecans. Abnormal centers of ossification, endocrine imbalances, and genetic factors have also been proposed as causes, but these have not been definitely shown to play a role in osteochondritis dissecans.
Another location of osteochondritis dissecans in the knee is the patella. In comparison to osteochondritis dissecans of the femoral condyle, this is a much rarer diagnosis and is possibly related to ligamentous laxity and patellar (sub)luxation. Lesions are generally found on the bottom half of the medial facet with involvement of the lateral facet in approximately 30% of patients.
Subchondral Insufficiency Fractures
Besides traumatic chondral and osteochondral lesions and osteochondritis dissecans, subchondral insufficiency fractures can also cause cartilage and osteochondral lesions. These subchondral insufficiency fractures can be associated with focal, subchondral areas of osteonecrosis or bone marrow edema.
According to recent theory, based on the work of Yamamoto and Bullough, the underlying cause of the fracture is thought to be osteoporosis and osseous insufficiency. Although it is still often referred to as spontaneous osteonecrosis of the knee, the osteonecrosis seen between the fracture line paralleling the articular surface and the bony end plate is probably secondary to vascular disruption caused by the fracture.
Other authors see subchondral insufficiency fractures and spontaneous osteonecrosis as two separate entities that need to be differentiated because of the therapeutic consequences. A subchondral insufficiency fracture is considered to be self-resolving, whereas spontaneous osteonecrosis can lead to collapse of the joint surface and must be treated surgically. Subchondral insufficiency fractures are classified by these authors in the same group as other self-resolving lesions presenting as bone marrow edema, such as transient bone marrow edema, transient osteoporosis, and reflex sympathetic dystrophy.
From a clinical point of view, however, an insufficiency fracture associated with osteonecrosis is still a distinct entity and unchanged since it was first described in 1968 by Ahlbäck and colleagues. It differs from classic osteonecrosis, which is associated with corticosteroid therapy, alcohol use, and hematologic diseases. An insufficiency fracture combined with osteonecrosis on the other hand is associated with obesity and age, with most patients being older than age 60 years. Although it is predominantly seen in elderly women with osteoporotic bone, men can be affected, too.
A subchondral insufficiency fracture is typically situated on the weight-bearing part of the medial femoral condyle. Clinically, it is characterized by an abrupt onset of pain without obvious trauma, allowing distinction of this entity from an acute traumatic (osteo)chondral lesion and osteochondritis dissecans of the knee. Typically, pain is worse at night in osteonecrosis. Other clinical symptoms, such as joint effusion, stiffness, and tenderness, are generally more pronounced than in osteochondritis dissecans but can also be absent.
Anatomy
The hyaline cartilage covering the articular surface of joints is composed of chondrocytes embedded in an extracellular matrix. This matrix contains dissolved gases, electrolytes, and small proteins, on the one hand, and macromolecules such as collagen and proteoglycans on the other.
A functional way of dividing cartilage is the four-layer model first proposed by Benninghoff in 1925 ( eFig. 29-2 ). The most superficial layer can be subdivided into two compartments: the lamina splendens, composed of tightly packed bundles of collagen arranged parallel to each other; and a second layer, made of collagen fibers that are oriented more perpendicularly to the surface. The transitional zone or middle layer is located underneath the superficial layer. It contains fewer chondrocytes that have a more rounded appearance. The collagen fibrils in this layer have a random orientation and larger diameters than those in the superficial zone.
The deep or radial zone is located between the transitional zone and the thin, calcified layer of cartilage overlying the subchondral bone. This layer has the highest proteoglycan concentration and lowest cellularity and collagen content. The diameter of the collagen fibrils, however, is maximal. The collagen fibers are oriented toward the surface and are arranged in large fibrils.
The calcified zone anchors the large collagen fibrils to the subchondral bone and has mechanical properties intermediate between those of uncalcified cartilage and subchondral bone. It is separated from the uncalcified cartilage by the tide mark, a wavy line representing the mineralized front of the calcified cartilage. The calcified cartilage is intimately connected to the subchondral bone plate, also called the cortical end plate or the articular bone plate. The interface between both structures is highly irregular with deep recesses and large protuberances, somewhat like the pieces of a jigsaw puzzle. Underneath the end plate is situated the subcortical space, containing fatty bone marrow, vascular structures, and trabecular bone. The density of this subchondral trabecular network and of the blood vessels is correlated with the compressive forces acting on the cartilage and subchondral bone. It also varies with age, from person to person, and from joint to joint. Directly underneath the subchondral end plate, the vascular structures have merged together to form a transverse sinus. It is fed by terminal arterial branches ending in irregular sinusoids. Originating from this transverse sinus are multiple small vascular branches that penetrate the cortical end plate and can reach through the calcified cartilage up to the tide mark. An estimated 50% of the oxygen and glucose required by cartilage is supplied by these vessels. The other 50% directly diffuses into the cartilage from the synovial fluid.
Macroscopically, the articular surface of the knee joint can be divided into several different regions. The members of the International Cartilage Repair Society proposed a gridlike mapping system of the femoral condyles ( eFig. 29-3 ), the tibial plateaus, and the patellar facets. The central and posterior areas of the femoral, the central areas of the tibial condyles, and the lateral patellar facet are subjected to the greatest forces in upright position and during flexion of the knee. As such, they are most often affected by osteochondral pathology.
Other ways of localizing osteochondral lesions have been devised ( eFig. 29-4 ).
Based on the lines along the posterior femoral cortex and the Blumensaat line, Cahill and Berg divided the lateral projection of the knee into three segments:
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A: Anterior to the Blumensaat line
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B: Between the Blumensaat line and the line along the posterior cortex of the femur
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C: Posterior to the line along the posterior cortex of the femur
They also divided the anteroposterior projection of the knee into five segments where 1 and 2 divided the medial femorotibial compartment into two equal parts, 3 encompassed the notch, and 4 and 5 divided the lateral compartment into two equal parts.
Biomechanics
Hyaline cartilage is a viscoelastic material that is resistant to compressive and shearing forces. Although elastic, cartilage attenuates only 1% to 3% of the load forces. The majority of the load forces (30%) are taken up by the subchondral bone. The main function of cartilage in weight bearing is dissipating the loading forces to a larger area.
Reaction of Cartilage to Loading
The collagen framework and the negatively charged hyaluron-aggrecan complexes confined within this framework provide a hydroelastic suspension mechanism. Loading of articular surfaces causes movement of fluid within the cartilage matrix that dampens and distributes the load within the cartilage and to the subchondral bone. When load is applied slowly, proteoglycan-bound water is squeezed out of the cartilage or into uncompressed regions of the matrix distributing the forces. After the load is removed, osmotic swelling pressure exerted by proteoglycans and dissolved electrolytes pulls water molecules back into the matrix and reestablishes equilibrium.
Reaction of Cartilage to Injury
In a traumatic event, the applied forces are too high or applied too rapidly for redistribution of fluid to occur. This results in rupture of the framework and, in more extreme cases, in fracturing of the subchondral bone.
When the articular surface is injured, there is damage not only to the cartilage matrix but also to the chondrocytes. This results in an area of cell death, through both necrosis and apoptosis, that extends further than the actual cartilaginous lesion. Because chondrocytes are responsible for the maintenance of the extracellular matrix, the framework in this acellular rim becomes prone to rapid degeneration, allowing the lesion to progress.
In a cartilaginous lesion caused by sharp trauma (e.g., a surgical tool), this rim of cell death is not seen. This is important in cartilage repair because an acellular region interferes with adhesion of the repair tissue to the surrounding cartilage.
Although the forces encountered by the articular surface during everyday use are easily redistributed, repetitive minor trauma can result in damage to the subchondral bone and the deeper regions of the cartilage without visible disruption of the surface. This damage results in subchondral bone marrow edema and possibly in associated microfractures of subchondral trabeculae. Healing of these fractures leads to microcallus formation and focal subchondral sclerosis. Owing to the rigidity of calcified cartilage, the cortical end plate, and, to a lesser extent, the subchondral bone, the probability of these regions sustaining microinjuries is higher than that of the softer cartilage. Especially at the periphery of these areas, small cracks can be found.
Eventually these changes lead to deterioration of both deep and superficial cartilage. On the surface, the cartilage starts to display fibrillation and fissuring. As explained earlier, these fissures are thought to play a role in the formation of subchondral cystic lesions, which are frequently seen in degenerative joint disease but can also appear after a traumatic event.
In the deeper regions of the cartilage, these changes lead to production of abnormal matrix proteins, which initiates swelling of the cartilage and can result in delamination of the articular surface if (repetitive) overloading persists.
Manifestations of the Disease
Traumatic Chondral or Osteochondral Lesions and Intraarticular Fractures
Grading of Cartilage Lesions
The most well-known arthroscopic staging method for articular cartilage lesions is that proposed by Outerbridge in 1961. In 1985, Shahriaree modified this classification, describing four grades of chondromalacia where grade 1 involved softening of the cartilage; grade 2, shallow fibrillation, ulceration, or blister-like swelling; grade 3, surface irregularities and areas of thinning; and grade 4, ulceration and exposure of subchondral bone. Based on the Shahriaree classification and in analogy with the Outerbridge classification, Yulish proposed three stages of chondromalacia patellae for use in MRI. In later studies, this classification was modified to five grades: 0, normal cartilage (corresponds arthroscopically to normal cartilage or softening of cartilage); I, slight swelling and signal heterogeneity; II, fissuring or ulcerations less than 50% of cartilage thickness ( Fig. 29-3 ); III, fissuring or ulcerations more than 50% of cartilage thickness ( Fig. 29-4 ); and IV, ulcerations and erosion with exposure of subchondral bone ( Fig. 29-5 ).
A correlation of these grades with arthroscopic findings is given in Table 47-1 (see also eTable 29-1 ). As these systems were based on the changes seen in degenerative cartilage, they are not ideally suited to describe acute cartilage lesions. Nevertheless, they are widely used for this purpose.
eTABLE 29–1
Comparison between MRI and Arthroscopic Findings in Grading Chondromalacia
| MRI | Arthroscopic Finding | |
|---|---|---|
| Grade 0 | Normal cartilage | Normal cartilage or moderate softening |
| Grade I | Normal contour or slight swelling and signal alteration | Extensive softening with swelling of the articular cartilage |
| Grade II | Superficial fraying; fissuring or ulcerations less than 50% of cartilage thickness | Surface irregularity less than half the cartilage thickness |
| Grade III | Ulcerations more than 50% of cartilage thickness | Surface irregularity greater than half the cartilage thickness |
| Grade IV | Full-thickness cartilage defect with exposure of subchondral bone | Ulceration and exposure of bone |
The grading system put forward by the International Cartilage Repair Society (ICRS) has a similar subdivision of cartilage lesions; however, full-thickness cartilage lesions are classified as grade IIIc. Only when the subchondral bone plate is compromised is a lesion called a grade IV defect. This grading system does not distinguish between acute and chronic lesions.
Size of a lesion is not taken into account in this classification. It should be reported as a separate parameter.
A limitation of the just-mentioned classification systems is the inability of routine MR sequences to reliably demonstrate grade I changes. Signal changes associated with changes in the extracellular matrix of the cartilage cannot be differentiated from imaging shortcomings such as truncation artifact, magic-angle artifact, or partial-volume artifact.
An alternative classification system was proposed by Bohndorf in 1999, based on a combination of arthroscopic and magnetic resonance findings. It differentiates between lesions with intact (A) or disrupted (B) cartilage and further subdivides based on the extent of cartilage damage, the involvement of subchondral bone, and the state of the bony end plate. (An overview can be found in eFigure 29-5 and also in eTable 29-2 .) The major advantage of this classification is it can be applied to acute chondral or osteochondral lesions in the knee and ankle as well as less frequently involved locations.
eTABLE 29–2
Classification of Acute Chondral and Osteochondral Lesions (According to Bohndorf)
From Bohndorf K. Osteochondritis (osteochondrosis) dissecans: a review and new MRI classification. Eur Radiol 1998; 8:103–12.
| A: Acute injury of the articular surface with intact cartilage | Subchondral microfracture and bone marrow edema |
| Subchondral impaction (linear or geographic) and bone marrow edema | |
| B: Acute injury of the articular surface with disrupted cartilage | Softening of cartilage with or without fissuring |
| Intracartilaginous tear or loose cartilage fragment | |
| Compression of cartilage and immediate subchondral bone | |
| Osteochondral compression with fracture of the bony end plate | |
| Partially or completely detached osteochondral fragment |
Radiography
A radiographic examination of patients with a suspected traumatic osteochondral lesion or an intraarticular fracture should include not only the standard anteroposterior and lateral views but also a posteroanterior view with the knee flexed 20 degrees (Schuss or MTP view). This view allows a better evaluation of the posterior articular surface, which is often affected in trauma to the flexed knee.
The axial view of the patella with 15 to 20 degrees of flexion is essential for evaluating the articular surface of the patella and the trochlear groove. Although it is important in evaluating the patellofemoral joint after patellar luxation, it will detect only 32% of osteochondral injuries caused by this trauma.
Long-leg views can help determine abnormal varus or valgus alignment after compression fractures of the medial or lateral tibial plateau but should not be taken routinely. Even with these different views, osteochondral fractures can easily go undetected on plain radiographs because the bone fragments tend to be small, even if a large osteochondral defect is present.
The main radiographic features of an osteochondral fracture include a linear radiodense area paralleling the subchondral bone plate ( Fig. 29-6 ). This is due to either impacted trabecular bone or callus around the fracture line. The double contour is typically seen in a depression fracture of a tibial condyle. An irregular bony contour, bony defect, or bony fragments are sometimes seen in osteochondral fractures ( Fig. 29-7 ). It is not always possible to detect the origin of this fragment because the natural healing processes tend to remodel the fracture site.
All osteochondral lesions can give rise to loose, intraarticular bodies, although they are more frequent in osteochondral fractures and osteochondritis dissecans. Most fragments become embedded in the synovial lining, especially in the posterior recesses of the knee, where the majority are broken down and reabsorbed. If these embedded fragments revascularize, growth and formation of trabecular bone can be seen on consecutive radiographs. The fragments that remain free can also disappear because of osteoclastic properties of the synovial fluid. Others develop degenerative calcifications, becoming denser on follow-up radiography, or acquire a laminated aspect as they add consecutive layers of new cartilage and even bone, nourished by the synovial fluid.
The radiologic appearance of intraarticular fractures is similar to that of any other fracture in the osteoarticular system: a discontinuity of cortical or subchondral bone, a more or less sharply demarcated radiolucent line extending into the articular surface, one or more bony fragments that may or may not be displaced, soft tissue damage, and excessive joint fluid.
Magnetic Resonance Imaging
The main advantage of MRI is the direct visualization of the articular cartilage. The ideal MR pulse sequence for the evaluation of articular cartilage in general and, more to the point, of acute cartilage injury should have a number of properties. Most importantly, it must display cartilage with an optimal contrast and spatial resolution. It must be able to show changes in the subchondral bone plate and display its exact thickness. It should detect bone marrow edema, subchondral cysts, and granulation tissue, on the one hand, and changes in the internal structure of cartilage on the other hand. These changes should be clearly visible, in both the superficial and the deep layers of cartilage. It should also allow segmentation, volume calculation, and three-dimensional (3D) reconstruction. At 1.5 T, two sequences broadly used in clinical practice allow good morphologic evaluation of cartilage and chondral abnormalities. These are the fast spin-echo (FSE) sequences, either 2D or 3D, and the 3D gradient-echo (GRE) sequences.
Proton-density and T2-weighted FSE images, especially with fat suppression, accurately detect chondral abnormalities owing to a higher signal in the joint fluid compared with the articular cartilage. The advantages of these sequences in 2D form are their short acquisition time, high signal-to-noise ratio (SNR), and resistance to artifacts. Unfortunately, they do not display the deepest cartilage layers well, which may lead to overestimation of the depth of a cartilage lesion.
3D-GRE images, using either water-selective excitation or fat-suppression techniques, are best suited for the evaluation of the deeper regions of cartilage. The sensitivity and specificity of these sequences in demonstrating cartilage lesions was reported to be higher than that of FSE sequences, but more recent studies report a similar accuracy. These sequences allow easy multiplanar reconstructions and cartilage volume measurements. They are, however, still hampered by image artifacts.
At 3 T, this sequence has been surpassed by other 3D gradient echo sequences, notably the double-echo steady-state (DESS) sequence with water excitation and the sampling perfection with application-optimized contrast using different flip-angle evolutions (SPACE) sequence, an FSE sequence. Both are 3D sequences with high SNR and contrast-to-noise ratio (CNR).
Detection and visualization of meniscus and cartilage pathologies with standard 3D-FSE is comparable to 2D-FSE at 3 T. According to Notohamiprodjo and colleagues, optimized 3D-SPACE even provides significantly higher signal and contrast than conventional 2D-FSE, most notably for fluid and cartilage, leading to improved diagnostic confidence, particularly in problematic areas such as the femoral trochlea. However, 3D-SPACE cannot be used as a single sequence in the MR evaluation of the knee at 3 T. Knee MR protocols at 3 T should include both 2D- and 3D-FSE sequences, as the combination of both leads to improved diagnostic yield in detecting meniscus, anterior cruciate ligament, and cartilage lesions.
The diagnosis of cartilage lesions on MRI is based on several criteria. First, a contour defect must be visualized. This is only possible on MR sequences that allow good differentiation between cartilage and intraarticular fluid.
In general, if the edges of the contour defect are sharp and the cartilaginous lesion is accompanied by bone marrow edema in the subjacent bone, an acute lesion must be suspected. A shallow lesion with wide margins and a more gradual slope to its edges suggests a chronic, degenerative lesion ( Fig. 29-8 ). Acute cartilage damage can also manifest itself as a tear in the cartilage, as discussed earlier.
A second criterion is focal thinning compared with the width of the surrounding cartilage. A third and more debated argument allowing the diagnosis of cartilage injury is the presence of circumscribed signal alterations. Although it is not always possible to differentiate these changes from imaging artifacts, focal areas of signal change are still considered suspect for cartilage injury.
Posttraumatic abnormalities in the subchondral bone are also well visualized on MRI. Minor trauma to the subchondral bone gives rise to a bone bruise, which is a combination of trabecular microfractures and bone marrow edema. On MRI, this is seen as a poorly demarcated area of high signal in the subchondral bone on fat-suppressed proton-density and T2-weighted images. It may be the only abnormality found on MRI because trabecular microfractures are not discernable. The patterns are indicative of the mechanism of the injury and provide clues to associated soft tissue injuries.
After more extensive trauma, curvilinear hypointense fracture lines can be seen on T1-weighted images. These tend to occur in trauma where the forces acting on the joint run approximately parallel to the articular surface. On T2-weighted images, their signal intensity can be either high or low, depending on the presence or absence of fluid or blood in the fracture line. As mentioned earlier, fracture lines can reenter the articular surface, creating completely or partially detached osteochondral fragments that may become displaced ( Fig. 29-9 ).
When the forces that arise during trauma run perpendicular to the joint surface, true compression fractures can occur. These are characterized by a flattened, hypointense area adjacent to the subchondral bone plate, with or without disruption of the bone end plate ( Fig. 29-10 ).
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